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CAR-T cell therapy for cancer: current challenges and future directions

Inés Zugasti, Lady Espinosa-Aroca, Klaudyna Fidyt and 7 more

Signal Transduction and Targeted Therapy · 2025 · Review · CC BY

Abstract

Chimeric antigen receptor T (CAR-T) cell therapies have transformed the treatment of relapsed/refractory (R/R) B-cell malignancies and multiple myeloma by redirecting activated T cells to CD19- or BCMA-expressing tumor cells. However, this approach has yet to be approved for acute myeloid leukemia (AML), the most common acute leukemia in adults and the elderly. Simultaneously, CAR-T cell therapies continue to face significant challenges in the treatment of solid tumors. The primary challenge in developing CAR-T cell therapies for AML is the absence of an ideal target antigen that is both effective and safe, as AML cells share most surface antigens with healthy hematopoietic stem and progenitor cells (HSPCs). Simultaneously targeting antigen expression on both AML cells and HSPCs may result in life-threatening on-target/off-tumor toxicities such as prolonged myeloablation. In addition, the immunosuppressive nature of the AML tumor microenvironment has a detrimental effect on the immune response. This review begins with a comprehensive overview of CAR-T cell therapy for cancer, covering the structure of CAR-T cells and the history of their clinical application. It then explores the current landscape of CAR-T cell therapy in both hematologic malignancies and solid tumors. Finally, the review delves into the specific challenges of applying CAR-T cell therapy to AML, highlights ongoing global clinical trials, and outlines potential future directions for developing effective CAR-T cell-based treatments for relapsed/refractory AML.

Full text

From PubMed Central, U.S. National Library of Medicine, as current on Oct 19, 2026. Paragraph numbers are ours, so an answer can point at one.

Introduction

1Acute myeloid leukemia (AML) is the predominant form of leukemia in adults, with a median age at diagnosis of 68 years., It is primarily characterized by a high degree of complex clonal heterogeneity., For patients eligible for high-dose chemotherapy, treatment typically involves a combination of cytarabine and daunorubicin or idarubicin. Additionally, for those classified as intermediate or high risk according to the European Leukemia Net 2022 (ELN22) risk stratification, allogeneic hematopoietic stem cell transplantation (alloHSCT) is often performed following initial chemotherapy. However, elderly patients or those with comorbidities who are ineligible for alloHSCT are typically treated with low-intensity regimens. These regimens include venetoclax combined with hypomethylating agents (HMAs),, low-dose cytarabine,, or targeted molecules such as FLT3-directed tyrosine kinase inhibitors,, as well as HMAs with IDH1/2 inhibitors.,

2Despite the great efforts that have been made in recent years and the approval of new targeted therapies, relapsed/refractory (R/R) AML remains the leading cause of treatment failure. This challenging scenario occurs in 40-50% of patients younger than 60 years of age, and in up to 80% of patients older than 65 years, many of whom are ineligible for alloHSCT or intensive chemotherapy.– There is currently no standardized treatment protocol for these patients, and the 5-year overall survival (OS) rate is below 20%. Therefore, R/R AML remains an unmet clinical need, and further investigation is urgent. For patients who meet eligibility criteria, alloHSCT is the only potentially curative option in this setting.

3The success of alloHSCT and other cell therapy-based strategies, such as donor lymphocyte infusion (DLI), relies on the capacity of T and natural killer (NK) cells to target and eliminate leukemic cells, underscoring the sensitivity of AML to immunotherapy. This has prompted interest in novel immunotherapeutic approaches, which are currently being explored. For example, some clinical trials have tested immune checkpoint blockade strategies, including the anti-TIM3 monoclonal antibody (mAb) sabatolimab (NCT04266301), with limited results, or antibodies targeting CD47 (e.g., magrolimab, lemzoparlimab). A clinical trial is currently underway (NCT03113643) testing a recombinant protein consisting of interleukin (IL)-3 fused to a truncated diphtheria toxin payload that targets CD123 (tagraxofusp). Additional ongoing strategies include the use of menin inhibitors targeting the HOX/MEIS1 transcriptional program, in combination with chemotherapy, for KMT2A rearranged- or NPM1-mutated AML, with encouraging results.,

4However, despite the excellent clinical outcomes observed with several chimeric antigen receptor T (CAR-T) cell products targeting CD19 or BCMA in the treatment of R/R B-cell malignancies and R/R multiple myeloma (MM), no CAR-T cell product has yet received regulatory approval for AML. This review offers an overview of the current development of CAR-T cell therapies for both hematologic and solid tumors, while examining the challenges associated with their application in AML, ongoing clinical trials, and future directions for optimizing CAR-T cell therapy in the treatment of AML.

CAR-T cell structure

5CARs are engineered receptors consisting of a combination of an endodomain, an anchoring transmembrane domain, and an ectodomain., The latter is a ligand-specific extracellular domain consisting of a single-chain variable-fragment (scFv) region and a hinge. The scFv is a fusion protein of the variable regions of the light and heavy chains of immunoglobulins linked by a short flexible peptide linker. The hinge, also known as a spacer, separates the binding units from the transmembrane domain. Most CAR-T cells are designed with immunoglobulin-like domain hinges, which provide flexibility in accessing the target antigen., The endodomain may consist of the intracellular T cell activation domain of CD3ζ as a single entity or by one or more intracellular co-stimulatory (or activation) domains. While the scFv provides antigen specificity, the co-stimulatory domains are key to the activation of effector T cells. CAR-T cells are classified into five generations based on the endodomain (Fig. 1).–

6The first-generation CAR-T cells comprised a single fragment derived from the CD3ζ chain.– These cells depended on exogenous cytokine production, exhibited insufficient persistence and T cell activation, and consequently, did not achieve the desired results in most studies.– Accordingly, first-generation CARs have been superseded by second-generation CARs, which feature an intracellular signaling domain comprising a variety of co-stimulatory protein receptors situated within the cytoplasmic tail of the CARs, such as CD28 or CD137 (4-1BB).– These co-stimulatory proteins can enhance proliferation, cytotoxicity, and prolong persistence.

7Third-generation CARs integrate multiple signaling domains, including CD28, 4-1BB, ICOS, and/or OX40.– Fourth-generation CAR-T cells, also known as “T cells redirected for universal cytokine-mediated killing” or “TRUCKs” are engineered to release cytokines into the tumor microenvironment (TME). They may also express additional proteins such as chemokine receptors, switch receptors, bispecific T cell engagers (BiTEs), and blockers/inducers of specific signaling pathways.–

8In this context, next-generation CAR-T cells are currently underway. The fifth-generation differs from the previous versions by integrating an additional membrane receptor. Several approaches are being explored, with one of the most promising involving the incorporation of IL-2 receptor signaling to enable antigen-dependent JAK/STAT pathway activation.– This signaling not only sustains CAR-T cell activity and promotes memory T cell formation but also reactivates and stimulates the broader immune system.

9Modifying T cells to express CARs typically involves transducing the cells with viral vectors containing the transgene, which leads to the semi-random integration of DNA into the T-cell genome. Interestingly, some fifth-generation strategies use specific site-integrations that provide additional features, which can be achieved through CRISPR mediated editing. One example is the insertion of the CAR into the TRAC locus (T cell receptor alpha constant). The TRAC locus is a constant region within the T cell receptor (TCR) alpha chain gene. This genetic editing allows the suppression of the expression of the endogenous TCR to ensure specific antigen recognition while avoiding potential interference from the natural TCR. By integrating TRAC, fifth-generation CAR-T cells maintain greater stability and identity over time, improving their ability to recognize and eliminate cancer cells. This genetic modification reduces the risk of T-cell exhaustion, graft-versus-host effect, and enhances the overall efficacy of CAR-T therapies, offering a more durable and potent treatment option. In line with this, an additional innovative strategy has integrated the CAR cassette into the PDCD1 gene locus demonstrating a superior ability to eradicate cancer cells both in vitro and in xenograft models.,

10All six of the currently approved CAR-T cell constructs are second-generation CARs. Axicabtagene ciloleucel (Yescarta®) and brexucabtagene autoleucel (Tecartus®) are CD28-based, whereas the remaining approved constructs are 4-1BB-based. Most approved products employ a murine scFv except for ciltacabtagene autoleucel (Carvykti®), which utilizes a camelid binding domain. As exposed in the following sections, to further improve the efficacy of CAR-T cell therapy, the different CAR components have been engineered, resulting in constructs with enhanced properties.,,

History of CAR-T cell implementation

11Modern CAR-T cell therapy is the culmination of decades of groundbreaking immunology and genetic engineering research. Here, we provide a brief overview of the key contributions that paved the way for its first approvals and subsequent use in thousands of patients worldwide (Fig. 2).

12The remarkable success of CAR-T cell therapy would not have been possible without foundational discoveries in immunology. The identification of T cell origin,, and the pioneering work of Dr. Eva and Dr. George Klein, who demonstrated that immune cells can eradicate cancer, were crucial milestones. In subsequent years, significant contributions were made by Dr. Steven Rosenberg at the National Cancer Institute (NCI), who pioneered the use of tumor-infiltrating lymphocytes (TILs) to treat selected solid tumors in patients.– While Rosenberg and colleagues highlighted the undeniable potential of cytotoxic T cells to combat cancer, TIL therapy faced challenges, including low reproducibility in TIL expansion and the restriction of its use to immunogenic tumors due to major histocompatibility complex (MHC) dependency. These limitations spurred researchers to address these challenges and explore ways to harness the anticancer potential of T cells across a broader range of malignancies, including poorly immunogenic tumors. This led to the groundbreaking concept of reprogramming T cells for enhanced specificity.

13The concept of CARs originated from two groundbreaking studies conducted in the late 1980s. In 1987, Dr. Yoshikazu Kurosawa and colleagues engineered modified cells expressing T cell receptors (TCRs) with their variable regions replaced by the antigen-binding site of an antibody, creating receptors that functioned independently of MHC interaction. Similarly, in 1989, Dr. Zelig Eshhar and his team developed analogous constructs. They successfully generated “T-bodies,” functional chimeric receptors that recognized a hapten, confirmed by their ability to kill target-expressing tumor cells and produce cytokines (Fig. 2). Notably, Eshhar and colleagues proposed for the first time the potential use of CAR-modified T cells to combat cancer, laying the groundwork for subsequent innovations. A few years later, the same team introduced pivotal constructs of what are now considered first-generation CARs (Fig. 1). These early receptors, containing an anti-hapten antibody-derived scFv linked to the intracellular CD3ζ chain, were successfully expressed in murine cytotoxic T lymphocyte (CTL) hybridoma cells. However, these first-generation CAR-T cells exhibited limited proliferation and killing capacities.,, Moreover, their introduction to murine cells highlighted the need for optimized CAR-T production protocols, particularly to effectively modify and expand human T cells ex vivo. At this time, Dr. Michel Sadelain at Memorial Sloan Kettering Cancer Center (MSKCC) made significant advancements in T-cell engineering by improving retroviral modification methods. Sadelain’s work on CAR design included the introduction of the CD28 co-stimulatory domain, which enhanced CAR T cell persistence and survival. These advances were influenced by earlier research led by Dr. Carl June at Children’s Hospital of Philadelphia (CHOP), whose pivotal study a decade earlier established the critical role of CD28 co-stimulation in T cell proliferation and cytokine production, complementing CD3 signaling. Collectively, the tremendous efforts of scientists in the late 20th century provided the foundational knowledge and technical advancements necessary for the eventual clinical implementation of CAR-T cell therapy.

14In the early 2000s, Sadelain’s team emerged as a leader in advancing CAR-T cell research. A pivotal breakthrough came with Maher et al. who introduced second-generation CARs to primary human T cells (Fig. 1). Although this was not the first report of CARs incorporating the CD28 co-stimulatory domain upstream of the CD3ζ chain, Maher and colleagues were the first to demonstrate successful modification of primary human T cells to express second-generation CARs targeting prostate-specific membrane antigen (PSMA). These anti-PSMA CAR-T cells exhibited sustained proliferation and responsiveness to repeated stimulation by PSMA-expressing cancer cells, achieving the first fully effective CAR-T product.

15Just one year later, researchers from MSKCC delivered another transformative milestone in immunotherapy. While early CAR-T development primarily focused on optimizing signaling constructs to enhance proliferation and persistence, selecting an ideal antigen to target became equally critical. Initial preclinical studies with first- and second-generation CARs targeted solid tumor-associated antigens, including disialogangliosides (GD2, GD3), carcinoembryonic antigen (CEA), and PSMA. However, Sadelain and his team shifted their focus to hematological malignancies, proposing CD19 as a promising antigen nearly 15 years before its clinical implementation in CAR-T therapy. In a landmark 2003 study, the MSKCC team demonstrated the feasibility of expanding CAR-T cells ex vivo using artificial antigen-presenting cells and IL-15. These CD19-targeted CAR-T cells achieved sustained persistence in immunodeficient murine models with established B-cell tumors. Around the same time, other research groups in the US—at institutions such as the National Cancer Institute (NCI), CHOP, and Baylor College of Medicine—also identified CD19 as a highly promising tumor-associated antigen.,– These efforts collectively focused on treating B-cell-derived malignancies, including B-cell acute lymphoblastic leukemia (B-ALL), chronic lymphocytic leukemia (CLL), and B-cell non-Hodgkin lymphoma (B-NHL), which uniformly express CD19 on their surfaces (Fig. 2). This concerted effort to target CD19 revolutionized the field and set the stage for CAR-T therapy’s transformative impact on hematologic cancers.

16After CD19 was identified as the optimal target for immunotherapy, a critical milestone was the development of scalable manufacturing protocols for clinical-grade CAR-T cells. Until 2010, the efficacy of CD19 CAR-T cells had been primarily evaluated in vitro and in murine models, which required relatively small numbers of effector cells. However, preparing CAR-T cells for clinical use demanded protocols capable of large-scale production. In 2009, Hollyman et al. described a process for autologous T cell activation, transduction, and expansion in bioreactors, enabling the generation of sufficient cell numbers for clinical applications. This advancement opened new opportunities for future clinical trials. By May 2010, nine independent single-center clinical trials were registered across the US, with three more under regulatory review. Investigators published data from individual case studies before collective clinical trial results were available. The first report of CD19 CAR-T therapy in a patient came from Rosenberg’s group at the NCI, detailing a case of relapsed B-NHL. This study used autologous T cells engineered with a second-generation CAR construct incorporating anti-CD19 scFv (anti-FMC63 epitope), a CD28 co-stimulatory domain, and a CD3ζ signaling chain. In the following months, additional studies reported the use of CD19 CAR-T cells in patients with B-cell-derived malignancies. The first clinical results from the CHOP described treating CLL,, while researchers at MSKCC reported outcomes for adult B-ALL., Notably, the CHOP trials utilized CD19 CAR-T cells designed with the 4-1BB co-stimulatory domain (CD19-BB-z), a construct initially introduced by Dr. Dario Campana and Dr. Chihaya Imai at St. Jude Children’s Research Hospital. These early clinical studies established the foundation for the rapid progression of CAR-T therapy from experimental models to transformative cancer treatments (Fig. 2).

17While early CD19 CAR-T cell clinical trials primarily enrolled R/R adult patients, a groundbreaking milestone was achieved in 2012 when physicians and scientists from CHOP administered CD19 CAR-T therapy to the first pediatric patient with B-ALL. The treatment garnered worldwide attention as the patient achieved morphologic remission within a month of CAR-T cell infusion. Remarkably, as of 2024, this patient remains cancer-free after 12 years, highlighting the life-saving potential of CAR-T therapy. The treatment, however, was not devoid of high-grade adverse effects and severe cytokine release syndrome (CRS), which was manifested by high IL-6 levels. Fortunately, the CHOP team, led by Dr. Carl June, obtained permission for the “off-label” use of tocilizumab—a humanized monoclonal antibody targeting the IL-6 receptor—originally approved for treating rheumatoid arthritis. The successful management of CRS with tocilizumab was a pivotal moment in CAR-T therapy, and IL-6 receptor antagonists are now the standard of care for CRS management in CAR-T-treated patients,, even prophylactically. This case showcased CAR-T cells’ efficacy in pediatric cancer., It underscored the importance of effective strategies to manage treatment-associated toxicities, paving the way for safer and more accessible CAR-T therapies.

18In the subsequent years, additional results from single-center trials demonstrated sustained remissions in patients treated with CD19 CAR-T, including adults and children with B-ALL, and adults with B-NHL or CLL., The successful responses in these pivotal trials prompted collaborations between scientists, clinicians, and biopharma companies to further develop and implement this treatment, ultimately acquiring the necessary regulatory approvals. Notably, June’s team at CHOP partnered with Novartis, Rosenberg’s team at NCI collaborated with Kite Pharma, and researchers from MSKCC, Seattle Children’s Research Institute, and Fred Hutchinson Cancer Research Center founded Juno Therapeutics. As a result, CD19 CAR-T received breakthrough therapy designation from the FDA in 2014, and the global multi-center trials culminated in the first approvals in 2017. Specifically, Kymriah® (CD19-BB-z) became the first approved cell-based therapy for R/R B-ALL in patients under 25 years old, while Yescarta® (CD19-28-z) was approved for adult R/R B-NHL, based on the ELIANA,, and and ZUMA-1 trials, respectively.

19These landmark approvals resulted from over 30 years of groundbreaking research and the dedicated efforts of scientists and clinicians. Despite the success of these CAR-T therapies, challenges remain in gaining approval for their use in all blood cancers and solid tumors. In the following sections, we will present an overview of the current role of CAR-T cells in hematologic malignancies with a major focus on AML and solid tumors, followed by the key difficulties involved in implementing adoptive cell therapies for patients with AML.

CAR-T therapies for hematologic malignancies and solid tumors: current scenario

20The US Food and Drug Administration (FDA) has approved six CAR-T cell therapies for the treatment of various hematologic malignancies. Kymriah®, a second-generation CAR-T cell therapy targeting the B cell antigen CD19, was the first CAR-T cell therapy to receive approval by the FDA and the European Medicines Agency (EMA) for the treatment of children and young adults with ALL.,, The FDA and EMA have subsequently approved three additional CAR-T cell therapies targeting the CD19 antigen: Yescarta®,– Tecartus®,, and lisocabtagene maraleucel (Breyanzi®)., In addition, two B cell maturation antigen (BCMA) CAR-T cell products have been approved for the treatment of R/R MM, idecabtagene vicleucel (Abecma®) in March 2021 and Carvykti® in February 2022.,, Currently, several clinical trials are ongoing testing these six CAR-T cells for further indications (Table 1).

21CAR-T therapy has been a breakthrough treatment for hematologic cancers, but its effectiveness in solid malignancies has been limited. To date, no CAR-T cell therapy has been granted FDA or EMA approval for solid tumors (Table 1), highlighting a critical need for progress in this context. Several factors may contribute to the limited effectiveness of CAR-T cells in solid malignancies, such as the antigen heterogeneity and the tumor microenvironment (TME). The TME is characterized for being highly immunosuppressive, hypoxic, and fibrotic, thus creating a physical and biological barrier that prevent CAR-T cells from accessing the tumor cells. Moreover, several studies have shown limited CAR-T cell expansion and shorter persistence in patients with solid tumors.–

22A clinical case report indicates a response to multiple doses of intracranial IL-13Ra-targeted CAR therapy in a patient with recurrent multifocal glioblastoma, which was sustained for 7.5 months after starting treatment. Some evidence regarding GD2-specific CAR-T cells in four pediatric patients with H3K27M-mutated glioma has also been reported, with three of four patients exhibiting clinical and radiographic improvement.

23Recent studies with larger cohorts in the solid tumor field have demonstrated significant antitumor effects. Notably, a claudin18.2-targeted CAR has proven effective in treating gastrointestinal tumors in a study including 37 patients (NCT04196413), with an overall response rate (ORR) and disease control rate (DCR) of 48.6% and 73.0%, respectively. Moreover, a GD2-specific CAR has shown strong results in 27 children with heavily pretreated neuroblastoma (NCT03373097). In this study, ORR was 63%; 9 patients had a complete response, and 8 had a partial response. Among those patients who received the recommended dose, the 3-year overall survival and event-free survival were 60% and 36%, respectively. The security profile was reasonable.

24While CAR-T cell therapies are not yet approved for solid tumors, other T lymphocyte-based treatments have recently been authorized. One of them is the gp100 peptide-MHC/CD3 bispecific T-cell engager (TCE) tebentafusp which was approved for uveal melanoma in 2022. Moreover, an autologous TCR T cell therapy named afami-cel is currently being tested in heavily pre-treated patients with HLA-A*02 and MAGE-A4-expressing synovial sarcoma. The phase 2 trial (NCT04044768) resulted in an ORR of 37% and durable responses. Other cellular therapies have also shown promising responses in treating certain solid tumors like HPV-associated cancers.–

25Collectively our understanding of the underlying reasons for the humble clinical activity observed in CAR-T cell trials involving solid tumors remains under investigation. In the following pages, we will examine the current application of CAR-T cells in the treatment of another disease, which, similar to solid tumors, remains challenging for CAR-T cell therapy: acute myeloid leukemia (AML).

CAR-T cell-associated challenges in AML

26The experience gained from treating R/R B-cell malignancies and R/R MM with CAR-T cell therapy has identified several characteristics associated with promising outcomes. These include the CAR molecular structure and co-stimulatory domains, the targeted antigen, the method of transduction, the lymphodepletion regimen prior to cell infusion, the infused cell doses, the heterogeneity of the patient population, and the intrinsic features of the tumor cells, among others. The primary challenges in the AML setting are three-fold: i) the clonal heterogeneity of the disease, ii) the highly immunosuppressive bone marrow (BM) microenvironment, and iii) the lack of tumor-specific target antigens (Fig. 3).,,

AML heterogeneity

27Nowadays, acute myeloid leukemia (AML) is a broad category that encompasses various diseases, each with distinct molecular and cytogenetic abnormalities.– This molecular and cytogenetic heterogeneity is reflected in the current diagnostic reality, where there are three major international classifications: the WHO 2022, which defines 11 AML groups based on genetic abnormalities; the ELN 2022, which is based on the previous one, but identifies 14 AML groups and is focused on prognosis and management; and the ICC 2022, which recognizes 18 entities. While new risk-stratifying molecular subgroups of AML may emerge over time, not all gene expression subtypes correlate well with disease-associated gene fusions or mutations.

28This heterogeneity arises from multiple factors influencing disease presentation, progression, and response to treatment. AML is characterized by a diverse array of genetic mutations that affect key pathways, including signal transduction (FLT3), epigenetic regulation (DNMT3A, IDH1/2, EZH2), and apoptosis (TP53). These mutations drive distinct transcriptional programs, contributing to variability in disease behavior and drug sensitivity. Additionally, chromosomal translocations (e.g., t(8;21), inv(16), t(15;17)) further influence AML prognosis and treatment strategies. Another layer of complexity comes from the clonal evolution of AML, where subclones with distinct genetic profiles contribute to intratumoral heterogeneity. These molecular and cytogenetic alterations serve as the foundation for prognostic classifications, as they are crucial factors influencing treatment outcomes and survival. For instance, AML with a complex or monosomal karyotype, structural abnormalities involving chromosome 3, TP53 mutations, high allelic ratio FLT3 mutations, or mutations in ASXL1, BCOR, EZH2, RUNX1, SF3B1, SRSF2, STAG2, U2AF1, and ZRSR2 (classified as AML with myelodysplasia-related gene mutations), are associated with treatment resistance and relapse, placing it in the ELN 2022 adverse prognostic group.

29AML is thought to mirror normal hematopoiesis, with leukemia stem cells (LSCs) sustaining the disease by driving the production of differentiated blasts. First described in the 1960s, LSCs are characterized by low cycling or quiescence, self-renewal capacity, and transcriptional or epigenetic signatures similar to hematopoietic stem cells (HSCs) and normal multipotent hematopoietic progenitors. LSCs exhibit therapy resistance due to their quiescent state and self-renewal potential. They originate from the sequential accumulation of somatic mutations in HSCs or HSPCs, or even more differentiated cells, where early mutations enhance self-renewal and impair differentiation, leading to the expansion of pre-leukemic clones. Common early mutations involve genes regulating epigenetics (DNMT3A, TET2, IDH1/2, ASXL1) and TP53, while later mutations, such as those in FLT3, drive proliferation, block differentiation, and ultimately lead to AML blast formation.

30This developmental hierarchy is even more complex at relapse, comprising distinct subclones of leukemia cells with disparate phenotypic, genetic and epigenetic features coexisting within a single patient.,, This complexity may impede CAR-T cell development by facilitating antigen escape.

BM microenvironment

31AML blasts and LSCs present immune evasion mechanisms, in addition to remodeling of the BM microenvironment, which collectively drives disease progression., While these factors were once considered to have a limited role, recent studies have highlighted their crucial contribution to the advancement of the disease.

32First, among the intrinsic factors directly related with the myeloid blast, mutations in NPM1 and FLT3 have been linked to alterations in immune response., Furthermore, the effects of mutant IDH1/2 and the subsequent increase of the oncometabolite R-2-hydroxyglutarate (R2-HG) have been associated with the augment of regulatory T cells (Tregs) in AML., TP53 mutations have also been shown to impede immune surveillance.– Other intrinsic features described in AML include downregulation of HLA molecules, leading to defective antigen presentation–; and alterations in cytokine balance.–

33Secondly, it is well documented that the highly immunosuppressive BM microenvironment deleteriously affects immune responses and T cell fitness. On one hand, metabolic products within the TME play a significant role in immune suppression, limiting the effectiveness of immunotherapies. AML cells exhibit altered metabolism, producing lactate, adenosine, and kynurenine, which contribute to a hostile microenvironment that impedes the function of CAR-T cells.– Elevated lactate levels, resulting from rapid glycolysis in AML blasts, can acidify the TME, suppressing T cell activation and proliferation. This acidic environment not only limits the effector functions of CAR-T cells but also promotes the accumulation of Tregs and myeloid-derived suppressor cells (MDSCs, pathologically activated neutrophils and monocytes with potent immunosuppressive activity–), both of which further dampen immune responses. Additionally, adenosine, often elevated in the TME, binds to receptors on CAR-T cells, leading to immune suppression and exhaustion., Similarly, kynurenine, generated through tryptophan catabolism by AML cells, also inhibits T cell function and promotes an immunosuppressive setting.

34On the other hand, AML is characterized by an increase in the number of T cells that infiltrate the BM compared to those observed in healthy individuals. These T cells exhibit an increase in the frequency of immune inhibitory and activating co-receptor expression, particularly in R/R AML.– This includes the expression of PD-1,, OX40, TIM3, and LAG3. Overall, T cells display insufficient potency, persistence, and functionality in this context. This T cell exhaustion, which may be present in the apheresis-derived T cells or emerge during the CAR-T cell manufacturing process,, is typically not only characterized by high expression of inhibitory receptors, but also is related to extensive transcriptional and epigenetic alterations, defective cytokine production, increased chemokine expression, and a shift from T cell to NK-like T cell phenotypes.,,

35In third place, in addition to intrinsic factors directly associated with the myeloid blast, its metabolism and other factors related to T cells, the expansion of M2 macrophages has also been shown to enhance AML immune escape., Moreover, poor immune synapse function and impaired NK cell function have been identified as mechanisms involved in this process.– Finally, it is also important to consider the role that the bone marrow structure may play beyond the cellular components. BM vascular remodeling may hinder anti-AML immune responses by reducing cell migration and inducing hypoxia.,

Target antigen

36The identification of an appropriate target for CAR-T cell therapy in AML is crucial. A suitable target should be an HLA-unrestricted antigen/protein expressed on the cell surface of malignant cells with a high expression level. Nonetheless, some preliminary evidence suggests that lower expression levels might be sufficient to direct CAR-T cells. Ideally, the antigen should also be expressed on LSCs to ensure complete disease eradication and minimize early relapses. Importantly, it must be absent in healthy tissues to prevent potentially fatal on-target/off-tumor toxicities. To date, no optimal target for CAR-T cell therapy in AML has been identified. AML neoantigens are relatively uncommon and are known to be mainly intracellular, requiring HLA presentation.

37One of the earliest demonstrations of the potential of CAR-T cells for AML was a construct developed by Ritchie and colleagues that targeted the Lewis Y (LeY) antigen. This CAR-T was tested in a Phase 1 clinical trial, demonstrating a favorable safety profile and durable in vivo persistence. However, the efficacy of this approach was limited, and all patients relapsed with the detection of LeY-positive AML blasts. In current clinical practice, CD33 and CD123 represent the most utilized molecules for CAR-T cell engineering (Table 2, Fig. 4).

CD123

38CD123, also known as the alpha chain of the IL-3 receptor (IL-3Ra), is a membrane protein highly expressed in AML (~90% of cases),, CD123 has also been identified in other myeloid malignancies, such as myelodysplastic syndrome, chronic myelomonocytic leukemia, chronic myeloid leukemia, and myeloproliferative neoplasms, CD123 is involved in the JAK, MAPK, and PI3K/AKT signaling pathways, which regulate cell proliferation and differentiation.

39Overexpression of CD123 has been identified in up to 95% of LSCs and AML blast cells. About on-target/off-tumor toxicities, there is controversy over its expression in healthy HSCs. Some reports have identified low CD123 expression patterns on HSCs, while other preclinical studies have described a myeloablative effect of CD123-directed CAR-T cells. A significant concern is the potential extra-hematologic toxicities, as CD123 is expressed in endothelial cells, which could result in capillary leak syndrome.,

40Several unconjugated monoclonal antibodies (mAbs), including the CD123-directed mAbs CSL360 and CSL362 (talacotuzumab), have demonstrated limited efficacy in the treatment of R/R AML., Consequently, current strategies predominantly entail the use of toxin-conjugated constructs or Bi-specific T-cell engagers (BiTEs). In this line, various agents targeting CD123 have been developed, including tagraxofusp, a recombinant protein comprising a truncated diphtheria toxin fused to IL-3, which has been approved for the treatment of blastic plasmacytoid dendritic cell neoplasm (BPDCN)., Tagraxofusp has demonstrated preliminary clinical activity in the context of AML. Additional strategies targeting CD123, including BiTEs such as pivekimab sunirine (PVK, IMGN632),, vibecotamab and flotetuzumab,; as well as other strategies such as JNJ-63709178, MGD024, and APVO436, are currently under investigation, with promising results (Fig. 4).

CD33

41CD33 is a transmembrane receptor stimulated by sialic acid residues that is expressed in approximately 85% of AML cases. CD33 undergoes internalization and dimerization upon binding, making it an attractive therapy and drug delivery target. Its primary role is related to the downregulation of cytokine production and monocyte activation., It is known to be present in over 85% of LSCs, with relatively low expression in HSCs.

42The humanized anti-CD33 antibody drug-conjugated gemtuzumab ozogamicin is EMA and FDA-approved for first line use in combination with intensive chemotherapy in treatment-naïve AML.– The primary toxicities reported are persistent thrombocytopenia and veno-occlusive disease (VOD). The latter was initially associated with CD33 expression in Kupffer cells within hepatic sinusoids following FDA approval in 2000. Upon reapproval in 2017 for administration in a fractionated dosing schedule, VOD was less frequent and was subsequently reported to be associated with the direct hepatotoxicity of the conjugated drug (calicheamicin).

43In line with the evidence reported with anti-CD123 unconjugated molecules, mAbs and antibody-drug conjugates directed against CD33 (lintuzumab,– SGN-CD33A, and IMGN779) have failed to demonstrate relevant antileukemic activity to date. Notably, several CD33 × CD3 BiTEs have shown promising results with an acceptable toxicity profile in clinical trials for R/R AML (AMG 330,, AMG 673, GEM333, JNJ-67571244, and SAR440234) (Fig. 4).

CLL-1

44CLL-1, also known as CLEC12A, myeloid inhibitory c-type lectin-like receptor, dendritic cell-associated C-type lectin 2 (DCAL-2), or CD371, is a C-type lectin-like type II transmembrane receptor with a role in cell adhesion and cell-to-cell signaling.– It is expressed in over 85% of patients with AML, both in blasts and LSCs., Furthermore, it is expressed exclusively in myeloid lineage cells and is absent in granulocyte-macrophage progenitors. In addition, CLL-1 does not show relevant expression on HSCs or extra-hematological tissues,,, limiting potential on-target/off-tumor risks and making it an exciting target for investigation.

NKG2D

45Natural killer group 2 member D (NKG2D) is a highly conserved activating receptor of NK cells and T lymphocytes that plays a pivotal role in immune recognition of tumoral cells through the engagement with a group of ligands, namely MICA, MICB, and the UL16-binding proteins.– NKG2D ligands are induced in response to DNA damage, inflammation, and malignant transformation.– Expression of NKG2D ligands has been documented in different hematologic malignancies, including AML, whereas expression is generally absent in healthy tissues., Consequently, there is growing interest in NKG2D and NKG2D ligands as potential targets for CAR-T cell therapy.

CD7

46CD7 is a transmembrane protein essential for T cell and T cell/B cell interactions in early lymphoid development., It is among the earliest T cell-associated antigens expressed during T-lymphocyte maturation and is aberrantly present in approximately 30-40% of adult AML patients., An important consideration is that CD7, present on T cells, requires CD7-directed CAR-T cells with CD7 gene-knockout strategies to prevent effector T cell fratricide.– Some strategies have been successful in preliminary studies, mainly for T cell leukemia/lymphoma., Consequently, CD7 may represent a viable target for CD7 + AML.,,

CD38

47CD38 is a surface glycoprotein that plays a role in cell adhesion, migration, and intracellular calcium mobilization.– It is known to be expressed in plasma cells but is also expressed heterogeneously in myeloid cells. Combinations of the humanized mAb targeting CD38, daratumumab, with other drugs, have demonstrated efficacy in the treatment of AML and T-ALL in clinical trials (NCT03067571 and NCT03384654), with no significant cytopenia reported. Similarly, another CD38 mAb, isatuximab,, has been employed in a second-stage study (NCT03860844), investigating its use in combination with standard salvage chemotherapy in children with R/R ALL or AML in first or second relapse. No unexpected safety issues were observed, and complete response (or complete response with incomplete peripheral blood count recovery) was observed in 50% of patients in the AML cohort. Then, targeting CD38 presents a promising strategy that may additionally hold potential benefits for a variety of malignancies.

CD44v6

48CD44, or the receptor for hyaluronic acid, is a cell surface adhesive molecule implicated in the aggregation, migration, activation, and malignant transformation of leukocytes.– It is expressed on multiple tissue types, although some splice isoforms of CD44 are relatively tumor-restricted. For example, the splice site variant CD44v6 is present in over 60% of AML samples and is not shared by non-tumoral cells or HSCs, indicating that this antigen is a promising target. The available data demonstrate promising results in in vitro and in vivo mouse models.–

CD70

49CD70, or the tumor necrosis factor receptor ligand, is expressed on antigen-presenting cells and is upregulated to promote an effector CD8 + T cell response and downregulate Th17 function. Reports have identified CD70 expression in 45% of AML blasts and in 30% of LSCs, or even lower. Other studies suggest its expression in up to 75% of AML LSCs. The targeting of CD70 with a mAb (cusatuzumab) has been demonstrated to successfully eliminate AML-LSCs when combined with HMAs, making it an exciting target for CAR-T cell therapy. The preclinical evidence for CAR-T cells targeting CD70 is encouraging.,

FLT3

50FLT3 is a very well-characterized receptor ligand for HSCs maintenance and differentiation. It is implicated in 30% of patients with AML (approximately 24% involving FLT3-ITD and 7-10% involving FLT3-TKD). Some FLT3 inhibitors have already received FDA approval (midostaurin, gilteritinib) with an acceptable safety profile. Additional FLT3 inhibitors under investigation include quizartinib, sorafenib and crenolanib. To date, most data regarding CAR-T cell therapy is preclinical,– and significant concerns have been raised regarding FLT3 expression in HSCs. In this context, some constructs in development include safety switches (described in the following sections) to reduce myeloablation.

51Other potential targets currently under investigation include CD19, ADGRE2,, and ILT3. However, there is limited data available regarding their efficacy and safety.

Current strategies implemented in clinical trials

52Currently, there are 75 registered clinical trials of CAR-T cell therapy for AML (Table 2), of which 53 (71%) are Phase 1 or early Phase 1 trials, with CD33 and CD123 being the most frequently targeted antigens (Fig. 4). Most of these trials recruit patients from China and the US. Past and ongoing clinical trials of CAR-T cells for treating AML are discussed below.

CD123-CAR-T cells in clinical trials

53In 2020, a German group testing CAR-T cell therapy directed to CD123 reported the preclinical efficacy of UniCAR-T-CD123, a two-component, rapidly switchable and second-generation CAR-T. The construct carries a CD28 co-stimulatory domain that, by itself, does not recognize any surface antigen apart from a soluble adaptor named targeting module (TM), which is included in the second component., The TM is administered intravenously and confers specificity against the antigen of choice. In this case, the TM included a scFv directed to the CD123 antigen (Fig. 3). Due to the brief half-life of the TM, the interruption of its continuous intravenous administration rapidly deactivates T cell activity, which mitigates the associated toxicities.

54This strategy is currently being investigated in a Phase 1a trial in R/R AML (NCT04230265), with early promising results and an acceptable toxicity profile. Indeed, the trial was modified to include a prolonged schedule of TM administration. To date, 19 patients who have undergone extensive prior treatment have received UniCAR-T-CD123, including 12 with previous alloHSCT. CRS was observed in 12 patients, mainly grade 1 or 2. No prolonged myelosuppression was observed, and therefore rescue alloHSCT was not required. The ORR for the R/R AML population was 53%. The same group developed the world’s first CRISPR-engineered switchable allogeneic CAR-T designed to circumvent graft-versus-host disease (GvHD) and cell rejection. The trial is currently in progress and is registered as Phase 1 (NCT05949125).

55A multicentric clinical trial (NCT03190278) conducted in the US has evaluated the efficacy of universal CD123-directed CAR-T cells. This approach involved gene-editing technology to modify allogeneic T cells to express a second-generation CAR targeting CD123 (comprising CD123 scFv-4-1BB-CD3ζ). The TCR αβ was inactivated by targeting the TRAC gene using TALEN® nucleases, which helps to reduce the risk of GvHD. Furthermore, a “safety switch” was incorporated by including an RQR8 deletion ligand containing epitopes from CD34 and CD20 antigens, thereby conferring susceptibility to rituximab on the modified cells.

56The CAR-T cell product demonstrated potent antitumor activity in vitro and long-term disease-free survival in a subset of primary patient-derived BPDCN xenograft (PDX) mouse models. Concerns arose during the transition to the clinic when the first patient treated (UCART123; NCT03203369) died after developing severe CRS and pulmonary capillary leak syndrome. The trial was discontinued and later reopened for R/R AML, with the addition of a CD52 knockout, dose reduction, and an upper age limit (AMELI-01; a Phase 1 open-label dose-escalation trial testing UCART123v1.2), which is still recruiting (NCT03190278, NCT04106076). Preliminary data presented at ASH (American Society of Hematology) 2022 congress indicated that the addition of alemtuzumab to the fludarabine and cyclophosphamide lymphodepletion regimen resulted in more robust and greater UCART123v1.2 expansion, which was an essential concern in an allogeneic context. Moreover, the expansion of UCART123v1.2 correlated with a reduction in tumor burden. CRS occurred in 100% of the cohort, with some cases being severe, and therefore, systematic tocilizumab is planned to be administered for future stages.

57Alternative approaches consider CAR-T cell treatment in the context of a bridge to alloHSCT. One example is the CATCHAML trial (NCT04318678) for pediatric R/R AML. This involves a second-generation CD28 co-stimulated CAR that incorporates a CD20 safety switch (Fig. 3). To date, preliminary data from 12 patients enrolled in the trial report the absence of grade ≥2 CRS or neurotoxicity despite the heterogeneous nature of the responses observed. A phenotypic analysis conducted by the researchers revealed that CD123-CAR-T cell products were predominantly effector memory cells. Accordingly, the next generation of CD123-CAR T-cell products will be manufactured in the presence of dasatinib, with the objective of limiting T cell differentiation and exhaustion.

58Several ongoing trials are employing additional approaches targeting CD123. There is compelling preclinical evidence from a soluble tumor-targeting protein (SPRX002) that exclusively binds to AML cells expressing CD123, thereby enabling their destruction by T cells transduced ex vivo. These are known as Antigen Receptor Complex (ARC) T cells. A Phase 1 clinical trial (NCT05457010) is currently enrolling and is projected to conclude in November 2025. A strategy involving the electroporation of anti-CD123-CAR mRNA into “biodegradable” T cells in patients with R/R AML (NCT02623582) was terminated due to an absence of an anti-tumor effect. Finally, a case report from a pivotal trial testing a fourth-generation, apoptosis-inducible lentiviral CAR targeting CD123 has been published, but there is no further evidence of this construct.

59More conventional strategies such as CD123CAR (autologous CD123CAR-CD28-CD3ζ-EGFRt) have demonstrated antileukemic efficacy with acceptable toxicities in seven patients with R/R AML who had undergone prior alloHSCT (NCT02159495).,

CD33-CAR-T cells in clinical trials

60A second-generation CD33-directed CAR construct comprising lintuzumab-CD28/CD3ζ has demonstrated promising outcomes in a Phase 1/2 dose-escalation interim analysis of children, adolescents, and young adults with R/R AML (NCT03971799). This construct includes a combination of a targeting motif derived from lintuzumab (HuM195, SGN-33; an antibody that targets the distal CD33 IgV domain) linked to CD28/CD3. The rationale was based on the observation that the rs12459419 C > T single nucleotide polymorphism, associated with decreased CD33 surface expression, is present in more than 50% of AML patients.– The lintuzumab-enhanced CD33 CAR-T cells are capable of recognizing low-antigen-density AML.

61A total of 24 subjects were enrolled in the trial, of whom 12 had undergone prior alloHSCT. CD33-CAR-T products were successfully manufactured for 23 patients and subsequently infused into 19, primarily due to the progression of the disease. Four patients experienced CRS grade 3 or 4, which was successfully managed. Responses were reported in those who achieved the highest dose level. Based on the rapid clinical efficacy observed at dose level 4, enrollment has resumed in Phase 2. The authors highlight that despite the considerable inter-patient heterogeneity of apheresis products, the centralized manufacturing of CD33-CAR-T cells was feasible for the 6 participant centers. Notably, the authors did not report sinusoidal obstruction syndrome, a complication that has been previously associated with gemtuzumab.

62A Phase 1 clinical trial conducted at MD Anderson Cancer Center evaluated the efficacy of a 4-1BB and CD3ζ endodomain co-expressed with a truncated human epidermal growth factor receptor but failed to demonstrate an anti-leukemic effect (NCT03126864). The researchers encountered difficulties regarding the efficiency of transduction and the complexity of the clinical setting, given the 2–4 weeks required for production (risk of AML progression and other clinical complications such as infections). As a consequence of this, the trial was closed after the enrollment of 11 patients. The current focus of research is on the development of a platform that will facilitate more rapid production and in vivo expansion of a product referred to as PRGN-3006 or UltraCAR-T. The preliminary responses were encouraging, reason why the product gained the fast-track designation by the FDA. The UltraCAR-T is based on a non-viral Sleeping Beauty system to express the CAR, as well as a membrane-bound IL-15 for stronger in vivo expansion and persistence. Furthermore, the construct contains a safety switch that can conditionally eliminate CAR-T cells, thereby improving the toxicity profile (Fig. 3).

63The addition of a potentiating molecule linked to human CD33 scFv via a self-cleaving P2A peptide has been reported to functionally enhance CD33-CAR-T cells and render them safe. Furthermore, this approach has demonstrated anti-leukemic efficacy, as revealed in a preliminary report at ASCO 2024 (NCT04835519). An intriguing strategy comprising a combination of VCAR33 (allogenic CARs with a lintuzumab-derived binding domain and a CD28 co-stimulatory domain) is currently enrolling patients in a Phase 1/2 study (NCT04849910), with the possibility of subsequent CD33-deleted alloHSCT consolidation.

64An additional conceptually appealing approach may be the drug-induced dimerization of split CAR designs, which allow for cycles of tumor killing interspersed with periods of myeloid recovery. These strategies may permit physicians to modulate CAR activity based on clinical needs. In this context, a CD33-targeted dimerizing agent-regulated immunoreceptor complex (DARIC) is currently being evaluated. The platform comprises separate antigen targeting and T cell signaling components, with embedded extracellular rapamycin-dependent heterodimerizing domains (Fig. 3). The targeting and signaling components undergo dimerization in the presence of rapamycin, thereby eliciting antigen-responsive T cell activation. Appelbaum et al. reported evidence of in vitro and in vivo antitumor activity against established CD33+ human tumor xenografts in NSG (NOD scid gamma) mouse models. However, the Phase 1, PLAT-08 trial of SC-DARIC33 in pediatric patients with AML was put on hold by the FDA following a severe grade 5 adverse event report.

65Finally, an interesting study performed multiplexed base editing to remove TCR, CD52, and the shared AML/T lineage antigen CD7 from T cells, which enabled the generation of universal donor CAR-T cells (BE-CAR33, BE-CAR7) for combinational use. Preclinical data demonstrated the robust activity of BE-CAR33 alone and in combination with BE-CAR7 against human CD7 + CD33 + AML cells in a PDX model from a KIT-mutated AML patient. Preliminary results from other early clinical trials of CAR-T cell strategies targeting CD33 have shown promising results with acceptable safety profiles.,,

CLL1-CAR-T cells in clinical trials

66A second-generation murine anti-CLL-1 scFv with an intracellular domain of CD28 and OX40 and a PD-1 silencing shRNA sequence, to strengthen CAR-T function, has been tested in a Phase 1 trial. Two patients who had previously undergone anti-CD38 CAR-T cell therapy and experienced treatment failure achieved a complete response, although no further follow-up has been provided. In a similar strategy, the CB-012 platform has been engineered with next-generation Cas12a CRISPR hybrid RNA-DNA (chRDNA) genome-editing technology to target both checkpoint function and immunomodulation, which has the potential to improve antitumor activity (AMpLify Phase 1 clinical trial) (Fig. 3). In other preliminary studies, CAR-T cells directed against the CLL1 antigen have also been reported to be safe and provide a promising response rate in heavily pretreated patients,

Other targets in clinical trials

67CD38 has been targeted in a Phase 1/2 CD38-CAR-T cell therapy in six patients with R/R AML post-alloHSCT (NCT04351022). CD38-CAR-T cells were manufactured without incident, with four products derived from an autologous source and two from a donor source. Four weeks after the infusion of CD38-CAR-T cells, the ORR was 66.7% (4/6 patients) including one patient who achieved complete remission (CR) and three patients who achieved complete remission with incomplete count recovery (CRi) and full donor chimerism. The 6-month OS and leukemia-free survival rates were both 50%, with a median of 7.9 and 6.4 months, respectively. Toxicities were considered acceptable.

68Some interesting strategies are being explored that target CD7. A recent study involving seven patients with R/R AML suggested that sequential treatment with CD7-CAR-T cells followed by haploidentical HSCT may be both safe and effective, leading to durable responses. Other strategies include autologous nanobody-derived fratricide-resistant CD7-CAR-T cells. Notably, an off-target CD7 blockade strategy was developed employing a tandem CD7 nanobody VHH6 coupled with an endoplasmic reticulum/Golgi-retention motif peptide, effectively sequestering the CD7 surface marker intracellularly (Fig. 3).

69A Phase 1 dose-escalation study was conducted to evaluate the efficacy of NKG2D-CAR-T cells for R/R AML and high-risk myelodysplastic syndrome without lymphodepletion conditioning (NCT02203825). However, no notable expansion or objective clinical efficacy was observed. The possible explanations for the observed results include the lack of a costimulatory domain in the CAR construct, heterogeneous NKG2D ligand expression in the patients, and the conserved nature of NKG2D, which may be related to the lack of immunogenicity.,

70Finally, a Phase 1 trial is currently evaluating a bispecific CLL1-CD33-CAR with two complete CAR constructs connected by a P2A cleavable linker (NCT03795779). Nine patients were treated until September 2019; eight treatments were manufactured from autologous cells, while a ninth was derived from an HLA-matched sibling donor. Two patients experienced grade 3 or 4 CRS, four patients experienced immune effector cell-associated neurotoxicity syndrome (in 3 cases, grade 3 or more), and all patients experienced grade four pancytopenia. On disease re-evaluation at four weeks post-CAR-T cell infusion, seven out of nine patients were negative for minimal residual disease by flow cytometry, and two patients had no response.

Manufacturing

71The primary elements of the CAR-T cell manufacturing process have largely been standardized. They can be divided into four main stages: isolation and enrichment of T cells, activation and expansion of T cells, gene transfer of a CAR vector, and ex vivo CAR-T cell expansion and cryopreservation.

72In the first stage, PBMCs (Peripheral Blood Mononuclear Cells) are isolated from peripheral blood by density gradient centrifugation to remove granulocytes, red blood cells, and platelets. In this initial phase, the patient with R/R AML may experience prolonged cytopenia, which could impede the success of apheresis. Notably, the cellular composition at the outset of production can impact the phenotype of the CAR-T cells. At this stage, it should be considered that patients with R/R AML may present with low numbers of effector T cells, besides an activated circulating cytokine profile, as reported in other hematological cancers at advanced stages.

73An alternative approach in this context is the selection of CD3 + T cells using magnetic bead-based systems, such as the CliniMACS® system. This enables T cell expansion and administration of the final cell product, ensuring a properly defined CD4:CD8 ratio– (Fig. 5).

74T cell activation is typically initiated by unconjugated mAbs, most commonly anti-CD3/anti-CD28 antibody-coated magnetic beads. Afterward, the method of delivery of the CAR transgene can significantly impact its expression level. At present, all FDA- and EMA-approved CAR-T cell products employ lentiviral or retroviral transduction to achieve CAR transgene integration. Still, several alternative non-viral gene delivery methods have been investigated, with promising results.

75It is important to note that production delays may prove fatal for this highly aggressive disease. Using donor-derived CAR-T cells, also known as allogeneic CAR-T, universal CAR-T (UCART), or off-the-shelf CAR-T,, could expand this strategy by being immediately available. Some of the currently engineered CAR-T cells, such as BE-CAR33 or BE-CAR7, are already based on this strategy and have shown efficacy in PDX models and are currently being tested in the CARAML clinical trial (NCT05942599).

76Furthermore, the optimal lymphodepleting therapy remains to be determined. Some evidence supports the use of HMAs concomitantly with the lymphodepleting regimen, which have been demonstrated to augment CD123 and other antigen expression on AML blast surfaces. Recent findings also suggest that combining CAR-T cells with cytokine signaling inhibitors could enhance immunotherapy efficacy in the specific AML context (NCT03766126).

77Finally, selecting eligible AML patients may require a more cautious approach than that employed in CAR-T cell therapy for other hematological malignancies. In the event of myeloid aplasia, the patient may require a rescue alloHSCT. Accordingly, a meticulous and multidisciplinary clinical strategy, including the identification of HSCT donors prior to CAR-T infusion, may be considered.

Strategies to circumvent antigen heterogeneity

78Given the molecular and cytogenetic heterogeneity of AML, a promising approach for effective CAR-T cell therapy with increased specificity might be to target two different antigens using tandem or bicistronic CARs. These strategies are still in the early stages of clinical development, with limited available information. Related to this, the emergence of antigen-low expression clones evading effector cell-mediated killing may constitute one mechanism of disease escape during AML evolution. In this context, both modifying the binding affinity and avidity of the scFv, and selecting appropriate costimulatory domains, can be used to enhance CAR sensitivity.

79The scFv determines the antigen-binding affinity and specificity of CAR-T cells. A high affinity scFv enhances the binding strength to the tumor antigen, improving tumor recognition and cytotoxicity. Additionally, the multivalent nature of CAR constructs facilitates a high-avidity effect, increasing overall binding efficiency and T cell activation, even in the presence of antigen heterogeneity. Optimizing both affinity and avidity can lead to more effective and sensitive CAR-T therapies, enabling better tumor targeting and improved clinical outcomes. However, achieving the right balance of affinity and specificity is complex. The affinity must be strong enough for the CAR-T cells to recognize tumor antigens and induce T cell-mediated destruction, but excessively high affinity may lead to off-target binding to healthy tissues., Furthermore, high-affinity CAR-T cells may exhibit reduced persistence in vivo due to activation-induced T cell exhaustion and apoptosis.

80Costimulatory elements may also influence CAR sensitivity. CD28 CARs typically exhibit a reduced requirement for target antigen density, as well as enhanced and accelerated expansion. These features make CD28 an interesting co-stimulator domain for the treatment of AML. Indeed, most strategies currently being tested in early clinical stages (discussed in this review) have selected the CD28 co-stimulator domain. Conversely, 4-1BB CARs typically exhibit more remarkable persistence, in part due to the reduction in T cell exhaustion induced by prolonged CAR signaling. This attribute may be particularly advantageous in contexts where an alloHSCT rescue is not anticipated as a component of the therapeutic strategy.

81Additionally, the signaling machinery can be enhanced by modifying the multimeric CD3 complex (CD3 complex-based receptors). This CD3 complex plays a pivotal role in TCR-mediated antigen recognition., Regarding this, preclinical evidence indicates that the substitution of chimeric VL–Cα and VH–Cβ chains for the endogenous TCR may improve sensitivity. This is the case of HIT receptors, STAR receptors,, TCAR, antibody-TCR (AbTCR), TCR fusion constructs (TRuC), and T cell antigen coupler (TAC) receptors. Specifically, STAR-T cells have demonstrated superior killing in low neoantigen density context and improved tumor control in mouse models in comparison with conventional CAR-T strategies., However, in contrast to CAR-T cells, most TCR-engineered T cells can only recognize intracellular tumor antigens presented by MHC molecules., Of note, CAR antigen sensitivity may also be enhanced without a structural modification by amplifying downstream activation signaling.

82The complexity of AML treatment may necessitate innovative strategies such as epitope-editing (Fig. 6). Early efforts in epitope-editing included CRISPR/Cas9-mediated CD33 knock-out in CD33-positive tumor cells and primary HSPCs, demonstrating its feasiblility.– More recent advancements, such as the work led by Casirati et al., successfully performed epitope engineering of donor CD34+ HSPCs to confer resistance to CAR-T cells targeting FLT3, CD123, and KIT antigens. The authors confirmed the resistance of epitope-edited hematopoiesis and the subsequent eradication of PDXs after CAR-T cell treatment. In the case of CD123, these results have been validated by other groups. Similarly, Wellhausen et al. generated CRISPR epitope-edited CD45-CAR-T cells to evade CAR-T cell recognition. These epitope-edited CD45-CAR-T cells exhibited fratricide resistance and efficacy against PDX AML. Thus, ex vivo epitope editing in HSCs and T cells could revolutionize CAR-T cell therapies for AML, offering a promising strategy to enhance treatment effectiveness and durability.

83When considering bispecific and complex editing approaches, it is crucial to control over cell killing to mitigate potential on-target/off-tumor toxicities, particularly in the context of AML (Fig. 7). One of the earliest strategies proposed to regulate toxicity is the use of switchable CAR-T cells. This approach involves introducing genes encoding surface proteins, antigens or intracellular effectors into the CAR-T cells. Upon gene expression, CAR-T cells become responsive to specific drugs, enabling the controlled cessation of their activity., An illustrative example is incorporating a truncated epidermal growth factor receptor (EGFRt) into CAR-T cells. The administration of cetuximab can target EGFRt, which could lead to the elimination of active CAR-T cells through antibody-dependent cellular cytotoxicity.

84A novel strategy recently published by He et al. involves the isolation of multiple nanobodies (heavy-chain-only antibodies with a small single variable domain) that bind to various epitopes. By employing a sequentially tumor-selected antibody and antigen retrieval (STAR) system, the researchers developed a bispecific and split CAR (BissCAR) targeting CD13 and TIM3. The BissCAR-T cells effectively eradicated patient-derived AML in murine and PDX models with limited toxicity to normal HSPCs.

85Other relevant platforms currently in development include a split, universal, and programmable (SUPRA) CAR system, which is designed to improve specificity and controllability, and the RevCAR-T platform, which employs an “AND” logic gate to target CD33 and CD123 in a versatile manner. In this context, the incorporation of the “OR” or “AND” logic gate strategies could also prove beneficial in reducing off-tumor side effects, as the tumor with both antigens will be selectively eliminated compared with tumors with a single antigen.–

86The “OR” logic gate is based on two completely independent CAR molecules able to recognize the presence of a single antigen or both antigens simultaneously. The SUPRA CAR system employs an AND or NOT logic gate design to target CD33 and FLT3. The construct comprises of a universal chimeric receptor expressed on the T cell, zipCAR, coupled to a soluble antigen-binding adapter, zipFv, which contains a leucine zipper and scFv. The “AND” logic gate would only achieve full activation status upon binding their cognate antigens simultaneously. Two distinct CARs are co-expressed on a single T cell, each with complementary signaling domains. However, the CAR-T cell attains full activation only when both of its receptors bind to their respective antigens simultaneously. For example, the use of synthetic Notch (synNotch) receptors in a dual CAR-T system enables synergistic and selective binding, minimizing on-target/off-tumor toxicity.– Upon recognition of the antigen by the first receptor, a transcription factor is activated, which in turn induces the expression of a second CAR. This subsequently binds to the secondary antigen.

87In addition to these two concepts, “NOT” gates are also noteworthy for their ability to turn off CAR-T cell activity upon encountering unintended target cells. For example, the “NOT”-gate CD93-CAR-T is an inhibitory CAR strategy designed to mitigate endothelial toxicity generated by CD93-CAR-T cells, which eliminates AML but exerts on-target/off-tumor toxicity to endothelial cells. “IF-THEN” gates (which allow spatiotemporal regulation of CAR expression) and “IF-BETTER” gates (in which a CAR-engaging antigen A performs better in the presence of antigen B) are also under investigation.

88Using different logic gate CAR-T designs could also mitigate AML relapse. Traditional CAR-T therapies can be limited by the heterogeneous nature of AML, where tumor cells may downregulate or lose expression of the targeted antigen, leading to relapse. By employing logic gate circuits, these therapies can be adapted to recognize more complex antigen expression patterns specific to AML., For example, incorporating “OR”-gate CARs – where two independent antigen recognition domains enable targeting multiple antigens – can enhance tumor recognition and reduce the likelihood of escape. Additionally, integrating a “safety switch” that responds to both tumor-associated markers and inhibitory signals from the TME can improve CAR-T cell persistence while minimizing off-target toxicity issue. Furthermore, optimizing costimulatory domains is essential to ensure adequate CAR-T cell proliferation and persistence, which are strongly correlated with durable leukemia remission. This multi-layered approach holds significant potential for reducing relapse rates and improving long-term outcomes in AML.

New antigens under development

89The major challenge encountered in CAR-T cell development for AML has been the inability to identify a specific targetable antigen. Further efforts are needed in whole-genome sequencing, surfaceome profiling of AML LSCs, and proteomic and transcriptomic studies comparing antigen expression in LSCs and healthy stem cells.,, Some antigens that have been the subject of early directed and promising strategies are shown in Fig. 8.

90In a notable advance, Lynn et al. developed an FRβ-specific CAR construct, supported by compelling preclinical evidence, targeted to a folate receptor (FR). The FR is expressed on approximately 70% of primary AML blasts. FRα and FRβ are cell surface-bound proteins through glycosyl-phosphatidylinositol linkages. This receptor is an attractive target because its expression is limited in normal tissue and can be upregulated by all-trans retinoic acid, a drug approved for acute promyelocytic leukemia.

91Additionally, Rafiq et al. successfully developed and tested WT1-CAR-T cells, demonstrating efficacy against cell lines in an in vitro model. Wilms tumor 1 (WT1) is an oncogenic zinc-finger transcription factor with low expression in the BM and notable overexpression in various hematological malignancies (AML and CLL), as well as in several solid tumors (such as glioblastoma, mesothelioma, and ovarian cancer).

92Moreover, LILRB4, a leukocytic immunoglobulin-like receptor belonging to the LILRB family,– has shown promising results in preclinical studies. The LILRB family is expressed on AML cells and has been reported to be uniquely expressed on normal monocytic cells at the promonocyte stage of development. An interesting first-in-human study presented at the last ASH congress (San Diego, December 2024) demonstrated that LILRB4 STAR-T therapy is a promising approach in LILRB4 -positive R/R AML patients. Further data from the Phase II trial is eagerly awaited. Additionally, exciting findings were reported on a humanized IgG1 monoclonal antibody with high affinity and specificity for LILRB4, tested in combination with azacytidine for CMML. This combination appears to be well tolerated, with preliminary efficacy outcomes showing superiority over azacytidine alone, leading to rapid and sustained responses.

93Similarly, a potential new target for developing CAR-T cells in AML is CD84, an immunoreceptor belonging to the SLAM family (SLAMF5,). CD84 is overexpressed on AML cells while displaying comparatively low expression in CD34+ HSCs and absent in other tissues. Perez-Amill et al. developed a CD84-CAR-T therapy with promising in vitro and in vivo results.

94Siglec-6 is expressed in primary AML blasts but is absent in normal HSCs., Building on this finding, Jetani et al. engineered a Siglec-6 CAR-T cell therapy utilizing a targeting domain derived from the mAb JML-1. Subsequent in vitro and in vivo studies demonstrated its remarkable efficacy against AML blasts while preserving regular HSCs activity. A similarly featured antigen is TIM-3 (T-cell immunoglobulin mucin-3), which is expressed in LSCs in almost all types of AML but not in HSCs.– TIM3-CAR-T cells exhibited robust antileukemia activity in xenograft models, accompanied by the production of IFN-γ, granzyme B, and perforin.

95Furthermore, tumor cells are known to express cancer-specific surface protein conformations that are difficult to detect using standard technologies assessing gene or protein expression. However, these unique conformations can be identified and selectively targeted. In this context, recent studies have applied structural surfaceomics to AML, integrating cross-linking mass spectrometry with glycoprotein surface capture. Although still an emerging field, preliminary findings suggests that AML exhibits a distinct conformational signature involving various proteins, including integrin β2, which has been proposed as a potential target for CAR-T therapy.

96Another emerging approach that could circumvent the challenges in AML treatment is the combination of antibodies and cell-based therapies, known as STAb (Secreting T-cell-engaging Antibody). This strategy is based on the endogenous secretion of T cell-redirecting bispecific antibodies (bsAbs). STAb immunotherapies involve genetically modifying T cells with nucleic acids or viral vectors to encode bsAbs. This approach not only offers therapeutic potential similar to CAR-T cells but also enables the secreted bispecific antibodies to bind and activate bystander T cells. As a result, all circulating T cells are effectively “converted” into CAR-T-like cells, enhancing overall efficacy., The ability to recruit and activate bystander T cells amplifies the immune response, making STAbs a promising strategy for targeting cancer and other diseases by broadening immune activation beyond the directly engineered T cells.

97This T cells engineered to produce bsAbs have demonstrated antitumor activity in preclinical models. For example, CD1a-, CD19-, and BCMA-STAb T cells have been tested in PDX models of cortical T-ALL, B-ALL and MM, respectively, showing higher efficacy than their respective second-generation CAR-based therapies. Similarly, dual-targeted STAb-T cells secreting BCMA TCE and CD19 TCE have been effectively tested in in vitro models of B-cell malignancies. This platform has also been studied in B-ALL, with promising results. An interesting example is a dual-target strategy based on T cells expressing an anti-CD22-CAR and also secreting an anti-CD19 T-cell engager antibody. This approach was compared with a previously validated anti-CD19/CD22 tandem CAR therapy, demonstrating that STAb-T cells exhibited an enhanced and faster in vitro cytotoxic activity. Given its ability to recruit bystander T cells, this innovative therapy is particularly promising for aggressive diseases prone to relapse with low effector T cells counts, such as AML. Indeed, some preliminary studies in AML have reported encouraging results.,

98There is mounting interest in gamma-delta (γδ) T cell-based products for adoptive immunotherapy.– Specifically, Delta One T (DOT) cells (Vδ1 + γδ T cells) have been identified as a promising avenue for cancer immunotherapy due to their reduced susceptibility to activation-induced cell death and their capacity to persist as tumor-reactive lymphocytes over extended periods (Fig. 9). Preclinical studies have demonstrated the safety and efficacy of this approach,, and it is undergoing testing in a Phase 1 clinical trial (NCT05015426) as a single infusion following alloHSCT.

Modulating the tumor microenvironment

99Given the T cell-inhibiting role of MDSCs,– concomitant administration of CAR-T cells with small molecules capable of depleting the MDSC population may be synergistic. Several strategies that enhance CAR-T cell efficacy in the context of B-cell malignancies may also be relevant in AML. These include the upregulation of IL-15 expression or the IL-18 transgene (TRUCKs) and the addition of exogenous IL-7, IL-15, and/or IL-21 cytokines during the ex vivo expansion of CAR-T cells– (Fig. 9).

100Because of the low mutational burden of AML and the correspondingly low frequency of AML-reactive T cells, CAR-T cell combinations with checkpoint inhibitors (e.g., anti-PD-1 or anti-CTLA-4 antibodies) might be an interesting future strategy, as it may also overcome T cell exhaustion and enhance CAR-T cell efficacy. This could be achieved either through exogenously administered inhibitors or genetic engineering, enabling the CAR-T cell to synthesize these antibodies. For example, the combination of immune checkpoint inhibitor PD-1/PD-L1 monoclonal antibodies and CAR-T cells has effectively prevented immune suppression and enhanced the anti-tumor activity of CAR-T cells. Similarly, novel strategies have been explored, such as the incorporation a Fc-mutant TIM3 receptor decoy to counteract inhibitory signals originating from the blasts or the TME in R/R B-ALL. In addition to TIM3, other immune checkpoint receptors, such as PD1, CLTA-4 and LAG3, can also be targeted as decoys to further disrupt these inhibitory signaling pathways. The flexibility to choose from a variety of inhibitory pathways to adapt this platform to different diseases offers a promising avenue for improving the overall efficacy and durability of CAR-based therapies.

101The combined use of apoptosis-regulating drugs, such as BCL-2 inhibitors, can lower the threshold for CAR-T cells to trigger tumor cell killing through pathways like death receptors. This strategy helps overcome tumor cell resistance to therapy, thereby enhancing the overall effectiveness of the treatment., Moreover, combination with cytoreductive chemotherapy or epigenetic modulators such as HMA (e.g., azacitidine or decitabine) can reduce the tumor burden and modulate the immune microenvironment. There are several clinical trials ongoing testing the synergistic function of epigenetic drugs and immunotherapy. Indeed, it has been proven that CAR-T cells treated with methylation inhibitors such as low-dose decitabine during CAR T cell manufacturing present stronger antitumour effector function, proliferation, memory phenotype maintenance, cytokine release capacities and a lower exhaustion-associated gene expression under tumor cell stimulation in vivo and in vitro. These epigenetic agents before CAR-T cell infusion may enhance CAR-T efficacy by reducing immunosuppressive cells or increasing antigen expression on AML blasts., Moreover, some studies have used histone, DNA, and miRNA modifications to downregulate inhibitory molecules such as PD1, CTLA-3, TIM2 and LAG3 resulting in T cell-intrinsic upregulation.– Additionally, the combination with immunomodulators like lenalidomide or TGF-β inhibitors can promote a more favorable microenvironment for CAR-T activity.,

102Combining CAR-T cells with metabolic modulators also represents a promising strategy, as metabolic pathways are integral to T cells’ function, persistence, and efficacy. CAR-T cells, require robust metabolic activity to support their proliferation, survival, and effector functions. Within the TME, however, metabolic stressors such as hypoxia, nutrient deprivation, and the accumulation of immunosuppressive metabolites can lead to CAR-T cell exhaustion and dysfunction. In this context, there is some preclinical evidence of the combination of metabolic modulators with CAR-T cell therapy. For instance, increasing L-arginine levels (crucial for CAR-T cell proliferation and cytotoxicity) by modulating PRODH2 enzyme seems a preclinical exciting strategy., A study modified CAR-T cells to overexpress kynureninase, increasing their cytotoxicity in the TME. Further publications combined IDO1 inhibitors (a key enzyme in kynurenine synthesis) with CAR-T cells.

Conclusions and perspectives

103Modern CAR-T cell therapy represents the culmination of decades of immunology and genetic engineering research. Foundational discoveries, such as the identification of T cells and the demonstration of immune-mediated cancer eradication, as well as the early efforts led by Dr. Steven Rosenberg highlighting the potential of TILs, paved the way for advancements in adoptive cell therapy.

104The first FDA-approved CAR-T therapies, Kymriah® and Yescarta®, revolutionized treatment for B-cell malignancies. Despite these successes, challenges remain, particularly in extending CAR-T therapy to solid tumors and certain hematological malignancies such as AML.

105Regarding solid tumors, the tumor microenvironment, antigen heterogeneity, and limited CAR-T cell persistence present significant obstacles. This review describes that while no CAR-T therapy has received FDA approval for solid malignancies, certain strategies such as intracranial IL-13Ra-targeted CAR therapy (multifocal glioblastoma), and ongoing clinical trials with Claudin18.2 (gastrointestinal tumors) and GD2 (H3K27M-mutated glioma; and neuroblastoma) show promise.

106Additionally, other T cell-based approaches, including ongoing trials targeting antigens like bispecific TCE and TCR-T therapies, are being explored in this specific solid tumor setting. For instance, the gp100 peptide-MHC/CD3 bispecific T-cell engager (TCE) tebentafusp, which was approved for uveal melanoma in 2022, is one strategy that holds great promise. In line with this, further approaches described in this review that are being currently tested show strong potential, such an autologous TCR T-cell therapy named afami-cel for synovial sarcoma, and other cellular therapies for HPV-associated cancers.– While significant challenges remain, the evolving landscape of CAR-T cell therapy offers promising avenues for expanding its impact beyond hematologic malignancies.

107Furthermore, CAR-T cell therapy holds great promise for the treatment of AML. However, several challenges must be addressed to fully realize its therapeutic potential. AML presents a highly heterogeneous landscape, driven by diverse genetic, cytogenetic, and epigenetic alterations that influence disease presentation, progression, and treatment response. The complexity of AML remains a challenge, particularly due to the presence of LSCs and clonal evolution mechanisms that contribute to therapy resistance and relapse.

108Additionally, as exposed in this work, the AML bone marrow microenvironment further exacerbates these challenges by fostering immune evasion, metabolic suppression, and a highly immunosuppressive setting that impairs immune-based therapies. The BM microenvironment in AML is characterized by metabolic byproducts such as lactate, adenosine, and kynurenine, which inhibit T cell function and drive immune exhaustion. Furthermore, the presence of myeloid-derived suppressor cells (MDSCs), T regulatory cells (Tregs), and inhibitory checkpoints, such as PD-1, TIM-3, and LAG-3, contributes to T cell dysfunction. These immunosuppressive factors not only hinder the effectiveness of conventional therapies but also pose significant obstacles to CAR-T cell therapy, which has demonstrated limited success in AML compared to its applications in B-cell malignancies.

109Moreover, a major limitation described in this review still to be faced in the development of CAR-T cell therapies for AML is the lack of an optimal target antigen. An ideal target should be highly expressed on AML blasts and LSCs while being absent in normal hematopoietic and extra-hematopoietic tissues to minimize on-target/off-tumor toxicity. Current CAR-T cell targets under investigation include CD123, CD33, CLL-1, NKG2D, CD7, CD38, CD44v6, CD70, and FLT3. Each of these antigens presents unique advantages and challenges, including concerns related to myeloablation, endothelial toxicity, and antigen escape mechanisms. Among these targets, CD123 and CD33 have been extensively studied, with various CAR-T cell constructs in preclinical and early clinical phases. However, toxicity concerns, particularly myelosuppression, remain a significant challenge. Emerging targets such as CLL-1 and NKG2D offer promising avenues due to their selective expression in AML while sparing normal HSCs. Additionally, strategies such as bispecific CARs, safety switches, and combinatorial approaches with immune checkpoint inhibitors or metabolic modulators are being explored to enhance CAR-T cell efficacy and safety.

110Overall, while significant progress has been made in understanding AML heterogeneity and immune evasion, further research is required to optimize CAR-T cell strategies and overcome the inherent challenges of AML treatment. The integration of multi-targeting approaches, improved manufacturing techniques, and a deeper understanding of the BM microenvironment may ultimately enhance the therapeutic potential of CAR-T cells in AML.

111Additionally, certain concerns regarding CAR-T cell therapy must be carefully evaluated in the context of AML. For instance, reports have highlighted potential long-term side effects, including the incidence of secondary myeloid neoplasms following CD19-CAR-T cell therapy., Studies estimate the incidence to range from 1% to 10%,– which is comparable to the risk of therapy-related myeloid neoplasms observed after chemotherapy or autologous HSCT in patients with NHL. Furthermore, the FDA had raised concerns following the diagnosis of 22 cases of T cell malignancies within two years of CAR-T infusion. While these findings warrant attention, further studies and long-term follow-up are necessary to draw definitive conclusions regarding the risks associated with CAR-T cell therapy.

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96.
Schneider, M. Carl June, first year Emily Whitehead reflect on experiences with Penn-pioneered cancer treatment. The Daily Pennsylvanian (2024).
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97.
Jain MD, Smith M, Shah NN. How I treat refractory CRS and ICANS after CAR T-cell therapy. Blood. 2023;141:2430-2442.
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98.
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99.
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101.
Maude SL, et al. Chimeric antigen receptor T cells for sustained remissions in leukemia. N. Engl. J. Med. 2014;371:1507-1517.
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102.
Park JH, et al. Long-term follow-up of CD19 CAR therapy in acute lymphoblastic leukemia. N. Engl. J. Med. 2018;378:449-459.
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103.
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104.
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105.
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106.
Costandi M. Kite and NCI partner on T cells. Nat. Biotechnol. 2013;31:10-10.
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107.
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109.
Maude SL, et al. Tisagenlecleucel in children and young adults with B-cell lymphoblastic leukemia. N. Engl. J. Med. 2018;378:439-448.
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110.
Neelapu SS, et al. Axicabtagene ciloleucel CAR T-cell therapy in refractory large B-cell lymphoma. N. Engl. J. Med. 2017;377:2531-2544.
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111.
Fowler NH, et al. Tisagenlecleucel in adult relapsed or refractory follicular lymphoma: the phase 2 ELARA trial. Nat. Med. 2022;28:325-332.
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112.
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113.
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114.
Frey NV. Approval of brexucabtagene autoleucel for adults with relapsed and refractory acute lymphocytic leukemia. Blood. 2022;140:11-15.
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115.
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117.
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118.
Munshi NC, et al. Idecabtagene vicleucel in relapsed and refractory multiple myeloma. N. Engl. J. Med. 2021;384:705-716.
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119.
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120.
Martin T, et al. Ciltacabtagene autoleucel, an anti–B-cell maturation antigen chimeric antigen receptor T-cell therapy, for relapsed/refractory multiple myeloma: CARTITUDE-1 2-year follow-up. J. Clin. Oncol. 2022;41:1265-1274.
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121.
Narayan V, et al. PSMA-targeting TGFβ-insensitive armored CAR T cells in metastatic castration-resistant prostate cancer: a phase 1 trial. Nat. Med. 2022;28:724-734.
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122.
Haas AR, et al. Phase I study of lentiviral-transduced chimeric antigen receptor-modified T cells recognizing mesothelin in advanced solid cancers. Mol. Ther. 2019;27:1919-1929.
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123.
O’Rourke, D. M. et al. A single dose of peripherally infused EGFRvIII-directed CAR T cells mediates antigen loss and induces adaptive resistance in patients with recurrent glioblastoma. Sci. Transl. Med.9, eaag3518 (2017).
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124.
Brown CE, et al. Regression of glioblastoma after chimeric antigen receptor T-cell therapy. N. Engl. J. Med. 2016;375:2561-2569.
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125.
GD2-CAR T cell therapy for H3K27M-mutated diffuse midline gliomas · 2022
No notice
126.
Claudin18.2-specific CAR T cells in gastrointestinal cancers: phase 1 trial interim results · 2022
No notice
127.
Del Bufalo F, et al. GD2-CART01 for relapsed or refractory high-risk neuroblastoma. N. Engl. J. Med. 2023;388:1284-1295.
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128.
Brudno JN, Maus MV, Hinrichs CS. CAR T-cells and T-cell therapies for cancer: a translational science review. JAMA. 2024;332:1924-1935.
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130.
Norberg SM, Hinrichs CS. Engineered T cell therapy for viral and non-viral epithelial cancers. Cancer Cell. 2023;41:58-69.
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131.
Nagarsheth NB, et al. TCR-engineered T cells targeting E7 for patients with metastatic HPV-associated epithelial cancers. Nat. Med. 2021;27:419-425.
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132.
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133.
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Vanhooren J, et al. CAR-T in the treatment of acute myeloid leukemia: barriers and how to overcome them. Hemasphere. 2023;7:e937.
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138.
The 5th edition of the World Health Organization Classification of Haematolymphoid Tumours: Myeloid and Histiocytic/Dendritic Neoplasms · 2022
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139.
Döhner H, et al. Diagnosis and management of AML in adults: 2022 recommendations from an international expert panel on behalf of the ELN. Blood. 2022;140:1345-1377.
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Corrected
146.
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Brummer T, Zeiser R. The role of the MDM2/p53 axis in antitumor immune responses. Blood. 2024;143:2701-2709.
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Bhagwat AS, et al. Cytokine-mediated CAR T therapy resistance in AML. Nat. Med. 2024;30:3697-3708.
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161.
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Catch me if you can: how AML and its niche escape immunotherapy · 2021
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164.
Mishra SK, Millman SE, Zhang L. Metabolism in acute myeloid leukemia: mechanistic insights and therapeutic targets. Blood. 2023;141:1119-1135.
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Gabrilovich DI. Myeloid-derived suppressor cells. Cancer Immunol. Res. 2017;5:3-8.
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169.
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Mabuchi R, et al. High serum concentration of L-kynurenine predicts unfavorable outcomes in patients with acute myeloid leukemia. Leuk. Lymphoma. 2016;57:92-98.
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171.
Ghobrial IM, Detappe A, Anderson KC, Steensma DP. The bone-marrow niche in MDS and MGUS: implications for AML and MM. Nat. Rev. Clin. Oncol. 2018;15:219-233.
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172.
Hao F, Sholy C, Wang C, Cao M, Kang X. The role of t cell immunotherapy in acute myeloid leukemia. Cells. 2021;10:3376.
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Zhang Z, et al. Single-cell RNA-seq reveals a microenvironment and an exhaustion state of T/NK cells in acute myeloid leukemia. Cancer Sci. 2023;114:3873-3883.
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Vadakekolathu J, Rutella S. Escape from T-cell–targeting immunotherapies in acute myeloid leukemia. Blood. 2024;143:2689-2700.
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175.
Bone marrow central memory and memory stem T-cell exhaustion in AML patients relapsing after HSCT · 2019
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176.
Haroun F, Solola SA, Nassereddine S, Tabbara I. PD-1 signaling and inhibition in AML and MDS. Ann. Hematol. 2017;96:1441-1448.
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177.
Single cell T cell landscape and T cell receptor repertoire profiling of AML in context of PD-1 blockade therapy · 2021
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178.
Nuebling T, et al. The immune checkpoint modulator OX40 and its ligand OX40L in NK-cell immunosurveillance and acute myeloid leukemia. Cancer Immunol. Res. 2018;6:209-221.
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179.
Atilla E, Benabdellah K. The black hole: CAR T cell therapy in AML. Cancers. 2023;15:2713.
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180.
Tikhonova AN, et al. The bone marrow microenvironment at single-cell resolution. Nature. 2019;569:222-228.
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181.
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182.
Labanieh L, Mackall CL. CAR immune cells: design principles, resistance and the next generation. Nature. 2023;614:635-648.
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183.
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184.
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185.
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186.
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187.
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188.
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189.
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190.
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191.
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193.
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194.
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196.
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197.
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198.
Coexpression profile of leukemic stem cell markers for combinatorial targeted therapy in AML · 2018
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199.
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201.
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203.
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206.
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207.
Naveen P, et al. Tagraxofusp in blastic plasmacytoid dendritic-cell neoplasm. N. Engl. J. Med. 2019;380:1628-1637.
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210.
Daver N, et al. Broad activity for the pivekimab sunirine (PVEK, IMGN632), azacitidine, and venetoclax triplet in high-risk patients with relapsed/refractory acute myeloid leukemia (AML). Blood. 2022;140:145-149.
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211.
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212.
Godwin JE, et al. Flotetuzumab (FLZ), an investigational CD123 x CD3 bispecific dart® protein-induced clustering of CD3+ T cells and CD123+ AML cells in bone marrow biopsies is associated with response to treatment in primary refractory AML patients. Blood. 2019;134:1410.
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213.
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Not in our library10.1182/blood-2022-159524
215.
Stein C, et al. Novel conjugates of single-chain Fv antibody fragments specific for stem cell antigen CD123 mediate potent death of acute myeloid leukaemia cells. Br. J. Haematol. 2010;148:879-889.
Not in our library10.1111/j.1365-2141.2009.08033.x
216.
Ehninger A, et al. Distribution and levels of cell surface expression of CD33 and CD123 in acute myeloid leukemia. Blood Cancer J. 2014;4:e218-e218.
Not in our library10.1038/bcj.2014.39
217.
Dinndorf P, et al. Expression of normal myeloid-associated antigens by acute leukemia cells. Blood. 1986;67:1048-1053.
Not in our library10.1182/blood.v67.4.1048.1048
218.
Walter RB, Appelbaum FR, Estey EH, Bernstein ID. Acute myeloid leukemia stem cells and CD33-targeted immunotherapy. Blood. 2012;119:6198-6208.
Not in our library10.1182/blood-2011-11-325050
219.
Castaigne S, et al. Effect of gemtuzumab ozogamicin on survival of adult patients with de-novo acute myeloid leukaemia (ALFA-0701): a randomised, open-label, phase 3 study. Lancet. 2012;379:1508-1516.
Not in our library10.1016/s0140-6736(12)60485-1
220.
Burnett AK, et al. Identification of patients with acute myeloblastic leukemia who benefit from the addition of gemtuzumab ozogamicin: results of the MRC AML15 trial. J. Clin. Oncol. 2011;29:369-377.
Not in our library10.1200/jco.2010.31.4310
221.
FDA. MYLOTARGTM (Gemtuzumab Ozogamicin) for Injection. Available online: https://www.accessdata.fda.gov/drugsatfda_docs/label/2017/761060lbl.pdf (accessed on 1 Sep 2024).
Not in our library
222.
EMA. EPAR—Summary for Mylotarg—Epar Product Information Public. Available online: https://www.ema.europa.eu/en/documents/product-information/mylotarg-epar-product-information_en.pdf (accessed on 1 Sep 2024).
Not in our library
223.
Norsworthy KJ, et al. FDA approval summary: mylotarg for treatment of patients with relapsed or refractory CD33-positive acute myeloid leukemia. Oncologist. 2018;23:1103-1108.
Not in our library10.1634/theoncologist.2017-0604
224.
He X, et al. Bispecific and split CAR T cells targeting CD13 and TIM3 eradicate acute myeloid leukemia. Blood. 2020;135:713-723.
Not in our library10.1182/blood.2019002779
225.
Godwin CD, McDonald GB, Walter RB. Sinusoidal obstruction syndrome following CD33-targeted therapy in acute myeloid leukemia. Blood. 2017;129:2330-2332.
Not in our library10.1182/blood-2017-01-762419
226.
Rajvanshi P, Shulman HM, Sievers EL, McDonald GB. Hepatic sinusoidal obstruction after gemtuzumab ozogamicin (mylotarg) therapy. Blood. 2002;99:2310-2314.
Not in our library10.1182/blood.v99.7.2310
227.
Schiller GJ, et al. Early clinical evaluation of potential synergy of targeted radiotherapy with lintuzumab-Ac225 and venetoclax in relapsed/refractory AML. Blood. 2022;140:3336-3337.
Not in our library10.1182/blood-2022-157588
228.
Abedin S, et al. Lintuzumab-Ac225 with combination with intensive chemotherapy yields high response rate and MRD negativity in R/R AML with adverse features. Blood. 2022;140:157-158.
Not in our library10.1182/blood-2022-157827
229.
Feldman EJ, et al. Phase III randomized multicenter study of a humanized anti-CD33 monoclonal antibody, lintuzumab, in combination with chemotherapy, versus chemotherapy alone in patients with refractory or first-relapsed acute myeloid leukemia. J. Clin. Oncol. 2005;23:4110-4116.
Not in our library10.1200/jco.2005.09.133
230.
Stein EM, et al. A phase 1 trial of vadastuximab talirine as monotherapy in patients with CD33-positive acute myeloid leukemia. Blood. 2018;131:387-396.
Not in our library10.1182/blood-2017-06-789800
231.
Cortes JE, et al. Maturing clinical profile of IMGN779, a next-generation CD33-targeting antibody-drug conjugate, in patients with relapsed or refractory acute myeloid leukemia. Blood. 2018;132:26.
Not in our library10.1182/blood-2018-99-112891
232.
Ravandi F, et al. Updated results from phase I dose-escalation study of AMG 330, a bispecific T-cell engager molecule, in patients with relapsed/refractory acute myeloid leukemia (R/R AML). J. Clin. Oncol. 2020;38:7508-7508.
Not in our library10.1200/jco.2020.38.15_suppl.7508
233.
Krupka C, et al. CD33 target validation and sustained depletion of AML blasts in long-term cultures by the bispecific T-cell–engaging antibody AMG 330. Blood. 2014;123:356-365.
Not in our library10.1182/blood-2013-08-523548
234.
Subklewe M, et al. Preliminary results from a phase 1 first-in-human study of AMG 673, a novel half-life extended (HLE) anti-CD33/CD3 BiTE® (bispecific T-cell engager) in patients with relapsed/refractory (R/R) acute myeloid leukemia (AML). Blood. 2019;134:833-833.
Not in our library10.1182/blood-2019-127977
235.
Marshall ASJ, et al. Human MICL (CLEC12A) is differentially glycosylated and is down-regulated following cellular activation. Eur. J. Immunol. 2006;36:2159-2169.
Not in our library10.1002/eji.200535628
236.
Chen C-H, et al. Dendritic-cell-associated C-type lectin 2 (DCAL-2) alters dendritic-cell maturation and cytokine production. Blood. 2006;107:1459-1467.
Not in our library10.1182/blood-2005-08-3264
237.
Ngai LL, et al. Bimodal expression of potential drug target CLL-1 (CLEC12A) on CD34+ blasts of AML patients. Eur. J. Haematol. 2021;107:343-353.
Not in our library10.1111/ejh.13672
238.
Zhao X, et al. Targeting C-type lectin-like molecule-1 for antibody-mediated immunotherapy in acute myeloid leukemia. Haematologica. 2010;95:71-78.
Not in our library10.3324/haematol.2009.009811
239.
Bakker ABH, et al. C-Type lectin-like molecule-1. Cancer Res. 2004;64:8443-8450.
Not in our library10.1158/0008-5472.can-04-1659
240.
Hutten TJA, et al. CLEC12A-mediated antigen uptake and cross-presentation by human dendritic cell subsets efficiently boost tumor-reactive t cell responses. J. Immunol. 2016;197:2715-2725.
Not in our library10.4049/jimmunol.1600011
241.
Toft-Petersen M, et al. The CLEC12A receptor marks human basophils: potential implications for minimal residual disease detection in acute myeloid leukemia. Cytom. B. Clin. Cytom. 2018;94:520-526.
Not in our library10.1002/cyto.b.21540
242.
Bill M, et al. Mapping the CLEC12A expression on myeloid progenitors in normal bone marrow; implications for understanding CLEC12A-related cancer stem cell biology. J. Cell Mol. Med. 2018;22:2311-2318.
Not in our library10.1111/jcmm.13519
243.
Zloza A, et al. NKG2D signaling on CD8+ T cells represses T-bet and rescues CD4-unhelped CD8+ T cell memory recall but not effector responses. Nat. Med. 2012;18:422-428.
Not in our library10.1038/nm.2683
244.
Sheppard S, et al. The immunoreceptor NKG2D promotes tumour growth in a model of hepatocellular carcinoma. Nat. Commun. 2017;8:13930.
Not in our library10.1038/ncomms13930
245.
Bauer S, et al. Activation of NK Cells and T Cells by NKG2D, a receptor for stress-inducible MICA. Science. 1999;285:727-729.
Not in our library10.1126/science.285.5428.727
246.
Mastaglio S, et al. Natural killer receptor ligand expression on acute myeloid leukemia impacts survival and relapse after chemotherapy. Blood Adv. 2018;2:335-346.
Not in our library10.1182/bloodadvances.2017015230
247.
Salih HR, et al. Functional expression and release of ligands for the activating immunoreceptor NKG2D in leukemia. Blood. 2003;102:1389-1396.
Not in our library10.1182/blood-2003-01-0019
248.
Zhang T, Lemoi BA, Sentman CL. Chimeric NK-receptor–bearing T cells mediate antitumor immunotherapy. Blood. 2005;106:1544-1551.
Not in our library10.1182/blood-2004-11-4365
249.
Lanier LL. NKG2D Receptor and its ligands in host defense. Cancer Immunol. Res. 2015;3:575-582.
Not in our library10.1158/2326-6066.cir-15-0098
250.
Rohner A, Langenkamp U, Siegler U, Kalberer CP, Wodnar-Filipowicz A. Differentiation-promoting drugs up-regulate NKG2D ligand expression and enhance the susceptibility of acute myeloid leukemia cells to natural killer cell-mediated lysis. Leuk. Res. 2007;31:1393-1402.
Not in our library10.1016/j.leukres.2007.02.020
251.
Diermayr S, et al. NKG2D ligand expression in AML increases in response to HDAC inhibitor valproic acid and contributes to allorecognition by NK-cell lines with single KIR-HLA class I specificities. Blood. 2008;111:1428-1436.
Not in our library10.1182/blood-2007-07-101311
252.
Themeli M. Selecting CD7− T cells for CAR T-cell therapy. Blood. 2022;140:2652-2653.
Not in our library10.1182/blood.2022017935
253.
Watanabe N, et al. Feasibility and preclinical efficacy of CD7-unedited CD7 CAR T cells for T cell malignancies. Mol. Ther. 2023;31:24-34.
Not in our library10.1016/j.ymthe.2022.09.003
254.
Tan Y, et al. Long-term follow-up of donor-derived CD7 CAR T-cell therapy in patients with T-cell acute lymphoblastic leukemia. J. Hematol. Oncol. 2023;16:34.
Not in our library10.1186/s13045-023-01427-3
255.
Hu Y, et al. Genetically modified CD7-targeting allogeneic CAR-T cell therapy with enhanced efficacy for relapsed/refractory CD7-positive hematological malignancies: a phase I clinical study. Cell Res. 2022;32:995-1007.
Not in our library10.1038/s41422-022-00721-y
256.
Base-edited CAR T cells for combinational therapy against T cell malignancies · 2021
No notice
257.
Png YT, et al. Blockade of CD7 expression in T cells for effective chimeric antigen receptor targeting of T-cell malignancies. Blood Adv. 2017;1:2348-2360.
Not in our library10.1182/bloodadvances.2017009928
258.
Lu, P. et al. Naturally selected CD7 CAR-T therapy without genetic manipulations for T-ALL/LBL: first-in-human phase i clinical trial. Blood, 140, 321–334 (2022).
Not in our library10.1182/blood.2021014498
259.
Gomes-Silva D, et al. CD7-edited T cells expressing a CD7-specific CAR for the therapy of T-cell malignancies. Blood. 2017;130:285-296.
Not in our library10.1182/blood-2017-01-761320
260.
Cao X, et al. CD7-directed CAR T-cell therapy: a potential immunotherapy strategy for relapsed/refractory acute myeloid leukemia. Exp. Hematol. Oncol. 2022;11:67.
Not in our library10.1186/s40164-022-00318-6
261.
Muñoz P, et al. Antigen-induced clustering of surface CD38 and recruitment of intracellular CD38 to the immunologic synapse. Blood. 2008;111:3653-3664.
Not in our library10.1182/blood-2007-07-101600
262.
Deterre, P. et al. CD38 in T- and B-cell functions. in Human CD38 and Related Molecules 146–168 (KARGER, 2000).
Not in our library10.1159/000058767
263.
Terhorst C, et al. Biochemical studies of the human thymocyte cell-surface antigens T6, T9 and T10. Cell. 1981;23:771-780.
Not in our library10.1016/0092-8674(81)90441-4
264.
Keyhani A, et al. Increased CD38 expression is associated with favorable prognosis in adult acute leukemia. Leuk. Res. 2000;24:153-159.
Not in our library10.1016/s0145-2126(99)00147-2
265.
Glisovic-Aplenc T, et al. CD38 as a pan-hematologic target for chimeric antigen receptor T cells. Blood Adv. 2023;7:4418-4430.
Not in our library10.1182/bloodadvances.2022007059
266.
Facon, T. et al. Isatuximab, bortezomib, lenalidomide, and dexamethasone for multiple myeloma. N. Engl. J. Med. 391, 1597–1609 (2024)
Not in our library10.1056/nejmoa2400712
267.
Attal M, et al. Isatuximab plus pomalidomide and low-dose dexamethasone versus pomalidomide and low-dose dexamethasone in patients with relapsed and refractory multiple myeloma (ICARIA-MM): a randomised, multicentre, open-label, phase 3 study. Lancet. 2019;394:2096-2107.
Not in our library10.1016/s0140-6736(19)32556-5
268.
Baruchel A, et al. P501: Isatuximab plus chemotherapy for pediatric relapsed/refractory acute lymphoblastic leukemia or acute myeloid leukemia (isakids): interim efficacy analysis. Hemasphere. 2023;7:e121813e.
Not in our library10.1097/01.hs9.0000968912.12181.3e
269.
Naik J, et al. CD38 as a therapeutic target for adult acute myeloid leukemia and T-cell acute lymphoblastic leukemia. Haematologica. 2019;104:e100-e103.
Not in our library10.3324/haematol.2018.192757
270.
Van Driel M, et al. CD44 variant isoforms are involved in plasma cell adhesion to bone marrow stromal cells. Leukemia. 2002;16:135-143.
Not in our library10.1038/sj.leu.2402336
271.
Heider K-H, Kuthan H, Stehle G, Munzert G. CD44v6: a target for antibody-based cancer therapy. Cancer Immunol. Immunother. 2004;53:567-579.
Not in our library10.1007/s00262-003-0494-4
272.
Wang, Z., Zhao, K., Hackert, T. & Zöller, M. CD44/CD44v6 a reliable companion in cancer-initiating cell maintenance and tumor progression. Front. Cell Dev. Biol.6, (2018).
Not in our library10.3389/fcell.2018.00097
273.
Casucci M, et al. CD44v6-targeted T cells mediate potent antitumor effects against acute myeloid leukemia and multiple myeloma. Blood. 2013;122:3461-3472.
Not in our library10.1182/blood-2013-04-493361
274.
Tang, L. et al. CD44v6 chimeric antigen receptor T cell specificity towards AML with FLT3 or DNMT3A mutations. Clin. Transl. Med.12, e1007 (2022).
Not in our library10.1002/ctm2.1043
275.
Stornaiuolo A, et al. Characterization and functional analysis of cd44v6.car t cells endowed with a new low-affinity nerve growth factor receptor-based spacer. Hum. Gene Ther. 2021;32:744-760.
Not in our library10.1089/hum.2020.216
276.
Wu, G. et al. Preclinical evaluation of CD70-specific CAR T cells targeting acute myeloid leukemia. Front. Immunol.14, 1093750 (2023).
Not in our library10.3389/fimmu.2023.1093750
277.
Sauer T, et al. CD70-specific CAR T cells have potent activity against acute myeloid leukemia without HSC toxicity. Blood. 2021;138:318-330.
Not in our library10.1182/blood.2020008221
278.
Riether C, et al. Targeting CD70 with cusatuzumab eliminates acute myeloid leukemia stem cells in patients treated with hypomethylating agents. Nat. Med. 2020;26:1459-1467.
Not in our library10.1038/s41591-020-0910-8
279.
Mirazee J, Shah NN. CD70 CAR T cells in AML: form follows function. Cell Rep. Med. 2022;3:100639.
Not in our library10.1016/j.xcrm.2022.100639
280.
Targeting FLT3 mutations in AML: review of current knowledge and evidence · 2019
No notice
281.
Short NJ, Kantarjian H, Ravandi F, Daver N. Emerging treatment paradigms with FLT3 inhibitors in acute myeloid leukemia. Ther. Adv. Hematol. 2019;10:204062071982731.
Not in our library10.1177/2040620719827310
282.
Erba HP, et al. Quizartinib plus chemotherapy in newly diagnosed patients with FLT3-internal-tandem-duplication-positive acute myeloid leukaemia (QuANTUM-First): a randomised, double-blind, placebo-controlled, phase 3 trial. Lancet. 2023;401:1571-1583.
Not in our library10.1016/s0140-6736(23)00464-6
283.
Wang ES, et al. Crenolanib and intensive chemotherapy in adults with newly diagnosed FLT3-mutated AML. J. Clin. Oncol. 2024;42:1776-1787.
Not in our library10.1200/jco.23.01061
284.
Loo S, et al. Sorafenib plus intensive chemotherapy in newly diagnosed FLT3 -ITD AML: a randomized, placebo-controlled study by the ALLG. Blood. 2023;142:1960-1971.
Not in our library10.1182/blood.2023020301
285.
Chien CD, et al. Preclinical development of FLT3-Redirected chimeric antigen receptor T cell immunotherapy for acute myeloid leukemia. Blood. 2016;128:1072.
Not in our library10.1182/blood.v128.22.1072.1072
286.
Jetani H, et al. CAR T-cells targeting FLT3 have potent activity against FLT3−ITD+ AML and act synergistically with the FLT3-inhibitor crenolanib. Leukemia. 2018;32:1168-1179.
Not in our library10.1038/s41375-018-0009-0
287.
Sleiman S, et al. Anti-FLT3 CAR T cells in acute myeloid leukemia. Blood. 2021;138:1703.
Not in our library10.1182/blood-2021-151196
288.
Sommer C, et al. Allogeneic FLT3 CAR T cells with an off-switch exhibit potent activity against AML and can be depleted to expedite bone marrow recovery. Mol. Ther. 2020;28:2237-2251.
Not in our library10.1016/j.ymthe.2020.06.022
289.
Barneh, F. et al. Repurposing CD19-directed immunotherapies for pediatric t(8;21) acute myeloid leukemia. Haematologica109, 4131–4136 (2024)
Not in our library10.3324/haematol.2024.285707
290.
Perna F, et al. Integrating proteomics and transcriptomics for systematic combinatorial chimeric antigen receptor therapy of AML. Cancer Cell. 2017;32:506-519.e5.
Not in our library10.1016/j.ccell.2017.09.004
291.
Dobrowolska H, et al. Expression of immune inhibitory receptor ILT3 in acute myeloid leukemia with monocytic differentiation. Cytom. B. Clin. Cytom. 2013;84B:21-29.
Not in our library10.1002/cyto.b.21050
292.
Loff S, et al. Rapidly switchable universal car-t cells for treatment of CD123-positive leukemia. Mol. Ther. Oncol. 2020;17:408-420.
Not in our library10.1016/j.omto.2020.04.009
293.
Switching CAR T cells on and off: a novel modular platform for retargeting of T cells to AML blasts · 2016
No notice
294.
Bachmann M. The UniCAR system: a modular CAR T cell approach to improve the safety of CAR T cells. Immunol. Lett. 2019;211:13-22.
Not in our library10.1016/j.imlet.2019.05.003
295.
Wermke M, et al. Updated results from a phase i dose escalation study of the rapidly-switchable universal CAR-T Therapy UniCAR-T-CD123 in relapsed/refractory AML. Blood. 2023;142:3465.
Not in our library10.1182/blood-2023-177867
296.
ClinicalTrials.gov. Available online: https://clinicaltrials.gov/study/NCT05949125.
Not in our library
297.
Sugita M, et al. Allogeneic TCRαβ deficient CAR T-cells targeting CD123 in acute myeloid leukemia. Nat. Commun. 2022;13:2227.
Not in our library10.1038/s41467-022-29668-9
298.
Cai T, et al. Targeting CD123 in blastic plasmacytoid dendritic cell neoplasm using allogeneic anti-CD123 CAR T cells. Nat. Commun. 2022;13:2228.
Not in our library10.1038/s41467-022-29669-8
299.
Pemmaraju N, et al. CD123-directed allogeneic chimeric-antigen receptor T-cell therapy (CAR-T) in blastic plasmacytoid dendritic cell neoplasm (BPDCN): clinicopathological insights. Leuk. Res. 2022;121:106928.
Not in our library10.1016/j.leukres.2022.106928
300.
Sallman DA, et al. Ameli-01: A phase I trial of UCART123v1.2, an anti-CD123 allogeneic CAR-T cell product, in adult patients with relapsed or refractory (R/R) CD123+ acute myeloid leukemia (AML). Blood. 2022;140:2371-2373.
Not in our library10.1182/blood-2022-169928
301.
Naik S, et al. Safety and anti-leukemic activity of CD123-CAR T cells in pediatric patients with AML: preliminary results from a phase 1 trial. Blood. 2022;140:4584-4585.
Not in our library10.1182/blood-2022-170201
302.
Edwards JP, et al. Abstract 587: ACLX-002, a novel CD123-targeted universal CAR-T cell therapy for relapsed or refractory acute myeloid leukemia that can be activated and silenced in vivo with soluble protein adapters in a dose dependent manner. Cancer Res. 2022;82:587.
Not in our library10.1158/1538-7445.am2022-587
303.
Cummins KD, et al. Treating relapsed / refractory (RR) AML with biodegradable anti-CD123 CAR modified T cells. Blood. 2017;130:1359.
Not in our library
304.
Budde LE, et al. Abstract PR14: CD123CAR displays clinical activity in relapsed/refractory (R/R) acute myeloid leukemia (AML) and blastic plasmacytoid dendritic cell neoplasm (BPDCN): Safety and efficacy results from a phase 1 study. Cancer Immunol. Res. 2020;8:PR14-PR14.
Not in our library10.1158/2326-6074.tumimm18-pr14
305.
Budde L, et al. Remissions of acute myeloid leukemia and blastic plasmacytoid dendritic cell neoplasm following treatment with CD123-specific CAR T cells: a first-in-human clinical trial. Blood. 2017;130:811-811.
Not in our library10.1182/blood.v130.suppl_1.811.811
306.
Qin H, et al. Systematic preclinical evaluation of CD33-directed chimeric antigen receptor T cell immunotherapy for acute myeloid leukemia defines optimized construct design. J. Immunother. Cancer. 2021;9:e003149.
Not in our library10.1136/jitc-2021-003149
307.
Lamba JK, et al. CD33 splicing SNP regulates expression levels of CD33 in normal regenerating monocytes in AML patients. Leuk. Lymphoma. 2018;59:2250-2253.
Not in our library10.1080/10428194.2017.1421756
308.
Mortland L, et al. Clinical significance of CD33 nonsynonymous single-nucleotide polymorphisms in pediatric patients with acute myeloid leukemia treated with gemtuzumab-ozogamicin–containing chemotherapy. Clin. Cancer Res. 2013;19:1620-1627.
Not in our library10.1158/1078-0432.ccr-12-3115
309.
Godwin CD, et al. The CD33 splice isoform lacking exon 2 as therapeutic target in human acute myeloid leukemia. Leukemia. 2020;34:2479-2483.
Not in our library10.1038/s41375-020-0755-7
310.
Shah NN, et al. CD33 CAR T-cells (CD33CART) for children and young adults with relapsed/refractory AML: dose-escalation results from a phase I/II multicenter trial. Blood. 2023;142:771-771.
Not in our library10.1182/blood-2023-179667
311.
Bowser B, et al. Success of centralized manufacturing of CD33 CAR T-cells (CD33CART) for children and young adults with relapsed/refractory AML. Transplant. Cell. Ther. 2024;30:S153-S154.
Not in our library10.1016/j.jtct.2023.12.195
312.
Autologous CD33-CAR-T cells for treatment of relapsed/refractory acute myelogenous leukemia · 2021
No notice
313.
Sallman DA, et al. Phase 1/1b safety study of prgn-3006 ultracar-T in patients with relapsed or refractory CD33-positive acute myeloid leukemia and higher risk myelodysplastic syndromes. Blood. 2022;140:10313-10315.
Not in our library10.1182/blood-2022-169142
314.
Pan J, et al. Phase I study of functionally enhanced CD33 CAR T cells in patients with relapsed or refractory acute myeloid leukemia. J. Clin. Oncol. 2024;42:6518-6518.
Not in our library10.1200/jco.2024.42.16_suppl.6518
315.
Shah NN, et al. Phase 1/2 Study of donor-derived anti-CD33 chimeric antigen receptor expressing T cells (VCAR33) in patients with relapsed or refractory acute myeloid leukemia after allogeneic hematopoietic cell transplantation. Blood. 2023;142:4862.
Not in our library10.1182/blood-2023-180990
316.
Appelbaum, J. et al. Drug-regulated CD33-targeted CAR T cells control AML using clinically optimized rapamycin dosing. J. Clin. Investig.134, e169155 (2024).
Not in our library10.1172/jci162593
317.
Liu, J. et al. Targeted CD7 CAR T-cells for treatment of T-lymphocyte leukemia and lymphoma and acute myeloid leukemia: recent advances. Front. Immunol.14, 1108959 (2023).
Not in our library10.3389/fimmu.2023.1170968
318.
O'Hear C, et al. Anti-CD33 chimeric antigen receptor targeting of acute myeloid leukemia. Haematologica100, 336–344 (2015).
Not in our library10.3324/haematol.2014.112748
319.
Ma, Y.-J. et al. CAR-T therapy in two AML patients with post-transplant relapse and failure of anti-CD38 CAR-T cell treatment. Am. J. Cancer Res.12, 1454–1463 (2022).
Not in our library
320.
Wainberg ZA, et al. AMPLIFY-7P: Phase 1 and randomized phase 2 study of amphiphile immunotherapy ELI-002 7P as adjuvant treatment for subjects with G12D, G12R, G12V, G12C, G12A, G12S and G13D Kirsten rat sarcoma (KRAS)-mutated pancreatic ductal adenocarcinoma. J. Clin. Oncol. 2024;42:TPS720-TPS720.
Not in our library10.1200/jco.2024.42.3_suppl.tps720
321.
First-in-human phase I study of CLL-1 CAR-T cells in adults with relapsed/refractory acute myeloid leukemia · 2022
No notice
322.
Francica B, et al. Abstract 6323: Preclinical evaluation of CB-012, an allogeneic anti-CLL-1 CAR-T cell therapy, that exhibits specific and potent toxicity in acute myeloid leukemia (AML) xenograft models. Cancer Res. 2024;84:6323-6323.
Not in our library10.1158/1538-7445.am2024-6323
323.
CD38-directed CAR-T cell therapy: a novel immunotherapy strategy for relapsed acute myeloid leukemia after allogeneic hematopoietic stem cell transplantation · 2021
No notice
324.
Hu Y, et al. Sequential CD7 CAR T-Cell therapy and allogeneic HSCT without GVHD prophylaxis. N. Engl. J. Med. 2024;390:1467-1480.
Not in our library10.1056/nejmoa2313812
325.
Zhang M, et al. Autologous nanobody-derived fratricide-resistant CD7-CAR T-cell therapy for patients with relapsed and refractory T-cell acute lymphoblastic leukemia/lymphoma. Clin. Cancer Res. 2022;28:2830-2843.
Not in our library10.1158/1078-0432.ccr-21-4097
326.
Baumeister SH, et al. Phase I trial of autologous CAR T cells targeting NKG2D ligands in patients with AML/MDS and multiple myeloma. Cancer Immunol. Res. 2019;7:100-112.
Not in our library10.1158/2326-6066.cir-18-0307
327.
Nikiforow S, et al. A first-in-human phase I trial of NKG2D chimeric antigen receptor-T cells in AML/MDS and multiple myeloma. J. Clin. Oncol. 2016;34:TPS3102-TPS3102.
Not in our library10.1200/jco.2016.34.15_suppl.tps3102
328.
Liu, F. et al. First-in-human CLL1-CD33 compound CAR (cCAR) T cell therapy in relapsed and refractory acute myeloid leukemia. EHA Library Abstract S149 (2020).
Not in our library
329.
Global Manufacturing of CAR T Cell Therapy · 2017
Not checked
330.
Stock S, et al. Idelalisib for optimized CD19-specific chimeric antigen receptor T cells in chronic lymphocytic leukemia patients. Int. J. Cancer. 2019;145:1312-1324.
Not in our library10.1002/ijc.32201
331.
Casati A, et al. Clinical-scale selection and viral transduction of human naïve and central memory CD8+ T cells for adoptive cell therapy of cancer patients. Cancer Immunol. Immunother. 2013;62:1563-1573.
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332.
Wang X, et al. Phenotypic and functional attributes of lentivirus-modified CD19-specific human CD8+ central memory t cells manufactured at clinical scale. J. Immunother. 2012;35:689-701.
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333.
Schmueck-Henneresse M, et al. Comprehensive approach for identifying the T cell subset origin of CD3 and CD28 antibody–activated chimeric antigen receptor-modified T cells. J. Immunother. 2017;199:348-362.
Not in our library10.4049/jimmunol.1601494
334.
CAR-T cell manufacturing: Major process parameters and next-generation strategies · 2024
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335.
Roth TL, et al. Reprogramming human T cell function and specificity with non-viral genome targeting. Nature. 2018;559:405-409.
Not in our library10.1038/s41586-018-0326-5
336.
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337.
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338.
Vishwasrao P, Li G, Boucher JC, Smith DL, Hui SK. Emerging CAR T cell strategies for the treatment of AML. Cancers. 2022;14:1241.
Not in our library10.3390/cancers14051241
339.
Ghorashian S, et al. Enhanced CAR T cell expansion and prolonged persistence in pediatric patients with ALL treated with a low-affinity CD19 CAR. Nat. Med. 2019;25:1408-1414.
Not in our library10.1038/s41591-019-0549-5
340.
Expanding the Therapeutic Window for CAR T Cell Therapy in Solid Tumors: The Knowns and Unknowns of CAR T Cell Biology · 2018
No notice
341.
Mao, R., Kong, W. & He, Y. The affinity of antigen-binding domain on the antitumor efficacy of CAR T cells: moderate is better. Front. Immunol.13, 900241 (2022).
Not in our library10.3389/fimmu.2022.1032403
342.
Mansilla-Soto J, et al. HLA-independent T cell receptors for targeting tumors with low antigen density. Nat. Med. 2022;28:345-352.
Not in our library10.1038/s41591-021-01621-1
343.
Zhao Z, et al. Structural design of engineered costimulation determines tumor rejection kinetics and persistence of CAR T cells. Cancer Cell. 2015;28:415-428.
Not in our library10.1016/j.ccell.2015.09.004
344.
Long AH, et al. 4-1BB costimulation ameliorates T cell exhaustion induced by tonic signaling of chimeric antigen receptors. Nat. Med. 2015;21:581-590.
Not in our library10.1038/nm.3838
345.
Hwang MS, et al. Structural engineering of chimeric antigen receptors targeting HLA-restricted neoantigens. Nat. Commun. 2021;12:5271.
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346.
MacKay M, et al. The therapeutic landscape for cells engineered with chimeric antigen receptors. Nat. Biotechnol. 2020;38:233-244.
Not in our library10.1038/s41587-019-0329-2
347.
Programming CAR T Cell Tumor Recognition: Tuned Antigen Sensing and Logic Gating · 2023
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348.
Mog, B. J. et al. Preclinical studies show that Co-STARs combine the advantages of chimeric antigen and T cell receptors for the treatment of tumors with low antigen densities. Sci. Transl. Med.16, eadh1696 (2024).
Not in our library10.1126/scitranslmed.adg7123
349.
Liu, Y. et al. Chimeric STAR receptors using TCR machinery mediate robust responses against solid tumors. Sci. Transl. Med.13, eabd8636 (2021).
Not in our library10.1126/scitranslmed.abb5191
350.
Synthetic TRuC receptors engaging the complete T cell receptor for potent anti-tumor response · 2019
No notice
351.
Yu, L. et al. Converting TCR-based chimeric antigen receptor STAR into dual-specific targeting receptor for cancer immunotherapy. Mol. Ther. 10.1016/j.ymthe.2025.02.001 (2025).
Not in our library10.1016/j.ymthe.2025.02.001
352.
Huang D, et al. TCR-mimicking STAR conveys superior sensitivity over CAR in targeting tumors with low-density neoantigens. Cell Rep. 2024;43:114949.
Not in our library10.1016/j.celrep.2024.114949
353.
Rosenberg SA, Restifo NP. Adoptive cell transfer as personalized immunotherapy for human cancer. Science. 2015;348:62-68.
Not in our library10.1126/science.aaa4967
354.
Weber EW, Maus MV, Mackall CL. The emerging landscape of immune cell therapies. Cell. 2020;181:46-62.
Not in our library10.1016/j.cell.2020.03.001
355.
RASA2 ablation in T cells boosts antigen sensitivity and long-term function · 2022
No notice
356.
Borot F, et al. Gene-edited stem cells enable CD33-directed immune therapy for myeloid malignancies. Proc. Natl. Acad. Sci. USA. 2019;116:11978-11987.
Not in our library10.1073/pnas.1819992116
357.
Kim MY, et al. Genetic inactivation of CD33 in hematopoietic stem cells to enable CAR T cell immunotherapy for acute myeloid leukemia. Cell. 2018;173:1439-1453.e19.
Not in our library10.1016/j.cell.2018.05.013
358.
Liu Y, et al. CD33-directed immunotherapy with third-generation chimeric antigen receptor T cells and gemtuzumab ozogamicin in intact and CD33-edited acute myeloid leukemia and hematopoietic stem and progenitor cells. Int. J. Cancer. 2022;150:1141-1155.
Not in our library10.1002/ijc.33865
359.
Casirati G, et al. Epitope editing enables targeted immunotherapy of acute myeloid leukaemia. Nature. 2023;621:404-414.
Not in our library10.1038/s41586-023-06496-5
360.
Ji R-J, et al. Epitope prime editing shields hematopoietic cells from CD123 immunotherapy for acute myeloid leukemia. Cell Stem Cell. 2024;31:1650-1666.e8.
Not in our library10.1016/j.stem.2024.09.003
361.
Wellhausen, N. et al. Epitope base editing CD45 in hematopoietic cells enables universal blood cancer immune therapy. Sci. Transl. Med.15, eabm2443 (2023).
Not in our library10.1126/scitranslmed.adi1145
362.
Liu D, Zhao J, Song Y. Engineering switchable and programmable universal CARs for CAR T therapy. J. Hematol. Oncol. 2019;12:69.
Not in our library10.1186/s13045-019-0763-0
363.
Cui Y, et al. T lymphocytes expressing the switchable chimeric Fc receptor CD64 exhibit augmented persistence and antitumor activity. Cell Rep. 2023;42:112797.
Not in our library10.1016/j.celrep.2023.112797
364.
Zarychta J, Kowalczyk A, Krawczyk M, Lejman M, Zawitkowska J. CAR-T cells immunotherapies for the treatment of acute myeloid leukemia-recent advances. Cancers. 2023;15:2944.
Not in our library10.3390/cancers15112944
365.
Engineering advanced logic and distributed computing in human CAR immune cells · 2021
No notice
366.
Kittel-Boselli E, et al. Targeting acute myeloid leukemia using the revCAR platform: a programmable, switchable and combinatorial strategy. Cancers. 2021;13:4785.
Not in our library10.3390/cancers13194785
367.
Lajoie MJ, et al. Designed protein logic to target cells with precise combinations of surface antigens. Science. 2020;369:1637-1643.
Not in our library10.1126/science.aba6527
368.
Roybal KT, et al. Precision tumor recognition by T cells with combinatorial antigen-sensing circuits. Cell. 2016;164:770-779.
Not in our library10.1016/j.cell.2016.01.011
369.
Tousley AM, et al. Co-opting signalling molecules enables logic-gated control of CAR T cells. Nature. 2023;615:507-516.
Not in our library10.1038/s41586-023-05778-2
370.
Cho JH, Collins JJ, Wong WW. Universal chimeric antigen receptors for multiplexed and logical control of T cell responses. Cell. 2018;173:1426-1438.e11.
Not in our library10.1016/j.cell.2018.03.038
371.
Synthetic cytokine circuits that drive T cells into immune-excluded tumors · 2022
No notice
372.
Zhu I, et al. Modular design of synthetic receptors for programmed gene regulation in cell therapies. Cell. 2022;185:1431-1443.e16.
Not in our library10.1016/j.cell.2022.03.023
373.
Roybal KT, et al. Engineering T cells with customized therapeutic response programs using synthetic notch receptors. Cell. 2016;167:419-432.e16.
Not in our library10.1016/j.cell.2016.09.011
374.
Morsut L, et al. Engineering customized cell sensing and response behaviors using synthetic notch receptors. Cell. 2016;164:780-791.
Not in our library10.1016/j.cell.2016.01.012
375.
Richards RM, et al. NOT-gated CD93 CAR T cells effectively target AML with minimized endothelial cross-reactivity. Blood Cancer Discov. 2021;2:648-665.
Not in our library10.1158/2643-3230.bcd-20-0208
376.
Simon S, Bugos G, Salter AI, Riddell SR. Synthetic receptors for logic gated T cell recognition and function. Curr. Opin. Immunol. 2022;74:9-17.
Not in our library10.1016/j.coi.2021.09.003
377.
Zah E, Lin M-Y, Silva-Benedict A, Jensen MC, Chen YY. T cells expressing CD19/CD20 bispecific chimeric antigen receptors prevent antigen escape by malignant B cells. Cancer Immunol. Res. 2016;4:498-508.
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378.
Grada Z, et al. TanCAR: A novel bispecific chimeric antigen receptor for cancer immunotherapy. Mol. Ther. Nucleic Acids. 2013;2:e105.
Not in our library10.1038/mtna.2013.32
379.
Wang, J.-Y. & Wang, L. CAR T cell therapy: where are we now, and where are we heading? Blood sci.5, 237–248 (2023).
Not in our library10.1097/bs9.0000000000000173
380.
Nelde A, et al. Immune surveillance of acute myeloid leukemia is mediated by HLA-presented antigens on leukemia progenitor cells. Blood Cancer Discov. 2023;4:468-489.
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381.
Lynn RC, et al. Targeting of folate receptor β on acute myeloid leukemia blasts with chimeric antigen receptor–expressing T cells. Blood. 2015;125:3466-3476.
Not in our library10.1182/blood-2014-11-612721
382.
Ross JF, Chaudhuri PK, Ratnam M. Differential regulation of folate receptor isoforms in normal and malignant tissues in vivo and in established cell lines. Physiologic and clinical implications. Cancer. 1994;73:2432-2443.
Not in our library10.1002/1097-0142(19940501)73:9<2432::aid-cncr2820730929>3.0.co;2-s
383.
Wang H, Zheng X, Behm FG, Ratnam M. Differentiation-independent retinoid induction of folate receptor type β, a potential tumor target in myeloid leukemia. Blood. 2000;96:3529-3536.
Not in our library10.1182/blood.v96.10.3529
384.
Rafiq S, et al. Optimized T-cell receptor-mimic chimeric antigen receptor T cells directed toward the intracellular Wilms Tumor 1 antigen. Leukemia. 2017;31:1788-1797.
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385.
Di Stasi, A., Jimenez, A. M., Minagawa, K., Al-Obaidi, M. & Rezvani, K. Review of the results of WT1 peptide vaccination strategies for myelodysplastic syndromes and acute myeloid leukemia from nine different studies. Front. Immunol.6, 236 (2015).
Not in our library10.3389/fimmu.2015.00036
386.
Li Z, et al. LILRB4 ITIMs mediate the T cell suppression and infiltration of acute myeloid leukemia cells. Cell Mol. Immunol. 2020;17:272-282.
Not in our library10.1038/s41423-019-0321-2
387.
Deng M, et al. LILRB4 signalling in leukaemia cells mediates T cell suppression and tumour infiltration. Nature. 2018;562:605-609.
Not in our library10.1038/s41586-018-0615-z
388.
Yang T, et al. LILRB4, an immune checkpoint on myeloid cells. Blood Sci. 2022;4:49-56.
Not in our library10.1097/bs9.0000000000000109
389.
John S, et al. A novel anti-LILRB4 CAR-T Cell for the treatment of monocytic AML. Mol. Ther. 2018;26:2487-2495.
Not in our library10.1016/j.ymthe.2018.08.001
390.
Kang X, et al. Inhibitory leukocyte immunoglobulin-like receptors: Immune checkpoint proteins and tumor sustaining factors. Cell Cycle. 2016;15:25-40.
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391.
Zhao X, et al. LILRB4 synthetic T-cell receptor and antigen receptor-T (STAR-T) for refractory/relapsed acute myeloid leukemia: first-in-human phase I clinical trial. Blood. 2024;144:4831-4831.
Not in our library10.1182/blood-2024-207297
392.
Mannis GN, et al. IO-202, a Novel Anti-LILRB4 antibody, with azacitidine for hypomethylating agent-naive chronic myelomonocytic leukemia: phase 1b expansion cohort results. Blood. 2024;144:1008-1008.
Not in our library10.1182/blood-2024-206538
393.
Wang Y, Quan Y, He J, Chen S, Dong Z. SLAM-family receptors promote resolution of ILC2-mediated inflammation. Nat. Commun. 2024;15:5056.
Not in our library10.1038/s41467-024-49466-9
394.
The survival and function of IL-10-producing regulatory B cells are negatively controlled by SLAMF5 · 2021
Not checked
395.
Pérez-Amill L, et al. CD84: a novel target for CAR T-cell therapy for acute myeloid leukemia. Blood. 2022;140:7379-7381.
Not in our library10.1182/blood-2022-165339
396.
Ghorashian S, Pule M. Siglec-6 CAR T: magic bullet for a moving target. Blood. 2021;138:1786-1787.
Not in our library10.1182/blood.2021013184
397.
Jetani H, et al. Siglec-6 is a novel target for CAR T-cell therapy in acute myeloid leukemia. Blood. 2021;138:1830-1842.
Not in our library10.1182/blood.2020009192
398.
Klaihmon P, Luanpitpong S, Kang X, Issaragrisil S. Anti-TIM3 chimeric antigen receptor-natural killer cells from engineered induced pluripotent stem cells effectively target acute myeloid leukemia cells. Cancer Cell. Int. 2023;23:297.
Not in our library10.1186/s12935-023-03153-9
399.
Wolf Y, Anderson AC, Kuchroo VK. TIM3 comes of age as an inhibitory receptor. Nat. Rev. Immunol. 2020;20:173-185.
Not in our library10.1038/s41577-019-0224-6
400.
Sabatos CA, et al. Interaction of Tim-3 and Tim-3 ligand regulates T helper type 1 responses and induction of peripheral tolerance. Nat. Immunol. 2003;4:1102-1110.
Not in our library10.1038/ni988
401.
Mandal K, et al. Structural surfaceomics reveals an AML-specific conformation of integrin β2 as a CAR T cellular therapy target. Nat. Cancer. 2023;4:1592-1609.
Not in our library10.1038/s43018-023-00652-6
402.
Blanco B, Compte M, Lykkemark S, Sanz L, Alvarez-Vallina L. T Cell-redirecting strategies to ‘STAb’ tumors: beyond CARs and bispecific antibodies. Trends Immunol. 2019;40:243-257.
Not in our library10.1016/j.it.2019.01.008
403.
Huehls AM, Coupet TA, Sentman CL. Bispecific T-cell engagers for cancer immunotherapy. Immunol. Cell Biol. 2015;93:290-296.
Not in our library10.1038/icb.2014.93
404.
Dunn GP, Bruce AT, Ikeda H, Old LJ, Schreiber RD. Cancer immunoediting: from immunosurveillance to tumor escape. Nat. Immunol. 2002;3:991-998.
Not in our library10.1038/ni1102-991
405.
Liu X, et al. Improved anti-leukemia activities of adoptively transferred T cells expressing bispecific T-cell engager in mice. Blood Cancer J. 2016;6:e430-e430.
Not in our library10.1038/bcj.2016.38
406.
Jiménez-Reinoso, A. et al. Efficient preclinical treatment of cortical T cell acute lymphoblastic leukemia with T lymphocytes secreting anti-CD1a T cell engagers. J. Immunother. Cancer10, e004042 (2022).
Not in our library10.1136/jitc-2022-005333
407.
Velasco-Sidro M, Arroyo-Ródenas J, Díez-Alonso L, Ramírez-Fernández Á, Álvarez-Vallina L. Dual-targeted STAb-T cells secreting BCMA and CD19 T cell engagers for improved control of haematological cancers. Oncoimmunology. 2025;14:2444701.
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408.
Arroyo-Rodenas J, et al. Effect of CD22-directed CAR-T cells secreting anti-CD19 T cell engagers on control of leukemia progression compared to tandem anti-CD19/CD22 CAR-T cells. J. Clin. Oncol. 2024;42:2550-2550.
Not in our library10.1200/jco.2024.42.16_suppl.2550
409.
Silva, H. et al. CD70 CAR T cells secreting an anti-CD33/anti-CD3 dual targeting antibody overcome antigen heterogeneity in AML. Blood 720–731 (2024).
Not in our library10.1182/blood.2023023210
410.
Yan Z, et al. A dual-targeting approach with anti-IL10R CAR-T cells engineered to release anti-CD33 bispecific antibody in enhancing killing effect on acute myeloid leukemia cells. Cell Oncol. 2024;47:1879-1895.
Not in our library10.1007/s13402-024-00971-5
411.
Silva-Santos B, Mensurado S, Coffelt SB. γδ T cells: pleiotropic immune effectors with therapeutic potential in cancer. Nat. Rev. Cancer. 2019;19:392-404.
Not in our library10.1038/s41568-019-0153-5
412.
Xin W, et al. Structures of human γδ T cell receptor–CD3 complex. Nature. 2024;630:222-229.
Not in our library10.1038/s41586-024-07439-4
413.
T cells in health and disease · 2023
No notice
414.
Ribot JC, Lopes N, Silva-Santos B. γδ T cells in tissue physiology and surveillance. Nat. Rev. Immunol. 2021;21:221-232.
Not in our library10.1038/s41577-020-00452-4
415.
Mensurado S, Blanco-Domínguez R, Silva-Santos B. The emerging roles of γδ T cells in cancer immunotherapy. Nat. Rev. Clin. Oncol. 2023;20:178-191.
Not in our library10.1038/s41571-022-00722-1
416.
Mensurado S, et al. CD155/PVR determines acute myeloid leukemia targeting by Delta One T cells. Blood. 2024;143:1488-1495.
Not in our library10.1182/blood.2023022992
417.
Di Lorenzo B, et al. Broad cytotoxic targeting of acute myeloid leukemia by polyclonal delta one T cells. Cancer Immunol. Res. 2019;7:552-558.
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418.
Veglia F, Perego M, Gabrilovich D. Myeloid-derived suppressor cells coming of age. Nat. Immunol. 2018;19:108-119.
Not in our library10.1038/s41590-017-0022-x
419.
Myeloid-derived suppressor cells as immunosuppressive regulators and therapeutic targets in cancer · 2021
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420.
Lasser SA, Ozbay Kurt FG, Arkhypov I, Utikal J, Umansky V. Myeloid-derived suppressor cells in cancer and cancer therapy. Nat. Rev. Clin. Oncol. 2024;21:147-164.
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421.
Recommendations for myeloid-derived suppressor cell nomenclature and characterization standards · 2016
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422.
Di, S. et al. Combined adjuvant of Poly I:C improves antitumor effects of CAR-T cells. Front. Oncol.9, 1208 (2019).
Not in our library10.3389/fonc.2019.00241
423.
Xu Y, et al. Closely related T-memory stem cells correlate with in vivo expansion of CAR.CD19-T cells and are preserved by IL-7 and IL-15. Blood. 2014;123:3750-3759.
Not in our library10.1182/blood-2014-01-552174
424.
Singh H, et al. Reprogramming CD19-specific T cells with IL-21 signaling can improve adoptive immunotherapy of B-lineage malignancies. Cancer Res. 2011;71:3516-3527.
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425.
Avanzi MP, et al. IL-18 secreting CAR T cells enhance cell persistence, induce prolonged B cell aplasia and eradicate CD19+ tumor cells without need for prior conditioning. Blood. 2016;128:816.
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426.
Sockolosky JT, et al. Selective targeting of engineered T cells using orthogonal IL-2 cytokine-receptor complexes. Science. 2018;359:1037-1042.
Not in our library10.1126/science.aar3246
427.
Analysis of 100,000 human cancer genomes reveals the landscape of tumor mutational burden · 2017
No notice
428.
Assi, R., Kantarjian, H., Ravandi, F. & Daver, N. Immune therapies in acute myeloid leukemia: a focus on monoclonal antibodies and immune checkpoint inhibitors. Curr. Opin. Hematol. 25 111–117 (2018).
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429.
Williams P, et al. The distribution of T-cell subsets and the expression of immune checkpoint receptors and ligands in patients with newly diagnosed and relapsed acute myeloid leukemia. Cancer. 2019;125:1470-1481.
Not in our library10.1002/cncr.31896
430.
CAR T Cells for Acute Myeloid Leukemia: State of the Art and Future Directions · 2020
No notice
431.
Song W, Zhang M. Use of CAR-T cell therapy, PD-1 blockade, and their combination for the treatment of hematological malignancies. Clin. Immunol. 2020;214:108382.
Not in our library10.1016/j.clim.2020.108382
432.
Lemoine J, Ruella M, Houot R. Overcoming intrinsic resistance of cancer cells to CAR T-cell killing. Clin. Cancer Res. 2021;27:6298-6306.
Not in our library10.1158/1078-0432.ccr-21-1559
433.
Karlsson H. Approaches to augment CAR T-cell therapy by targeting the apoptotic machinery. Biochem. Soc. Trans. 2016;44:371-376.
Not in our library10.1042/bst20150253
434.
Epi-drugs in combination with immunotherapy: a new avenue to improve anticancer efficacy · 2017
No notice
435.
Low-dose decitabine priming endows CAR T cells with enhanced and persistent antitumour potential via epigenetic reprogramming · 2021
No notice
436.
James SR, Link PA, Karpf AR. Epigenetic regulation of X-linked cancer/germline antigen genes by DNMT1 and DNMT3b. Oncogene. 2006;25:6975-6985.
Not in our library10.1038/sj.onc.1209678
437.
Zhou J, et al. Demethylating agent decitabine disrupts tumor-induced immune tolerance by depleting myeloid-derived suppressor cells. J. Cancer Res. Clin. Oncol. 2017;143:1371-1380.
Not in our library10.1007/s00432-017-2394-6
438.
Khan O, et al. TOX transcriptionally and epigenetically programs CD8+ T cell exhaustion. Nature. 2019;571:211-218.
Not in our library10.1038/s41586-019-1325-x
439.
Otáhal, P. et al. Lenalidomide enhances antitumor functions of chimeric antigen receptor modified T cells. Oncoimmunology5, e1226723 (2016).
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440.
Works M, et al. Anti–B-cell maturation antigen chimeric antigen receptor T cell function against multiple myeloma is enhanced in the presence of lenalidomide. Mol. Cancer Ther. 2019;18:2246-2257.
Not in our library10.1158/1535-7163.mct-18-1146
441.
Ai K, et al. Optimizing CAR-T cell therapy for solid tumors: current challenges and potential strategies. J. Hematol. Oncol. 2024;17:105.
Not in our library10.1186/s13045-024-01625-7
442.
PRODH2-mediated proline metabolism boosts CAR T-cell effector function. Cancer Discov.12, 1405 (2022).
Not in our library10.1158/2159-8290.cd-rw2022-054
443.
Ye L, et al. A genome-scale gain-of-function CRISPR screen in CD8 T cells identifies proline metabolism as a means to enhance CAR-T therapy. Cell Metab. 2022;34:595-614.e14.
Not in our library10.1016/j.cmet.2022.02.009
444.
Yang, Q. et al. Superior antitumor immunotherapy efficacy of kynureninase modified CAR-T cells through targeting kynurenine metabolism. Oncoimmunology11, 2093402 (2022).
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445.
Heslop HE. Data mining for second malignancies after CAR-T. Blood. 2024;143:2023-2024.
Not in our library10.1182/blood.2024024446
446.
Hamilton MP, et al. Risk of second tumors and T-cell lymphoma after CAR T-cell therapy. N. Engl. J. Med. 2024;390:2047-2060.
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447.
Strati P, et al. Hematopoietic recovery and immune reconstitution after axicabtagene ciloleucel in patients with large B-cell lymphoma. Haematologica. 2021;106:2667-2672.
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448.
Elsallab M, et al. Second primary malignancies after commercial CAR T-cell therapy: analysis of the FDA adverse events reporting system. Blood. 2024;143:2099-2105.
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449.
National Library of Medicine (US). NCT04134117. Tisagenlecleucel in primary CNS lymphoma. ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT04134117?cond=NCT04134117&rank=1 (2019).
Not in our library
450.
Frigault MJ, et al. Tisagenlecleucel demonstrates safety, efficacy and CNS trafficking in primary CNS lymphoma. Blood. 2021;138:258-258.
Not in our library10.1182/blood-2021-148444
451.
Dietrich, J. et al. CAR-T cell therapy in recurrent primary CNS lymphoma (PCNSL): a phase 2 clinical trial (S27.009). Neurology98, S27.009 (2022).
Not in our library
452.
National Library of Medicine (US). NCT03630159. Study of tisagenlecleucel in combination with pembrolizumab in R/R diffuse large B-cell lymphoma patients (PORTIA). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT03630159?cond=tisagenlecleucel&checkSpell=&rank=9 (2018).
Not in our library
453.
Jaeger U, et al. Safety and efficacy of tisagenlecleucel plus pembrolizumab in patients with R/R DLBCL: phase 1b PORTIA study results. Blood Adv. 2023;7:2283-2286.
Not in our library10.1182/bloodadvances.2022007779
454.
National Library of Medicine (US). NCT03876028. Study of tisagenlecleucel in combination with ibrutinib in R/R diffuse large B-cell lymphoma patients. ClinicalTrials.gov [Internet]. https://clinicaltrials.gov/study/NCT03876028?cond=tisagenlecleucel&checkSpell=&page=2&rank=11 (2019).
Not in our library
455.
national library of medicine (us). nct06003179. optimizing lymphodepletion to improve outcomes in patients receiving cell therapy with kymriah (LOKI). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT06003179?cond=tisagenlecleucel&checkSpell=&page=3&rank=22 (2023).
Not in our library
456.
National Library of Medicine (US). NCT05310591. Combination of an anti-PD1 antibody with tisagenlecleucel reinfusion in children, adolescents and young adults with acute lymphoblastic leukemia after loss of persistence (CAPTiRALL). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT05310591?cond=tisagenlecleucel&checkSpell=&page=2&rank=16 (2022).
Not in our library
457.
National Library of Medicine (US). NCT03876769. Study of efficacy and safety of tisagenlecleucel in HR B-ALL EOC MRD positive patients (CASSIOPEIA). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT03876769?cond=NCT03876769&rank=1 (2018).
Not in our library
458.
Buechner, J. et al. Chimeric antigen receptor T-cell therapy in paediatric B-cell precursor acute lymphoblastic leukaemia: curative treatment option or bridge to transplant? Front. Pediatr.9 (2022).
Not in our library10.3389/fped.2021.784024
459.
National Library of Medicine (US). NCT03568461.Efficacy and safety of tisagenlecleucel in adult patients with refractory or relapsed follicular lymphoma (ELARA). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT03568461?cond=NCT03568461&rank=1&tab=results (2018).
Not in our library
460.
National Library of Medicine (US). NCT04234061. Clinical Trial to Assess The efficacy and safety of the combination of tisagenlecleucel and ibrutinib in mantle cell lymphoma (TARMAC). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT04234061?cond=tisagenlecleucel&checkSpell=&page=2&rank=18&tab=table (2020).
Not in our library
461.
National Library of Medicine (U.S.). NCT02445248. Study of efficacy and safety of CTL019 in adult DLBCL patients (JULIET). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT02445248?cond=NCT02445248&rank=1 (2015).
Not in our library
462.
Schuster SJ, et al. Long-term clinical outcomes of tisagenlecleucel in patients with relapsed or refractory aggressive B-cell lymphomas (JULIET): a multicentre, open-label, single-arm, phase 2 study. Lancet Oncol. 2021;22:1403-1415.
Not in our library10.1016/s1470-2045(21)00375-2
463.
National Library of Medicine (US). NCT03610724. Phase II open label trial to determine safety & efficacy of tisagenlecleucel in pediatric non-Hodgkin lymphoma patients. ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT03610724?cond=NCT03610724&rank=1 (2018).
Not in our library
464.
National Library of Medicine (U.S.). NCT02228096. Study of efficacy and safety of CTL019 in pediatric ALL patients (ENSIGN). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT02228096?tab=results (2014).
Not in our library
465.
Awasthi R, et al. Long term durable responses in relapsed/refractory (R/R) ALL, DLBCL, and FL patients treated with tisagenlecleucel and its association with persistence of CAR T-cells. Blood. 2023;142:4872-4872.
Not in our library10.1182/blood-2023-181663
466.
Laetsch TW, et al. Tisagenlecleucel in pediatric and young adult patients with down syndrome-associated relapsed/refractory acute lymphoblastic leukemia. Leukemia. 2022;36:1508-1515.
Not in our library10.1038/s41375-022-01550-z
467.
Thudium Mueller K, et al. Tisagenlecleucel immunogenicity in relapsed/refractory acute lymphoblastic leukemia and diffuse large B-cell lymphoma. Blood Adv. 2021;5:4980-4991.
Not in our library10.1182/bloodadvances.2020003844
468.
National Library of Medicine (US). NCT05460533. A second infusion (early reinfusion) of tisagenlecleucel in children and young adults with B-cell acute lymphoblastic leukemia(B-ALL). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT05460533?cond=tisagenlecleucel&checkSpell=&page=2&rank=19 (2022).
Not in our library
469.
National Library of Medicine (US). NCT04225676. Study of efficacy and safety of reinfusion of tisagenlecleucel in pediatric and young adult patients with acute lymphoblastic leukemia (ALL). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT04225676?cond=NCT04225676&rank=1 (2020).
Not in our library
470.
Boyer MW, et al. ALL-026: evaluating efficacy and safety of tisagenlecleucel reinfusion following loss of B-cell aplasia in pediatric and young adult patients with acute lymphoblastic leukemia: HESTER phase II study. Clin. Lymphoma Myeloma Leuk. 2021;21:S262-S263.
Not in our library10.1016/s2152-2650(21)01641-4
471.
Boyer MW, et al. HESTER: A phase II study evaluating efficacy and safety of tisagenlecleucel reinfusion in pediatric and young adult patients with acute lymphoblastic leukemia experiencing loss of B-cell aplasia. Blood. 2020;136:23-24.
Not in our library10.1182/blood-2020-136340
472.
National Library of Medicine (US). NCT04161118. Tisagenlecleucel in elderly patients with first-relapsed or primary refractory aggressive B-cell non-Hodgkin lymphoma (TIGER-CTL019). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT04161118?term=tisagenlecleucel&rank=19 (2019).
Not in our library
473.
National Library of Medicine (US). NCT04156659. Study of tisagenlecleucel in chinese pediatric and young adult subjects with relapsed or refractory B-cell ALL. ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT04156659?cond=tisagenlecleucel&checkSpell=&page=2&rank=13 (2019).
Not in our library
474.
National Library of Medicine (US). NCT04456023. Study of tisagenlecleucel in chinese adult patients with relapsed or refractory diffuse large b-cell non-Hodgkin lymphoma (DLBCL). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT04456023?cond=tisagenlecleucel&checkSpell=&page=2&rank=17 (2020).
Not in our library
475.
National Library of Medicine (US). NCT03570892. Tisagenlecleucel in adult patients with aggressive B-cell non-Hodgkin lymphoma. ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT03570892?cond=NCT03570892&rank=1 (2018).
Not in our library
476.
Bishop MR, et al. Second-line tisagenlecleucel or standard care in aggressive B-cell lymphoma. N. Engl. J. Med. 2022;386:629-639.
Not in our library10.1056/nejmoa2116596
477.
National Library of Medicine (US). NCT05888493. A phase III trial comparing tisagenlecleucel to standard of care (SoC) in adult participants with R/R follicular lymphoma (LEDA). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT05888493?term=tisagenlecleucel&rank=21&tab=table (2023).
Not in our library
478.
National Library of Medicine (US). NCT04094311. Study of out of specification for tisagenlecleucel. ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT04094311?cond=tisagenlecleucel&checkSpell=&rank=2.(2021)
Not in our library
479.
National Library of Medicine (US). NCT05199961. Quality of life of adults with diffuse large B-cell lymphoma treated with tisagenlecleucel. ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT05199961?term=tisagenlecleucel&rank=22 (2022).
Not in our library
480.
National Library of Medicine (US). NCT05541341. Effectiveness and safety of tisagenlecleucel therapy in brazilian patients with B-lymphocyte malignancies. ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT05541341?cond=tisagenlecleucel&checkSpell=&rank=6 (2022).
Not in our library
481.
National Library of Medicine (US). NCT03153462. Axicabtagene ciloleucel expanded access study (ZUMA-9). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT03153462?cond=Axicabtagene%20ciloleucel&sort=StudyFirstPostDate&rank=23 (2017).
Not in our library
482.
Jacobson CA, et al. Outcomes of patients (Pts) in ZUMA-9, a multicenter, open-label study of axicabtagene ciloleucel (axi-cel) in relapsed/refractory large B cell lymphoma (R/R LBCL) for expanded access and commercial out-of-specification (OOS) product. Blood. 2020;136:2-3.
Not in our library10.1182/blood-2020-136136
483.
National Library of Medicine (US). NCT04608487. Axi-cel in CNS lymphoma. ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT04608487?cond=Axicabtagene%20ciloleucel&sort=StudyFirstPostDate&rank=15 (2020).
Not in our library
484.
Nayak L, et al. A pilot study of axicabtagene ciloleucel (axi-cel) for relapsed/refractory primary and secondary central nervous system lymphoma (PCNSL and SCNSL). J. Clin. Oncol. 2024;42:2006-2006.
Not in our library10.1200/jco.2024.42.16_suppl.2006
485.
National Library of Medicine (US). NCT05077527. Immune cell therapy (CAR-T) for the treatment of patients with HIV and B-cell non-Hodgkin lymphoma. ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT05077527?cond=Axicabtagene%20ciloleucel&sort=StudyFirstPostDate&rank=13 (2021).
Not in our library
486.
National Library of Medicine (US). NCT05794958. Evaluate safety of axicabtagene ciloleucel reinfusion (axi-cel-2) in patients with relapsed and/or refractory second line high-risk non-Hodgkin lymphoma after standard of care Axi-Cel. ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT05794958?cond=NCT05794958.%20&rank=1 (2023).
Not in our library
487.
National Library of Medicine (US). NCT05950802. Optimizing lymphodepletion to improve outcomes in patients receiving cell therapy with yescarta (ODIN). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT05950802?cond=yescarta&rank=1 (2023).
Not in our library
488.
National Library of Medicine (US). NCT03704298. Safety and efficacy of axicabtagene ciloleucel in combination with utomilumab in adults with refractory large B-cell lymphoma (ZUMA-11). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT03704298?cond=Axicabtagene%20ciloleucel&sort=StudyFirstPostDate&rank=21 (2018).
Not in our library
489.
National Library of Medicine (US). NCT04314843. Study of lenzilumab and axicabtagene ciloleucel in participants with relapsed or refractory large B-cell lymphoma (ZUMA-19). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT04314843?cond=Axicabtagene%20ciloleucel&sort=StudyFirstPostDate&rank=17 (2020).
Not in our library
490.
Kenderian SS, et al. ZUMA-19: A phase 1/2 multicenter study of lenzilumab use with axicabtagene ciloleucel (axi-cel) in patients (Pts) with relapsed or refractory large B cell lymphoma (R/R LBCL). Blood. 2020;136:6-7.
Not in our library10.1182/blood-2020-135988
491.
Oluwole OO, et al. ZUMA-19: A phase 1/2 study of axicabtagene ciloleucel plus lenzilumab in patients with relapsed or refractory large B-cell lymphoma. Blood. 2022;140:10318-10320.
Not in our library10.1182/blood-2022-167688
492.
National Library of Medicine (US). NCT03105336. A phase 2 multicenter study of axicabtagene ciloleucel in subjects with relapsed/refractory indolent non-Hodgkin lymphoma (ZUMA-5). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT03105336?cond=Axicabtagene%20ciloleucel&sort=StudyFirstPostDate&rank=24 (2017).
Not in our library
493.
Neelapu SS, et al. Three-year follow-up analysis of axicabtagene ciloleucel in relapsed/refractory indolent non-Hodgkin lymphoma (ZUMA-5). Blood. 2024;143:496-506.
Not in our library10.1182/blood.2023021243
494.
Ghione P, et al. Comparative effectiveness of ZUMA-5 (axi-cel) vs SCHOLAR-5 external control in relapsed/refractory follicular lymphoma. Blood. 2022;140:851-860.
Not in our library10.1182/blood.2021014375
495.
Leslie, L. et al. P1159 ZUMA-24 Preliminary analysis: a phase 2 study of axicabtagene ciloleucel in the outpatient setting with prophylactic corticosteroids in patients with relapsed/refractory large B-cell lymphoma. In Eha2024 2093402 (2024).
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496.
Leslie L, et al. Pb2346: ZUMA-24: a phase 2, open-label, multicenter study of axicabtagene ciloleucel in patients with relapsed/refractory large B-cell lymphoma given with corticosteroids in the outpatient setting. Hemasphere. 2023;7:e50042ff.
Not in our library10.1097/01.hs9.0000976104.50042.ff
497.
National Library of Medicine (US). NCT05459571. Study of axicabtagene ciloleucel given with steroids in participants with relapsed or refractory large B-cell lymphoma (ZUMA-24). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT05459571?cond=NCT05459571&rank=1.
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498.
Neelapu SS, et al. A phase 2, open-label, multicenter study evaluating the safety and efficacy of axicabtagene ciloleucel in combination with either rituximab or lenalidomide in patients with refractory large B-cell lymphoma (ZUMA-14). Blood. 2019;134:4093-4093.
Not in our library10.1182/blood-2019-126369
499.
Strati P, et al. Axicabtagene ciloleucel (axi-cel) in combination with rituximab (Rtx) for the treatment (Tx) of refractory large B-cell lymphoma (R-LBCL): outcomes of the phase 2 ZUMA-14 study. J. Clin. Oncol. 2022;40:7567-7567.
Not in our library10.1200/jco.2022.40.16_suppl.7567
500.
National Library of Medicine (US). NCT04002401. Safety and efficacy of axicabtagene ciloleucel in combination with rituximab in participants with refractory large B-cell lymphoma (ZUMA-14). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT04002401?cond=Axicabtagene%20ciloleucel&sort=StudyFirstPostDate&rank=18 (2019).
Not in our library
501.
National Library of Medicine (US). NCT03761056. Study to evaluate the efficacy and safety of axicabtagene ciloleucel as first-line therapy in participants with high-risk large B-cell lymphoma. ClinicalTrials.gov [Internet]https://clinicaltrials.gov/search?cond=Axicabtagene%20ciloleucel&sort=StudyFirstPostDate (2018).
Not in our library
502.
Neelapu SS, et al. Primary analysis of ZUMA-12: a phase 2 study of axicabtagene ciloleucel (axi-cel) as first-line therapy in patients with high-risk large B-cell lymphoma (LBCL). Blood. 2021;138:739-739.
Not in our library10.1182/blood-2021-148009
503.
Neelapu SS, et al. Interim analysis of ZUMA-12: a phase 2 study of axicabtagene ciloleucel (axi-cel) as first-line therapy in patients (pts) with high-risk large B cell lymphoma (LBCL). Blood. 2020;136:49-49.
Not in our library10.1182/blood-2020-134449
504.
Neelapu SS, et al. ZUMA-12: a phase 2 multicenter study of axicabtagene ciloleucel (axi-cel) as a first-line therapy in patients (pts) with high-risk large B-cell lymphoma (LBCL). J. Clin. Oncol. 2019;37:TPS7574-TPS7574.
Not in our library10.1200/jco.2019.37.15_suppl.tps7574
505.
Axicabtagene ciloleucel as first-line therapy in high-risk large B-cell lymphoma: the phase 2 ZUMA-12 trial · 2022
No notice
506.
Chavez JC, et al. 3-year analysis of ZUMA-12: a phase 2 study of axicabtagene ciloleucel (axi-cel) as first-line therapy in patients with high-risk large B-cell lymphoma (LBCL). Blood. 2023;142:894-894.
Not in our library10.1182/blood-2023-174510
507.
National Library of Medicine (US). NCT06218602. Pilot trial of fecal microbiota transplantation for lymphoma patients receiving axicabtagene ciloleucel therapy. ClinicalTrials.gov [Internethttps://clinicaltrials.gov/study/NCT06218602?cond=Axicabtagene%20ciloleucel&sort=StudyFirstPostDate&rank=4 (2024).
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508.
National Library of Medicine (US). NCT06043323. A phase II study of axicabtagene ciloleucel, an anti-CD19 chimeric antigen receptor (CAR) T cell therapy, in combination with radiotherapy (RT) in relapsed/refractory follicular lymphoma. ClinicalTrials.gov [Internethttps://clinicaltrials.gov/study/NCT06043323?cond=Axicabtagene%20ciloleucel&sort=StudyFirstPostDate&rank=6 (2023).
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509.
National Library of Medicine (US). NCT06213311. A study of axicabtagene ciloleucel and glofitamab as second-line therapy for relapsed or refractory patients with large B cell lymphoma. ClinicalTrials.gov [Internethttps://clinicaltrials.gov/study/NCT06213311?cond=Axicabtagene%20ciloleucel&sort=StudyFirstPostDate&rank=5 (2024).
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510.
National Library of Medicine (US). NCT03391466. Study of effectiveness of axicabtagene ciloleucel compared to standard of care therapy in patients with relapsed/refractory diffuse large B cell lymphoma (ZUMA-7). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT03391466?cond=Axicabtagene%20ciloleucel&sort=StudyFirstPostDate&rank=22 (2017).
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511.
Ghobadi A, et al. Outcomes of subsequent anti-lymphoma therapies in patients (pts) with large B-cell lymphoma (LBCL) treated with axicabtagene ciloleucel (axi-cel) or standard of care (SOC) in the second-line (2L) ZUMA-7 study. Blood. 2022;140:1595-1597.
Not in our library10.1182/blood-2022-158303
512.
Locke FL, et al. Association of metabolic tumor volume (MTV) and clinical outcomes in second-line (2L) relapsed/refractory (R/R) large B-cell lymphoma (LBCL) following axicabtagene ciloleucel (axi-cel) versus standard-of-care (Soc) therapy in ZUMA-7. Blood. 2022;140:638-640.
Not in our library10.1182/blood-2022-158492
513.
Westin JR, et al. Survival with axicabtagene ciloleucel in large B-cell lymphoma. N. Engl. J. Med. 2023;389:148-157.
Not in our library10.1056/nejmoa2301665
514.
Westin JR, et al. Safety and efficacy of axicabtagene ciloleucel versus standard of care in patients 65 years of age or older with relapsed/refractory large B-cell lymphoma. Clin. Cancer Res. 2023;29:1894-1905.
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515.
National Library of Medicine (US). NCT05605899. Study to compare axicabtagene ciloleucel with standard of care therapy as first-line treatment in participants with high-risk large B-cell lymphoma (ZUMA-23). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT05605899?cond=NCT05605899&rank=1 (2022).
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516.
National Library of Medicine (US). NCT05371093. Study of axicabtagene ciloleucel versus standard of care therapy in participants with relapsed/refractory follicular lymphoma (ZUMA-22). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT05371093?cond=NCT05371093&rank=1 (2022).
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517.
Flinn IW, et al. P1107: ZUMA-22: a phase 3, randomized controlled study of axicabtagene ciloleucel versus standard-of-care therapy in patients with relapsed or refractory follicular lymphoma. Hemasphere. 2023;7:e6350662.
Not in our library10.1097/01.hs9.0000971324.63506.62
518.
National Library of Medicine (US). NCT06609304. Axicabtagene ciloleucel for consolidation after first-line treatment of high-risk large B-cell lymphoma (axi-cel). ClinicalTrials.gov [Internethttps://clinicaltrials.gov/study/NCT06609304?cond=Axicabtagene%20ciloleucel&sort=StudyFirstPostDate&rank=1 (2024).
Not in our library
519.
National Library of Medicine (US). NCT05800067. Axi-cel retreatment in relapsed/refractory LBCL. ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT05800067?cond=Axicabtagene%20ciloleucel&sort=StudyFirstPostDate&rank=7 (2022).
Not in our library
520.
Goy A, et al. Outcomes of patients with relapsed/refractory mantle cell lymphoma (R/R MCL) treated with brexucabtagene autoleucel (brexu-cel) in ZUMA-2 and ZUMA-18, an expanded access study. Blood. 2023;142:106-106.
Not in our library10.1182/blood-2023-174273
521.
National Library of Medicine (US). NCT04162756. Study of brexucabtagene autoleucel (KTE-X19) for the treatment of individuals with relapsed/refractory B-cell malignancies (ZUMA-18). ClinicalTrials.gov [Internet] (2019).
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522.
NCT05776134. Expanded access study for the treatment of patients with commercially out-of-specification brexucabtagene autoleucel. ClinicalTrials.gov [Internet].
Not in our library
523.
National Library of Medicine (US). NCT05993949. Study of brexucabtagene autoleucel plus dasatinib in adults with acute lymphoblastic leukemia. ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT05993949?cond=brexucabtagene%20autoleucel&rank=3 (2023).
Not in our library
524.
Davids MS, et al. ZUMA-8: a phase 1 study of KTE-X19, an anti-CD19 chimeric antigen receptor (CAR) T-cell therapy, in patients with relapsed/refractory chronic lymphocytic leukemia. Blood. 2022;140:7454-7456.
Not in our library10.1182/blood-2022-167868
525.
Flinn I, et al. ZUMA-8: a phase 1/2 multicenter study evaluating KTE-X19 in patients (pts) with relapsed/refractory (R/R) chronic lymphocytic leukemia (CLL). J. Clin. Oncol. 2019;37:TPS7566-TPS7566.
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526.
National Library of Medicine (US). NCT03624036. Study to evaluate the safety and tolerability of brexucabtagene autoleucel (KTE-X19) in people with relapsed/refractory chronic lymphocytic leukemia and small lymphocytic lymphoma (ZUMA-8). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT03624036?cond=brexucabtagene%20autoleucel&rank=9#publications (2018).
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527.
National Library of Medicine (U.S.). NCT02625480. Study evaluating brexucabtagene autoleucel (KTE-X19) in pediatric and adolescent participants with relapsed/refractory B-precursor acute lymphoblastic leukemia or relapsed/refractory B-cell non-Hodgkin lymphoma (ZUMA-4). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT02625480?cond=brexucabtagene%20autoleucel&rank=10 (2015).
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528.
Wayne AS, et al. Three-year results from phase I of ZUMA-4: KTE-X19 in pediatric relapsed/refractory acute lymphoblastic leukemia. Haematologica. 2022;108:747-760.
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National Library of Medicine (U.S.). NCT02614066. A study evaluating the safety and efficacy of brexucabtagene autoleucel (KTE-X19) in adult subjects with relapsed/refractory B-precursor acute lymphoblastic leukemia (ZUMA-3) (ZUMA-3). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT02614066?cond=NCT02614066&rank=1 (2015).
Not in our library
530.
Shah BD, et al. KTE-X19 anti-CD19 CAR T-cell therapy in adult relapsed/refractory acute lymphoblastic leukemia: ZUMA-3 phase 1 results. Blood. 2021;138:11-22.
Not in our library10.1182/blood.2020009098
531.
Shah BD, et al. KTE-X19 for relapsed or refractory adult B-cell acute lymphoblastic leukaemia: phase 2 results of the single-arm, open-label, multicentre ZUMA-3 study. Lancet. 2021;398:491-502.
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532.
National Library of Medicine (US). NCT06287229. Phase Ib/II study assessing the clinical activity and safety of brexucabtagene autoleucel as a consolidation in patients with relapsed/refractory (R/R) and newly diagnosed b-cell acute lymphocytic leukemia (ALL) post cytoreduction with mini-HCVD-inotuzumab-blinatumomab/HCVAD-inotuzumab-blinatumomab. ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT06287229?cond=brexucabtagene%20autoleucel&rank=2 (2024).
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533.
National Library of Medicine (US). NCT05537766. Study of brexucabtagene autoleucel in adults with rare B-cell malignancies (ZUMA-25). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT05537766?cond=brexucabtagene%20autoleucel&rank=5 (2022).
Not in our library
534.
Wayne AS, et al. ZUMA-4: A phase 1/2 multicenter study evaluating the safety and efficacy of KTE-C19 (anti-CD19 CAR T cells) in pediatric and adolescent subjects with relapsed/refractory B-precursor acute lymphoblastic leukemia (R/R ALL). J. Clin. Oncol. 2016;34:TPS7075-TPS7075.
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535.
Wang M, et al. ZUMA-2: Phase 2 multicenter study evaluating efficacy of kte-C19 in patients with relapsed/refractory mantle cell lymphoma. J. Clin. Oncol. 2018;36:TPS3102-TPS3102.
Not in our library10.1200/jco.2018.36.15_suppl.tps3102
536.
National Library of Medicine (U.S.). NCT02601313. Study of brexucabtagene autoleucel (KTE-X19) in participants with relapsed/refractory mantle cell lymphoma (cohort 1 and cohort 2) (ZUMA-2). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT02601313?cond=brexucabtagene%20autoleucel&rank=12 (2015).
Not in our library
537.
National Library of Medicine (US). NCT06553872. Phase 2 open label randomized study of pirtobrutinib and brexucabtagene autoleucel in R/R MCL. ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT06553872?cond=brexucabtagene%20autoleucel&rank=1 (2024).
Not in our library
538.
National Library of Medicine (US). NCT04880434. Study of brexucabtagene autoleucel (KTE-X19) in participants with relapsed/refractory mantle cell lymphoma (cohort 3) (ZUMA-2). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT04880434?cond=NCT04880434&rank=1 (2021).
Not in our library
539.
van Meerten T, et al. Primary analysis of ZUMA-2 cohort 3: brexucabtagene autoleucel (brexu-cel) in patients (pts) with relapsed/refractory mantle cell lymphoma (R/R MCL) who were naive to bruton tyrosine kinase inhibitors (BTKi). Blood. 2024;144:748-748.
Not in our library10.1182/blood-2024-198021
540.
National Library of Medicine (US). NCT03274219. Study of bb21217 in multiple myeloma. ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT03274219?cond=idecabtagene%20vicleucel&rank=17 (2017).
Not in our library
541.
Alsina M, et al. Updated results from the phase I CRB-402 study of anti-Bcma CAR-T cell therapy bb21217 in patients with relapsed and refractory multiple myeloma: correlation of expansion and duration of response with T cell phenotypes. Blood. 2020;136:25-26.
Not in our library10.1182/blood-2020-140410
542.
National Library of Medicine (US). NCT04771078. Expanded access protocol (EAP) for participants receiving idecabtagene vicleucel that is nonconforming for commercial release. ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT04771078?cond=NCT04771078&rank=1.
Not in our library
543.
Paul B, et al. Idecabtagene vicleucel (ide-cel) in patients (pts) with newly diagnosed multiple myeloma (NDMM) with an inadequate response to front-line autologous stem cell transplantation (ASCT): karMMa-2 cohort 2c extended follow-up. Blood. 2024;144:3388-3388.
Not in our library10.1182/blood-2024-200829
544.
National Library of Medicine (US). NCT06048250. Mezigdomide (CC-92480) post idecabtagene vicleucel in treating patients with relapsed multiple myeloma. ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT06048250?cond=idecabtagene%20vicleucel&rank=7 (2023).
Not in our library
545.
Anderson JLD, et al. Idecabtagene vicleucel (ide-cel, bb2121), a BCMA-directed CAR T cell therapy, in relapsed and refractory multiple myeloma: Updated KarMMa results. J. Clin. Oncol. 2021;39:8016-8016.
Not in our library10.1200/jco.2021.39.15_suppl.8016
546.
Raje NS, et al. KarMMa-7, a phase 1/2, dose-finding and dose-expansion study of combination therapies with idecabtagene vicleucel (ide-cel, bb2121), a BCMA-directed CAR T cell therapy for relapsed/refractory multiple myeloma (rrmm). Blood. 2021;138:4830-4830.
Not in our library10.1182/blood-2021-147412
547.
National Library of Medicine (US). NCT04855136. Safety and efficacy of bb2121 (ide-cel) combinations in multiple myeloma (KarMMa-7). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT04855136?cond=idecabtagene%20vicleucel&rank=13 (2021).
Not in our library
548.
National Library of Medicine (US). NCT06518551. Elotuzumab + iberdomide + dexamethasone post ide-cel in rrmm. ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT06518551?cond=idecabtagene%20vicleucel&rank=3 (2024).
Not in our library
549.
National Library of Medicine (US). NCT05032820. MM CAR-T to upgrade response BMTCTN1902. ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT05032820?cond=idecabtagene%20vicleucel&rank=12 (2021).
Not in our library
550.
National Library of Medicine (US). NCT06523621. Nivolumab in multiple myeloma patients after idecabtagene vicleucel. ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT06523621?cond=idecabtagene%20vicleucel&rank=2 (2024).
Not in our library
551.
National Library of Medicine (US). NCT05393804. A study of whether ide-cel (bb2121) can be made from people with multiple myeloma who have had a hematopoietic cell transplant. ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT05393804?cond=idecabtagene%20vicleucel&rank=10 (2022).
Not in our library
552.
National Library of Medicine (US). NCT06179888. Iberdomide versus observation off therapy after idecabtagene vicleucel CAR-T for multiple myeloma. ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT06179888?cond=idecabtagene%20vicleucel&rank=4 (2023).
Not in our library
553.
National Library of Medicine (US). NCT06045806. A study to compare the efficacy and safety of idecabtagene vicleucel with lenalidomide maintenance therapy versus lenalidomide maintenance therapy alone in adult participants with newly diagnosed multiple myeloma who have suboptimal response after autologous stem cell transplantation (KarMMa-9). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT06045806?cond=idecabtagene%20vicleucel&rank=8 (2023).
Not in our library
554.
Raje N, et al. MM-493 Efficacy and safety of idecabtagene vicleucel (ide-cel) with lenalidomide (R) maintenance versus R maintenance alone in adult patients with newly diagnosed multiple myeloma (NDMM) who have suboptimal response to autologous stem cell transplantation (ASCT): phase 3 KarMMa-9 trial. Clin. Lymphoma Myeloma Leuk. 2024;24:S562-S563.
Not in our library10.1016/s2152-2650(24)01690-2
555.
National Library of Medicine (US). NCT06698887. A study to evaluate the long-term safety of idecabtagene vicleucel treatment in adults with newly diagnosed multiple myeloma in korea. ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT06698887?cond=idecabtagene%20vicleucel&rank=1 (2024).
Not in our library
556.
Abramson JS, et al. Two-year follow-up of lisocabtagene maraleucel in relapsed or refractory large B-cell lymphoma in TRANSCEND NHL 001. Blood. 2024;143:404-416.
Not in our library10.1182/blood.2023020854
557.
Abramson JS, et al. Lisocabtagene maraleucel as second-line therapy for large B-cell lymphoma: primary analysis of the phase 3 TRANSFORM study. Blood. 2023;141:1675-1684.
Not in our library10.1182/blood.2022018730
558.
Abramson JS, et al. Updated safety and long term clinical outcomes in TRANSCEND NHL 001, pivotal trial of lisocabtagene maraleucel (JCAR017) in R/R aggressive NHL. J. Clin. Oncol. 2018;36:7505-7505.
Not in our library10.1200/jco.2018.36.15_suppl.7505
559.
National Library of Medicine (US). NCT02631044. Study evaluating the safety and pharmacokinetics of JCAR017 in B-cell non-Hodgkin lymphoma (TRANSCEND-NHL-001). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT02631044?intr=Lisocabtagene%20maraleucel&rank=20 (2015).
Not in our library
560.
Ogasawara K, et al. In vivo cellular expansion of lisocabtagene maraleucel and association with efficacy and safety in relapsed/refractory large B-cell lymphoma. Clin. Pharm. Ther. 2022;112:81-89.
Not in our library10.1002/cpt.2561
561.
National Library of Medicine (US). NCT05075603. Relapsed/refractory large B-cell lymphoma with NT-I7 Post-CD19 CAR T-cell therapy. ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT05075603?cond=NCT05075603&rank=1 (2021).
Not in our library
562.
Siddiqi T, et al. Phase 1 TRANSCEND CLL 004 study of lisocabtagene maraleucel in patients with relapsed/refractory CLL or SLL. Blood. 2022;139:1794-1806.
Not in our library10.1182/blood.2021011895
563.
Siddiqi T, et al. Lisocabtagene maraleucel in chronic lymphocytic leukaemia and small lymphocytic lymphoma (TRANSCEND CLL 004): a multicentre, open-label, single-arm, phase 1–2 study. Lancet. 2023;402:641-654.
Not in our library10.1016/s0140-6736(23)01052-8
564.
National Library of Medicine (US). NCT03331198. Study evaluating safety and efficacy of JCAR017 in subjects with relapsed or refractory chronic lymphocytic leukemia (CLL) or small lymphocytic lymphoma (SLL). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT03331198?intr=Lisocabtagene%20maraleucel&rank=19 (2017).
Not in our library
565.
National Library of Medicine (US). NCT03743246. A study to evaluate the safety and efficacy of JCAR017 in pediatric subjects with relapsed/refractory (R/R) B-cell Acute Lymphoblastic Leukemia (B-ALL) and B-cell non-Hodgkin lymphoma (B-NHL). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT03743246?cond=jcar017&sort=StudyFirstPostDate&limit=25&rank=5 (2018).
Not in our library
566.
National Library of Medicine (US). NCT03483103. Lisocabtagene maraleucel (JCAR017) as SECOND-LINE THERApy (TRANSCEND-PILOT-017006). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT03483103?intr=Lisocabtagene%20maraleucel&rank=18 (2018).
Not in our library
567.
Ernst, M. et al. Chimeric antigen receptor (CAR) T-cell therapy for people with relapsed or refractory diffuse large B-cell lymphoma. Cochrane Database of Systematic Reviews (2021).
Not in our library10.1002/14651858.cd013365.pub2
568.
Ghosh N, et al. Comparative effectiveness of lisocabtagene maraleucel (liso-cel) in PILOT in patients (pt) with relapsed or refractory (R/R) large B-cell lymphoma (LBCL) for whom transplant was not intended (TNI) versus conventional second-line (2L) chemotherapy regimens in the real world. Blood. 2022;140:10430-10431.
Not in our library10.1182/blood-2022-159686
569.
National Library of Medicine (US). NCT03484702. Trial to determine the efficacy and safety of JCAR017 in adult participants with aggressive B-cell non-Hodgkin lymphoma (TRANSCENDWORLD). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT03484702?intr=Lisocabtagene%20maraleucel&rank=17&tab=results (2018).
Not in our library
570.
National Library of Medicine (US). NCT03744676. A safety trial of lisocabtagene maraleucel (JCAR017) for relapsed and refractory (R/R) B-cell non-Hodgkin lymphoma (NHL) in the outpatient setting (TRANSCEND-OUTREACH-007). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT03744676?cond=Lisocabtagene%20maraleucel&sort=StudyFirstPostDate&limit=25&page=1&rank=10 (2018).
Not in our library
571.
Godwin JE, et al. Outreach: preliminary safety and efficacy results from a phase 2 study of lisocabtagene maraleucel (liso-cel) in the nonuniversity setting. J. Clin. Oncol. 2021;39:e19513-e19513.
Not in our library10.1200/jco.2021.39.15_suppl.e19513
572.
Linhares Y, et al. OUTREACH: phase 2 study of lisocabtagene maraleucel as outpatient or inpatient treatment at community sites for R/R LBCL. Blood Adv. 2024;8:6114-6126.
Not in our library10.1182/bloodadvances.2024013254
573.
National Library of Medicine (US). NCT05583149. Acalabrutinib + liso-cel in R/R aggressive B-cell lymphomas. ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT05583149?cond=Lisocabtagene%20maraleucel&sort=StudyFirstPostDate&limit=25&page=1&rank=7 (2022).
Not in our library
574.
National Library of Medicine (US). NCT05672173. Lisocabtagene maraleucel, nivolumab and ibrutinib for the treatment of richter’s transformation. ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT05672173?cond=Lisocabtagene%20maraleucel&sort=StudyFirstPostDate&limit=25&page=1&rank=4 (2023).
Not in our library
575.
National Library of Medicine (US). NCT05873712. Zanubrutinib and lisocabtagene maraleucel for the treatment of Richter’s syndrome. ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT05873712?cond=Lisocabtagene%20maraleucel&sort=StudyFirstPostDate&limit=25&page=1&rank=3 (2023).
Not in our library
576.
National Library of Medicine (US). NCT04245839. A study to evaluate the efficacy and safety of JCAR017 in adult subjects with relapsed or refractory indolent B-cell non-Hodgkin lymphoma (NHL) (TRANSCEND FL). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT04245839?cond=jcar017&sort=StudyFirstPostDate&limit=25&rank=3 (2020).
Not in our library
577.
National Library of Medicine (US). NCT03575351. A study to compare the efficacy and safety of JCAR017 to standard of care in adult subjects with high-risk, transplant-eligible relapsed or refractory aggressive B-cell non-Hodgkin lymphomas (TRANSFORM). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT03575351?cond=Lisocabtagene%20maraleucel&sort=StudyFirstPostDate&limit=25&page=1&rank=11&tab=results (2018).
Not in our library
578.
Kamdar M, et al. Lisocabtagene maraleucel versus standard of care with salvage chemotherapy followed by autologous stem cell transplantation as second-line treatment in patients with relapsed or refractory large B-cell lymphoma (TRANSFORM): results from an interim analysis of an open-label, randomised, phase 3 trial. Lancet. 2022;399:2294-2308.
Not in our library10.1016/s0140-6736(22)00662-6
579.
Kamdar MK, et al. Lisocabtagene maraleucel (liso-cel) vs standard of care (SOC) with salvage chemotherapy (CT) followed by autologous stem cell transplantation (ASCT) as second-line (2L) treatment in patients (pt) with R/R large B-cell lymphoma (LBCL): 3-year follow-up (FU) from the randomized, phase 3 TRANSFORM study. J. Clin. Oncol. 2024;42:7013-7013.
Not in our library10.1200/jco.2024.42.16_suppl.7013
580.
National Library of Medicine (US). NCT06313996. A study to evaluate the efficacy and safety of liso-cel compared to standard of care in adults with relapsed or refractory follicular lymphoma. ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT06313996?cond=Lisocabtagene%20maraleucel&sort=StudyFirstPostDate&limit=25&page=1&rank=1 (2024).
Not in our library
581.
National Library of Medicine (US). NCT06205290. A study to compare the efficacy and safety of lisocabtagene maraleucel vs investigator’s choice options in adult participants with relapsed or refractory chronic lymphocytic leukemia or small lymphocytic lymphoma, whose disease has failed treatment with both BTKi and BCL2i therapies. ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT06205290?cond=Lisocabtagene%20maraleucel&sort=StudyFirstPostDate&limit=25&page=1&rank=2 (2023).
Not in our library
582.
National Library of Medicine (US). NCT06623630. Lymphodepleting total body irradiation (TBI) plus cyclophosphamide prior to ciltacabtagene autoleucel (carvykti; cilta-cel) for multiple myeloma (MM) patients with impaired renal function. ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT06623630?cond=ciltacabtagene%20autoleucel&rank=1 (2024).
Not in our library
583.
National Library of Medicine (U.S.). NCT03090659. LCAR-B38M Cells in treating relapsed/refractory (R/R) multiple myeloma (LEGEND-2). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT03090659?cond=ciltacabtagene%20autoleucel&sort=StudyFirstPostDate&limit=25&rank=15 (2017).
Not in our library
584.
Four-year follow-up of LCAR-B38M in relapsed or refractory multiple myeloma: a phase 1, single-arm, open-label, multicenter study in China (LEGEND-2) · 2022
No notice
585.
A phase 1, open-label study of LCAR-B38M, a chimeric antigen receptor T cell therapy directed against B cell maturation antigen, in patients with relapsed or refractory multiple myeloma · 2018
No notice
586.
Xu J, et al. Long-term remission and survival in patients with relapsed or refractory multiple myeloma after treatment with LCAR-B38M CAR T cells: 5-year follow-up of the LEGEND-2 trial. J. Hematol. Oncol. 2024;17:23.
Not in our library10.1186/s13045-024-01530-z
587.
Liu R, et al. Outcomes in patients with multiple myeloma receiving salvage treatment after BCMA -specific CAR-T therapy: A retrospective analysis of LEGEND-2. Br. J. Haematol. 2024;204:1780-1789.
Not in our library10.1111/bjh.19340
588.
Berdeja JG, et al. Ciltacabtagene autoleucel, a B-cell maturation antigen-directed chimeric antigen receptor T-cell therapy in patients with relapsed or refractory multiple myeloma (CARTITUDE-1): a phase 1b/2 open-label study. Lancet. 2021;398:314-324.
Not in our library10.1016/s0140-6736(21)00933-8
589.
National Library of Medicine (US). NCT03548207. A study of JNJ-68284528, a chimeric antigen receptor T cell (CAR-T) therapy directed against B-cell maturation antigen (BCMA) in participants with relapsed or refractory multiple myeloma (CARTITUDE-1). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT03548207?cond=ciltacabtagene%20autoleucel&sort=StudyFirstPostDate&limit=25&rank=14 (2018).
Not in our library
590.
National Library of Medicine (US). NCT05347485. A study of JNJ-68284528 out-of-specification (OOS) for commercial release in participants with multiple myeloma. ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT05347485?cond=ciltacabtagene%20autoleucel&rank=6 (2022).
Not in our library
591.
A phase 1, open-label study of LCAR-B38M, a chimeric antigen receptor T cell therapy directed against B cell maturation antigen, in patients with relapsed or refractory multiple myeloma · 2018
No notice
592.
Mi J-Q, et al. Phase II, open-label study of ciltacabtagene autoleucel, an anti–B-cell maturation antigen chimeric antigen receptor–T-cell therapy, in chinese patients with relapsed/refractory multiple myeloma (CARTIFAN-1). J. Clin. Oncol. 2023;41:1275-1284.
Not in our library10.1200/jco.22.00690
593.
National Library of Medicine (US). NCT04133636. A study of JNJ-68284528, a chimeric antigen receptor T cell (CAR-T) therapy directed against B-cell maturation antigen (BCMA) in Participants with multiple myeloma (CARTITUDE-2). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT04133636?cond=ciltacabtagene%20autoleucel&rank=12 (2019).
Not in our library
594.
Cohen AD, et al. Efficacy and safety of cilta-cel in patients with progressive multiple myeloma after exposure to other BCMA-targeting agents. Blood. 2023;141:219-230.
Not in our library10.1182/blood.2022015526
595.
National Library of Medicine (US). NCT06550895. A study of ciltacabtagene autoleucel and talquetamab for the treatment of participants with high-risk multiple myeloma (MonumenTAL-8). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT06550895?cond=ciltacabtagene%20autoleucel&rank=4 (2024).
Not in our library
596.
National Library of Medicine (US). NCT06574126. Ciltacabtagene autoleucel in high-risk smoldering multiple myeloma (CAR-HiRiSMM). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT06574126?cond=ciltacabtagene%20autoleucel&rank=3 (2024).
Not in our library
597.
National Library of Medicine (US). NCT06577025. A study of different sequences of cilta-cel, talquetamab in combination with daratumumab and teclistamab in combination with daratumumab following induction with daratumumab, bortezomib, lenalidomide and dexamethasone in participants with standard-risk newly diagnosed multiple myeloma (aMMbition). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT06577025?cond=ciltacabtagene%20autoleucel&rank=2 (2024).
Not in our library
598.
National Library of Medicine (US). NCT04181827. A study comparing JNJ-68284528, a CAR-T therapy directed against B-cell maturation antigen (BCMA), versus pomalidomide, bortezomib and dexamethasone (pvd) or daratumumab, pomalidomide and dexamethasone (DPd) in participants with relapsed and lenalidomide-refractory multiple myeloma (CARTITUDE-4). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT04181827?cond=ciltacabtagene%20autoleucel&rank=11 (2019).
Not in our library
599.
National Library of Medicine (US). NCT04923893. A study of bortezomib, lenalidomide and dexamethasone (VRd) followed by cilta-cel, a CAR-T therapy directed against BCMA versus VRd followed by lenalidomide and dexamethasone (Rd) therapy in participants with newly diagnosed multiple myeloma for whom ASCT is not planned as initial therapy (CARTITUDE-5). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT04923893?cond=ciltacabtagene%20autoleucel&rank=9 (2021).
Not in our library
600.
Dytfeld D, et al. Bortezomib, lenalidomide and dexamethasone (VRd) followed by ciltacabtagene autoleucel versus Vrd followed by lenalidomide and dexamethasone (Rd) Maintenance in patients with newly diagnosed multiple myeloma not intended for transplant: a randomized, phase 3 study (CARTITUDE-5). Blood. 2021;138:1835-1835.
Not in our library10.1182/blood-2021-146210
601.
National Library of Medicine (US). NCT05257083. A study of daratumumab, bortezomib, lenalidomide and dexamethasone (DVRd) followed by ciltacabtagene autoleucel versus daratumumab, bortezomib, lenalidomide and dexamethasone (DVRd) followed by autologous stem cell transplant (ASCT) in participants with newly diagnosed multiple myeloma (CARTITUDE-6). ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT05257083?cond=ciltacabtagene%20autoleucel&rank=7 (2022).
Not in our library
602.
National Library of Medicine (US). NCT05201781. A long-term study for participants previously treated with ciltacabtagene autoleucel. ClinicalTrials.gov [Internet]https://clinicaltrials.gov/study/NCT05201781?cond=ciltacabtagene%20autoleucel&rank=8 (2022).
Not in our library
603.
Ehninger G, et al. Phase 1 dose escalation study of the rapidly switchable universal CAR-T therapy Unicar-T-CD123 in relapsed/refractory AML. Blood. 2022;140:2367-2368.
Not in our library10.1182/blood-2022-168877
604.
Wermke M, et al. Proof of concept for a rapidly switchable universal CAR-T platform with UniCAR-T-CD123 in relapsed/refractory AML. Blood. 2021;137:3145-3148.
Not in our library10.1182/blood.2020009759
605.
Feldmann A, et al. A novel revcar platform for switchable and gated tumor targeting. Blood. 2019;134:5611-5611.
Not in our library10.1182/blood-2019-128436
606.
A. Ehninger, et al. Preclinical characterization of switchable allogeneic chimeric antigen receptor T cells to support first in human clinical study in CD123-positive hematologic and lymphatic malignancies. [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 4095.
Not in our library
607.
Sallman DA, et al. Phase 1/1b safety study of Prgn-3006 Ultracar-T in patients with relapsed or refractory CD33-positive acute myeloid leukemia and higher risk myelodysplastic syndromes. Blood. 2021;138:825.
Not in our library10.1182/blood-2021-152692
608.
Zuo S, et al. C-JUN overexpressing CAR-T cells in acute myeloid leukemia: preclinical characterization and phase I trial. Nat. Commun. 2024;15:6155.
Not in our library10.1038/s41467-024-50485-9
609.
Wang Q, et al. Treatment of CD33-directed Chimeric antigen receptor-modified T cells in one patient with relapsed and refractory acute myeloid leukemia. Mol. Ther. 2015;23:184-191.
Not in our library10.1038/mt.2014.164
610.
Shah N., et al. G. Phase 1/2 study of donor-derived anti-CD33 chimeric antigen receptor expressing T cells (VCAR33 ALLO) in patients with relapsed or refractory acute myeloid leukemia after allogeneic hematopoietic cell transplantation (trial in progress). Presented at the 65 th ASH annual meeting and exposition; December 9-12, San Diego, USA. 2023. Abstract nr 4862.
Not in our library
611.
Canesin G., et al. G-CSF/plerixafor dual-mobilized donor derived CD33CAR T-cells as potent and effective AML therapy in pre-clinical models. Presented at 63rd ASH annual meeting & exposition, December 11–14, 2021. Abstract nr 1716.
Not in our library
612.
Moeller R, K. S. S. J. Construction and evaluation of interleukin 3 (IL3)-zetakine–redirected cytolytic T cells for treatment of CD123-expressing acute myeloid leukemia. Presented at SITC 2021, November 10–14, 2021. Abstract nr 871.
Not in our library
613.
Cooper TM, et al. Pediatric and young adult leukemia adoptive therapy (PLAT)-08: A phase 1 study of SC-DARIC33 in pediatric and young adults with relapsed or refractory CD33+ AML. J. Clin. Oncol. 2022;40:TPS7078-TPS7078.
Not in our library10.1200/jco.2022.40.16_suppl.tps7078
614.
Petrov JC, et al. Compound CAR T-cells as a double-pronged approach for treating acute myeloid leukemia. Leukemia. 2018;32:1317-1326.
Not in our library10.1038/s41375-018-0075-3
615.
Daver NG, et al. A first-in-human phase 1, multicenter, open-label study of CB-012, a next-generation CRISPR-edited allogeneic anti-CLL-1 CAR-T cell therapy for adults with relapsed/refractory acute myeloid leukemia (AMpLify). J. Clin. Oncol. 2024;42:TPS6586-TPS6586.
Not in our library10.1200/jco.2024.42.16_suppl.tps6586
616.
Liu F, et al. First-in-human CLL1-CD33 compound CAR T cell therapy induces complete remission in patients with refractory acute myeloid leukemia: update on phase 1 clinical trial. Blood. 2018;132:901-901.
Not in our library10.1182/blood-2018-99-110579
617.
Chen L, et al. Targeting FLT3 by chimeric antigen receptor T cells for the treatment of acute myeloid leukemia. Leukemia. 2017;31:1830-1834.
Not in our library10.1038/leu.2017.147
618.
Karbowski CM, et al. Nonclinical safety assessment of AMG 553, an investigational anti-FLT3 CAR-T therapy. J. Clin. Oncol. 2019;37:7032-7032.
Not in our library10.1200/jco.2019.37.15_suppl.7032
619.
Karbowski C, et al. Nonclinical safety assessment of AMG 553, an investigational chimeric antigen receptor T-cell therapy for the treatment of acute myeloid leukemia. Toxicol. Sci. 2020;177:94-107.
Not in our library10.1093/toxsci/kfaa098
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Cui, Q. et al. Case report: CD38-directed CAR-T cell therapy: a novel immunotherapy targeting CD38-positive blasts overcomes TKI and chemotherapy resistance of myeloid chronic myeloid leukemia in blastic phase. Front. Immunol.13, 1012981 (2022).
Not in our library10.3389/fimmu.2022.1012981
621.
Murad JM, et al. Manufacturing development and clinical production of NKG2D chimeric antigen receptor–expressing T cells for autologous adoptive cell therapy. Cytotherapy. 2018;20:952-963.
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Carrabba MG, et al. Phase I-IIa clinical trial to assess safety and efficacy of MLM-CAR44.1, a CD44v6-directed CAR-T in relapsed/refractory acute myeloid leukemia (AML) and multiple myeloma (MM). Blood. 2018;132:5790-5790.
Not in our library10.1182/blood-2018-99-117974
623.
Salman H, et al. Preclinical targeting of human acute myeloid leukemia using CD4-specific chimeric antigen receptor (CAR) T Cells and NK Cells. J. Cancer. 2019;10:4408-4419.
Not in our library10.7150/jca.28952
624.
Pei K, et al. Anti-CLL1-based CAR T-cells with 4-1-BB or CD28/CD27 stimulatory domains in treating childhood refractory/relapsed acute myeloid leukemia. Cancer Med. 2023;12:9655-9661.
Not in our library10.1002/cam4.5916
625.
Zhang H, et al. Characteristics of anti-CLL1-based CAR-T therapy for children with relapsed or refractory acute myeloid leukemia: the multi-center efficacy and safety interim analysis. Leukemia. 2022;36:2596-2604.
Not in our library10.1038/s41375-022-01703-0
626.
Hazelton W, Ghorashian S, Pule M. Nanobody-based tri-specific chimeric antigen receptor to treat acute myeloid leukaemia. Blood. 2020;136:10-11.
Not in our library10.1182/blood-2020-141214

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