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Molecular and Translational Classifications of DAMPs in Immunogenic Cell Death

Abhishek D. Garg, Lorenzo Galluzzi, Lionel Apetoh and 49 more (opens in a new tab)

Frontiers in Immunology · 2015

doi:10.3389/fimmu.2015.00588 (opens in a new tab)

Abstract

The immunogenicity of malignant cells has recently been acknowledged as a critical determinant of efficacy in cancer therapy. Thus, besides developing direct immunostimulatory regimens, including dendritic cell-based vaccines, checkpoint-blocking therapies, and adoptive T-cell transfer, researchers have started to focus on the overall immunobiology of neoplastic cells. It is now clear that cancer cells can succumb to some anticancer therapies by undergoing a peculiar form of cell death that is characterized by an increased immunogenic potential, owing to the emission of the so-called "damage-associated molecular patterns" (DAMPs). The emission of DAMPs and other immunostimulatory factors by cells succumbing to immunogenic cell death (ICD) favors the establishment of a productive interface with the immune system. This results in the elicitation of tumor-targeting immune responses associated with the elimination of residual, treatment-resistant cancer cells, as well as with the establishment of immunological memory. Although ICD has been characterized with increased precision since its discovery, several questions remain to be addressed. Here, we summarize and tabulate the main molecular, immunological, preclinical, and clinical aspects of ICD, in an attempt to capture the essence of this phenomenon, and identify future challenges for this rapidly expanding field of investigation.

Full text

From PubMed Central, U.S. National Library of Medicine, as current on Oct 17, 2026. Paragraph numbers are ours, so an answer can point at one.

Introduction and Historical Background

Augmenting the immunogenicity of cancer cells to improve the efficacy of cancer therapy is a paradigm that has gained significant momentum over the past 5 years. Researchers have realized that besides therapeutically exploiting innate or adaptive immune cells directly (e.g., through dendritic cell (DC)-based vaccines or adoptive T-cell transfer) and/or improving the effector functions of T cells (through checkpoint-blocking therapies), cancer cells also need to be made immunogenic. This has diverted attention toward studying the interface between stressed or dying cancer cells and the immune system, in the hope of efficiently exploiting it for therapeutic purposes.

Early indications regarding immune system-driven tumor control emerged in the eighteenth century, when feverish infections in cancer patients were circumstantially associated with tumor remission. The first evidence that immunotherapy can be applied to achieve tumor regression emerged from the work of William Coley, who in the 1890s achieved tumor regression in some sarcoma/lymphoma patients upon the intra-tumoral injection of streptococcal cultures (provided by Robert Koch). In the following 43 years, Coley injected nearly 900 (mostly sarcoma) patients with his bacterial preparation (achieving a cure rate >10%), which later became known as “Coley’s toxin”. However, the Coley’s toxin came under intense scrutiny owing to an elevated toxicity and some difficulties in reproducing remission rates. Eventually, the first experimental evidence that virus-unrelated tumors can indeed be recognized by the host immune system emerged in the 1940s, and by the 1960s, coupled with the discovery of T cells, it was proposed that the human immune system may also react against tumors. The ability of anticancer therapies to enhance the immunogenic potential of malignant cells gained some appreciation by the 1970s. It was recognized that if specific treatments are applied (e.g., radiotherapy, the bacillus Calmette–Guerin, or some chemotherapeutics), the immunogenicity of malignant cells increases enough to induce durable anti-tumor immunity. By the 1980s, researchers started to report more specific observations regarding the therapeutic impact of cancer cell immunogenicity, e.g., the ability of curative hyperthermia to cause the (heat-shock based) generation of circumstantial anti-tumor immunity, the fact that the immunogenicity of cancer cells influences patient prognosis after radiotherapy, and the increase in tumor immunogenicity due to hydrostatic pressure. However, these early studies (especially those published before the 1980s) had several issues linked to a lack in consensus. For instance, due to early controversies on the existence of tumor-associated antigens (TAAs), the target of tumor-specific immune responses was unclear, and the mechanism of action of some therapies came under scrutiny. Moreover, such therapies could operate by directly modulating immune effector cells rather than improving the immunogenic potential of tumors. In particular, the death of cancer cells exposed to therapy was never suspected to drive anti-tumor immunity, since it was considered to be a relatively “silent” process in terms of immunogenicity. Moreover, the classical “self/non-self” theory was unable to explain the possibility that dying cancer cells could elicit an immune response.

By the early 1990s, the molecular characterization of mice and human TAAs clarified the entities targeted by anti-tumor immune responses. Similarly, the so-called “danger theory” started to emerge, challenging the classical model of “self/non-self” immune recognition, especially in a diseased or damaged tissue. This model proposed that the immune recognition is not restricted to “non-self” entities, but rather discriminates between “dangerous” and “safe” entities, irrespective of source. Indeed, “dangerous” entities include pathogens as well as injured, infected, diseased and necrotic tissues, or cells undergoing non-physiological cell death which emit danger signals (or alarmins) with pro-inflammatory activity. These danger signals are now collectively referred to as “damage-associated molecular patterns” (DAMPs). DAMPs are endogenous molecules that are concealed intracellularly in normal conditions, but are exposed or released upon stress, injury, cell death, thereby becoming able to bind cognate receptors on immune cells. Table 1 summarizes the most prominent DAMPs characterized to date and their mode of emission, the cell death pathway they are associated with, and their known cognate receptors. It is important to consider that not all DAMPs may act as immunogenic danger signals. Several DAMPs exist that are crucial for the maintenance of tissue homeostasis, and the avoidance of auto-immune responses, as they exert immunosuppressive effects, including phosphatidylserine (PS), annexin A1 (ANXA1), death domain 1α (DD1α), B-cell CLL/lymphoma 2 (BCL2) and some extracellular matrix-derived molecules (Table 1). Accordingly, the blockade of these anti-inflammatory DAMPs accentuates the immunogenic potential of dying cells, or renders immunogenic otherwise tolerogenic forms of cell death. Moreover, some danger signals are not always involved in the immunogenicity of cell death, but act as “bystanders.” This is the case for heat shock protein 90 kDa alpha (cytosolic), class A member 1 (HSP90AA1, best known as HSP90) exposed on the cell surface after melphalan treatment. Last (but not least), several DAMPs may be subjected to post-translational modifications (e.g., oxidation, reduction, citrullination) that may potentially neutralize, increase, or change their immunogenic properties – a process that is still incompletely understood.

Despite these advances, the overall role of regulated cell death (RCD) in augmenting cancer immunogenicity remained obscure. Initial observations involving the immunogenicity of cell death in the efficacy of cancer therapy were published between 1998 and 2004, when it was proposed that the non-apoptotic demise of malignant cells (within the context of the so-called “immunogenic death”) could be associated with the emission of the danger signal heat shock 70 kDa protein 1A (HSPA1A, best known as HSP70) (Table 1), enhancing the immunogenic potential of dying cancer cells in vivo. The dogmatic view that only necrotic or non-apoptotic (as postulated by the “immunogenic death” concept) cancer cells are characterized by an elevated immunogenic potential started to be questioned by a series of studies published between 2005 and 2007. These publications outlined that cancer cells undergoing apoptosis in response to specific anticancer therapies are immunogenic [a subroutine termed immunogenic cell death (ICD)], as long as they emit precise DAMPs in a spatiotemporally defined fashion. Cells succumbing to ICD are sufficient for the elicitation of durable anti-tumor immune responses. ICD is indeed paralleled by the redirection and emission of DAMPs, owing to the stimulation of distinct danger signaling pathways occurring in synchrony with cell death signaling. Table 2 summarizes the main signaling pathways that play a role in the trafficking and emission of DAMPs. ICD-associated DAMPs and other immunostimulatory factors released by cells destined to undergo ICD favor the establishment of a productive interface between dying cancer cells and innate immune cells (like DCs or macrophages), thereby leading to the initiation of a therapeutically relevant adaptive immune response (Figure 1). In some contexts, DAMPs may regulate the function of specific innate immune cell subsets, e.g., following anthracycline treatment, extracellular adenosine triphosphate (ATP) assists in recruitment and differentiation of CD11c+Cd11b+Ly6Chigh cells into CD11c+CD86+MHCII+ DCs; similarly, necrosis associated F-actin exposure activates an immune response by directing the dead cell debris to specifically CD8α+ DCs. Indeed, DCs and other antigen-presenting cells exposed to cancer cells succumbing to ICD can then prime CD4+ T cells (and polarize them into TH1, TH17, or TH1/TH17-like phenotype), CD8+ cytotoxic T lymphocytes (CTLs) and γδ T lymphocytes against one or several TAAs (Figure 1). Of note, residual cancer cells that survive ICD inducers can also show some enduring immunogenic characteristics that make them susceptible to immunological control by CTLs.

Immunogenic Cell Death Inducers

Over the past few years, a number of single-agent ICD inducers have been discovered, encompassing conventional chemotherapeutics, targeted anticancer agents and various other ­biological and physicochemical therapies. Table 3 summarizes single-agent ICD inducers characterized so far, as per consensus guidelines, and the spectra of DAMPs and other immunostimulatory signals associated with them. For combinatorial therapeutic strategies capable of achieving ICD, readers may want to refer to other recent publications. It is clear that a general structure–function relationship capable of clustering all existing ICD inducers and predicting new ones does not exist, an issue that makes discovering new ICD-inducing therapies based on cheminformatic analyses challenging, if not impossible. A peculiar characteristic of most, if not all, ICD inducers is their ability to induce reactive oxygen species (ROS)-based/associated endoplasmic reticulum (ER) stress, as first delineated for anthracyclines. This peculiarity was exploited for the targeted discovery of hypericin-based photodynamic therapy (Hyp-PDT) – a therapeutic modality that can trigger ICD through the induction of ROS that target the ER. Along with an ever more precise characterization of the links between ROS, ER stress, and ICD induction, it became clear that the more “focused” ER stress is, the higher the probability of inducing ICD. These observations paved way for a classification system based on how ICD inducers engage ER stress for cell death and danger signaling. Based on this classification, Type I ICD inducers are defined as anticancer agents that act on non-ER proteins for the induction of cell death, but promote collateral ER stress for danger signaling, thereby operating on multiple targets, while Type II ICD inducers are anticancer agents that target the ER for both cell death induction and danger signaling. Table 4 summarizes the classification of current ICD inducers into Type I and Type II, and their cell death/danger signaling targets. Such a classification suggest that while Type I ICD inducers can be discovered through various approaches (e.g., DAMP-based drug screening platforms), putative Type II ICD inducers can be characterized rapidly on the basis of their ability to selectively or predominantly target the ER. Recent findings comforted the purpose and usefulness of this classification system, as two novel Type II ICD inducers [i.e., PtII N-heterocyclic carbene complex and Newcastle disease virotherapy (NDV)] were identified based on the notion that they induce predominant ROS-based ER stress. Nevertheless, as more ICD inducers and features are discovered, this classification system is expected to evolve or be substituted by a more refined one.

Since its discovery, a plethora of molecular and immunological components responsible for ICD have been discovered (Figure 1). Table 5 summarizes the molecular and immunological determinants of ICD characterized so far, as well as the models of ICD in which they operate (in a positive, negative or dispensable manner). Anthracyclines and oxaliplatin are the most common ICD inducers employed in experimental settings, followed by Hyp-PDT. According to current understanding, cancer cell-associated determinants of ICD can be subdivided into those that are common to all ICD inducers (i.e., “core” signaling components), and those that operate in an ICD inducer-dependent manner (i.e., “private” signaling components). Thus, eukaryotic translation initiation factor 2-alpha kinase 3 (EIF2AK3, best known as PERK) and the ER-to-Golgi secretory machinery are considered “core” signaling components on the cancer cell side. Similarly, from the immune system side, a general role for (IFNγ-producing) CD4+ and CD8+ T cells has been confirmed for most, if not all, ICD inducers (Table 5). Interestingly, some components that are required for ICD induction by some agents (like autophagy for anthracyclines and oxaliplatin) might be either dispensable for ICD induction by other agents, e.g., autophagy for NDV and phosphorylation of eukaryotic translation initiation factor 2α (eIF2α), caspase-8 (CASP8) activation or cytosolic Ca2+ levels for Hyp-PDT; or even negatively regulate ICD in some settings, e.g., autophagy in case of Hyp-PDT (Table 5). Thus, it will be important to expand our molecular knowledge of ICD to as many experimental settings as possible.

Immunogenic Cell Death from Bench to Bedside

The relevance of ICD has been verified in a number of rodent models, with a variety of chemical and physicochemical ICD inducers. Table 6 summarizes the most prominent mouse or rat models used so far for the characterization and study of ICD. For the moment, ICD has been mostly investigated in heterotopic syngeneic subcutaneous models. Within such models, inter-species differences (mouse versus rats), inter-strain differences (among BALB/c, C57BL/6, C3H and KMF mice), and inter-cell line differences, as well as differences in therapeutic setups (prophylactic versus curative) have been amply accounted for (Table 6). Nevertheless, there is predominance in the use of cancer cells derived from carcinogen-induced tumors and transplanted subcutaneously (Table 6). In very few cases, ICD has been characterized in either orthotopic (for NDV) or spontaneous (for anthracyclines) tumor murine models (Table 6). This has been questioned as a prominent Achilles’ heel of ICD research. While this criticism is valid, it has to be recognized that no rodent model is perfect at all immunological levels.

As a recent systematic review summarized, heterotopic murine models suffer from a number of caveats, including the inability to recapitulate the early interaction between transformed cells and the immune system and the incompatibility between the cancer type and the site-of-transplantation. Orthotopic murine models are useful as they overcome the cancer cell-tissue type incompatibility issue. While genetically engineered tumor murine models (GEMMs) overcome most of the issues mentioned above, they come with their own set of shortcomings, including a limited genetic mosaicism, a low tumor heterogeneity, a lack of well-defined immunogenic TAAs, the presence of unintended “passenger” genetic modifications, and a reduced mutational spectrum. Many of these parameters are critical for responses to immunotherapy/ICD. For instance, the lack of well-defined immunogenic TAAs was the reason why preliminary results obtained in spontaneously developing murine tumors disputed the very existence of TAAs. Similarly, a high mutational spectrum (which produces considerable amounts of neo-antigens) has been found to be mandatory for the clinical efficacy of checkpoint blockers. Last (but not least), laboratory rodent models in general are associated with some critical issues, including the fact that a high level of inbreeding (which produces a number of shortcomings e.g., homozygous recessive defects) reduces the general immunological fitness, responsiveness and diversity in these models. Moreover, numerous immunological differences between mouse and humans tend to affect the translational relevance of the findings obtained. Also, the time frames of tumor growth rates between rodent models and humans are relatively divergent. This further complicates clinical translation of immunotherapeutic paradigms since the level of immunosurveillance and immunoediting experienced by human tumors can be much higher than any rodent tumor model.

In summary, it would be ideal to test ICD across as many different rodent models as possible, in order to determine the features that can be exploited for therapeutic purposes in humans. Moreover, if ICD fails in a specific experimental model, active effort should be made to characterize the mechanisms behind such failure, since resistance phenotypes can have profound clinical implications. This emerges from various studies summarized in Table 7. Indeed, several ICD resistance mechanisms exist operating at both the cancer cell and the immune system level, which have been characterized in different experimental models. Several of these resistance mechanisms have also been identified in cancer patients, thereby justifying further studies along these lines Table 7.

A considerable amounts of clinical findings support the relevance of ICD or ICD-related signatures in (at least subsets of) cancer patients. As summarized in Table 8, various ICD-linked (specific) parameters have been associated with the prognosis of cancer patients treated with clinically relevant ICD inducers (like anthracyclines, oxaliplatin, paclitaxel, or radiotherapy). Moreover, it is becoming clear that ICD-related or ICD-derived (immunological) genetic signatures (e.g., a MX1-centered metagene, a CXCR3-PRF1-CASP1-centered metagene, an ASAH1-centered metagene) can be positively associated with good prognosis in patients affected by various neoplasms, including breast, lung, and ovarian malignancies. These observations indicate that ICD or ICD-relevant parameters may have prognostic or predictive relevance in at least a subset of cancer patients. It will be important to characterize new and more specific ICD-associated parameters linked to patient prognosis as well as biomarkers that may predict improved disease outcome in cancer patient treated with ICD inducers. Of note, considering the current clinical experience with immunotherapies, the patients with an increased likelihood to benefit from ICD inducers are probably those that display pre-existing (baseline) immune reactivity against cancer cells. This may depend on the ability of ICD to reboot and/or revive pre-existing TAA-directed immunity rather to prime de novo immune reactivity. In future, it would be crucial to characterize biomarkers that allow clinicians to delineate patients with reduced baseline immune reactivity against malignant cells so that proper combinatorial therapies involving ICD inducers can be implemented.

Confronting the Clinical Realities of Anti-Tumor Immunity

It is well-established that the response of cancer patients to immunotherapy relies on the activity of effector T cells [that employ their T-cell receptors (TCRs) for recognizing TAAs]. However, these TAA-targeting T cells may also constitute obstacles for effective anti-tumor immunity. As opposed to T lymphocytes recognizing pathogen-associated antigens (PAAs) (Figure 2), indeed, T cells directed against some TAAs (derived from non-mutated proteins that are source of self or near-to-self antigens) are developmentally subjected to negative selection in the thymus and peripheral lymphoid organs (Figure 2). As a result, T cells bearing TCRs with high affinity for self antigens (including some TAAs) are clonally deleted to avoid auto-immunity (Figure 2). However, some “leakiness” in this process allows TAA-specific T cells possessing TCRs with low affinity to escape deletion and persist, although at low precursor frequencies (Figure 2). Unfortunately, as compared to PAA-specific T cells, which bear high-affinity TCRs (Figure 2), TAA-specific T cells exhibit limited effector and memory functions. Coupled with the tendency of progressing tumors to generate a highly immunosuppressive microenvironment, this renders the insurgence of lifelong protective immunity nearly impossible. Of note, central and peripheral tolerance may not affect T cells reactive toward neo-tumor-specific antigens (neo-TSAs) e.g., tumor-specific neo-antigens that are generated de novo in the course of tumor progression because of mutational events. However, the extent to which such neo-TSAs can elicit consistent “immunodominant” T cell reactivity is still a matter of investigation. Nevertheless, in this context, inefficient T-cell stimulation can be overcome through the ICD-based improvement of effector T-cell functions. ICD can be further combined with checkpoint-blocking therapies, which potently reverse immunosuppression. However, the lifelong maintenance of anti-tumor T cells remains a particularly hard challenge.

In the clinical reality, anticancer agents are administered to patients in a limited number of cycles. Even if these therapeutic regimens may attain optimal efficacy in terms of ICD induction, they are unlikely to ensure the lifelong persistence of TAA-directed T cells with low-affinity TCR. This probably reflects the contraction of TAA-targeting T cells occurring once the immunostimulatory stimulus provided by ICD ceases, owing to peripheral tolerance mechanisms. Clinically, it may not be feasible to administer ICD inducers repeatedly over time, since many of them can cause lymphopenia (which negatively affects disease outcome), or are associated with other side effects. It has been proposed that active immunization with ICD-based anticancer vaccines (which are associated with robust immunogenicity) given in a repetitive manner may achieve this goal (Figure 2). Thus, it will be important to test whether the long-term administration of ICD-based anticancer vaccines can sustain the effector function of TAA-specific T cells bearing low-affinity TCRs, hence, ensuring lifelong disease-free survival. Of note, in the case of hematological malignancies, this issue could be overcome upon the adoptive transfer of CTLs expressing chimeric antigen receptors (CARs). However, whether CAR-expressing CTLs generate protective immunological memory in the absence of considerable side effects remains to be determined. Moreover, the use of this therapeutic strategy against solid malignancies is relatively challenging owing to lack of well-defined “unique” TAAs.

Conclusion

The model of ICD has been considerably refined since the initial identification of a cell death modality manifesting apoptotic features but able to induce an adaptive immune response. This model strives to integrate several phenomena observed throughout the second half of the twentieth century in one therapeutically relevant platform. However, as discussed above, several challenges still need to be addressed. First, comprehensive testing should be performed in advanced experimental settings like GEMMs or orthotopic tumor models. Second, ICD resistance mechanisms should be characterized with precision. Third, various issues linked to the successful translation of ICD to cancer therapy will have to be resolved, including (but not limited to) treatment schedules, dosages, and combinatorial strategies. This translational drive also needs to be coupled with effective strategies for the discovery of new and effective ICD inducers. Drug screening programs are often complicated by the possibility of false-positive (due to bystander presence of DAMPs) or false-negative (due to limited number of biomarkers used for screening) hits. This issue can only be ironed out by discovering new and common regulators of ICD, and integrating them into existing screening platforms. Last, but not least, it will be important to identify new ICD-related/derived biomarkers that can be used to improve current protocols of patient stratification and clinical decision making. We are positive that all these objectives are at reach.

Author Contributions

ADG did the literature study, data collection, as well as conceived and wrote the manuscript. PA provided senior supervision and guidance, conceived the paper, helped in writing, and critically revised the manuscript. LG improved and edited the manuscript. JMBSP helped with the preparation of figures. All authors participated in the critical reading of the manuscript (wherever applicable), approved content and conclusions, as well as helped in ensuring the accuracy of cited literature.

Conflict of Interest Statement

Akseli Hemminki is shareholder in Targovax AG and TILT Biotherapeutics Ltd. The remaining authors have no conflict of interest to declare.

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    Not in our library10.1371/journal.pone.0009103 (opens in a new tab)

  39. 39.

    Babelova A Moreth K Tsalastra-Greul W Zeng-Brouwers J Eickelberg O Young MF Biglycan, a danger signal that activates the NLRP3 inflammasome via toll-like and P2X receptors. J Biol Chem (2009 ) 284(36):24035–48.

    Not in our library10.1074/jbc.m109.014266 (opens in a new tab)

  40. 40.

    Schaefer L. Extracellular matrix molecules: endogenous danger signals as new drug targets in kidney diseases. Curr Opin Pharmacol (2010 ) 10(2):185–90.

    Not in our library10.1016/j.coph.2009.11.007 (opens in a new tab)

  41. 41.

    Obeid M Tesniere A Ghiringhelli F Fimia GM Apetoh L Perfettini JL Calreticulin exposure dictates the immunogenicity of cancer cell death. Nat Med (2007 ) 13(1):54–61.

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  42. 42.

    Garg AD Elsen S Krysko DV Vandenabeele P de Witte P Agostinis P. Resistance to anticancer vaccination effect is controlled by a cancer cell-autonomous phenotype that disrupts immunogenic phagocytic removal. Oncotarget (2015 ) 6(29):26841–60.

    Not in our library10.18632/oncotarget.4754 (opens in a new tab)

  43. 43.

    Koks CA Garg AD Ehrhardt M Riva M Vandenberk L Boon L Newcastle disease virotherapy induces long-term survival and tumor-specific immune memory in orthotopic glioma through the induction of immunogenic cell death. Int J Cancer (2015 ) 136(5):E313–25.

    Not in our library10.1002/ijc.29202 (opens in a new tab)

  44. 44.

    Gardai SJ McPhillips KA Frasch SC Janssen WJ Starefeldt A Murphy-Ullrich JE Cell-surface calreticulin initiates clearance of viable or apoptotic cells through trans-activation of LRP on the phagocyte. Cell (2005 ) 123(2):321–34.

    Not in our library10.1016/j.cell.2005.08.032 (opens in a new tab)

  45. 45.

    Garcia Fernandez M Troiano L Moretti L Nasi M Pinti M Salvioli S Early changes in intramitochondrial cardiolipin distribution during apoptosis. Cell Growth Differ (2002 ) 13(9):449–55.

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  46. 46.

    Sorice M Circella A Cristea IM Garofalo T Di Renzo L Alessandri C Cardiolipin and its metabolites move from mitochondria to other cellular membranes during death receptor-mediated apoptosis. Cell Death Differ (2004 ) 11(10):1133–45.

    Not in our library10.1038/sj.cdd.4401457 (opens in a new tab)

  47. 47.

    Korbelik M Banath J Sun J Canals D Hannun YA Separovic D. Ceramide and sphingosine-1-phosphate act as photodynamic therapy-elicited damage-associated molecular patterns: cell surface exposure. Int Immunopharmacol (2014 ) 20(2):359–65.

    Not in our library10.1016/j.intimp.2014.03.016 (opens in a new tab)

  48. 48.

    Horino K Nishiura H Ohsako T Shibuya Y Hiraoka T Kitamura N A monocyte chemotactic factor, S19 ribosomal protein dimer, in phagocytic clearance of apoptotic cells. Lab Invest (1998 ) 78(5):603–17.

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  49. 49.

    Nishimura T Horino K Nishiura H Shibuya Y Hiraoka T Tanase S Apoptotic cells of an epithelial cell line, AsPC-1, release monocyte chemotactic S19 ribosomal protein dimer. J Biochem (2001 ) 129(3):445–54.

    Not in our library10.1093/oxfordjournals.jbchem.a002876 (opens in a new tab)

  50. 50.

    Peter C Wesselborg S Lauber K Role of attraction and danger signals in the uptake of apoptotic and necrotic cells and its immunological outcome. In: Krysko DV Vandenabeele P, editors. Phagocytosis of Dying Cells. Berlin: Springer Science + Business Media B.V. (2009 ). p. 63–101.

    Not in our library

  51. 51.

    Yamamoto T. Roles of the ribosomal protein S19 dimer and the C5a receptor in pathophysiological functions of phagocytic leukocytes. Pathol Int (2007 ) 57(1):1–11.

    Not in our library10.1111/j.1440-1827.2007.02049.x (opens in a new tab)

  52. 52.

    Struck J Uhlein M Morgenthaler NG Furst W Hoflich C Bahrami S Release of the mitochondrial enzyme carbamoyl phosphate synthase under septic conditions. Shock (2005 ) 23(6):533–8.

    Not in our library

  53. 53.

    Krysko DV Garg AD Kaczmarek A Krysko O Agostinis P Vandenabeele P. Immunogenic cell death and DAMPs in cancer therapy. Nat Rev Cancer (2012 ) 12(12):860–75.

    Not in our library10.1038/nrc3380 (opens in a new tab)

  54. 54.

    Pullerits R Bokarewa M Jonsson IM Verdrengh M Tarkowski A. Extracellular cytochrome c, a mitochondrial apoptosis-related protein, induces arthritis. Rheumatology (Oxford) (2005 ) 44(1):32–9.

    Not in our library10.1093/rheumatology/keh406 (opens in a new tab)

  55. 55.

    Codina R Vanasse A Kelekar A Vezys V Jemmerson R. Cytochrome c-induced lymphocyte death from the outside in: inhibition by serum leucine-rich alpha-2-glycoprotein-1. Apoptosis (2010 ) 15(2):139–52.

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  56. 56.

    Yoon KW Byun S Kwon E Hwang SY Chu K Hiraki M Control of signaling-mediated clearance of apoptotic cells by the tumor suppressor p53. Science (2015 ) 349(6247):1261669.

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  57. 57.

    Kao J Houck K Fan Y Haehnel I Libutti SK Kayton ML Characterization of a novel tumor-derived cytokine. Endothelial-monocyte activating polypeptide II. J Biol Chem (1994 ) 269(40):25106–19.

    Not in our library

  58. 58.

    Knies UE Behrensdorf HA Mitchell CA Deutsch U Risau W Drexler HC Regulation of endothelial monocyte-activating polypeptide II release by apoptosis. Proc Natl Acad Sci U S A (1998 ) 95(21):12322–7.

    Not in our library10.1073/pnas.95.21.12322 (opens in a new tab)

  59. 59.

    Ahrens S Zelenay S Sancho D Hanc P Kjaer S Feest C F-actin is an evolutionarily conserved damage-associated molecular pattern recognized by DNGR-1, a receptor for dead cells. Immunity (2012 ) 36(4):635–45.

    Not in our library10.1016/j.immuni.2012.03.008 (opens in a new tab)

  60. 60.

    Chiba S Baghdadi M Akiba H Yoshiyama H Kinoshita I Dosaka-Akita H Tumor-infiltrating DCs suppress nucleic acid-mediated innate immune responses through interactions between the receptor TIM-3 and the alarmin HMGB1. Nat Immunol (2012 ) 13(9):832–42.

    Not in our library10.1038/ni.2376 (opens in a new tab)

  61. 61.

    Zitvogel L Kepp O Kroemer G. Decoding cell death signals in inflammation and immunity. Cell (2010 ) 140(6):798–804.

    Not in our library10.1016/j.cell.2010.02.015 (opens in a new tab)

  62. 62.

    Pletjushkina OY Fetisova EK Lyamzaev KG Ivanova OY Domnina LV Vyssokikh MY Long-distance apoptotic killing of cells is mediated by hydrogen peroxide in a mitochondrial ROS-dependent fashion. Cell Death Differ (2005 ) 12(11):1442–4.

    Not in our library10.1038/sj.cdd.4401685 (opens in a new tab)

  63. 63.

    Garg AD Nowis D Golab J Agostinis P. Photodynamic therapy: illuminating the road from cell death towards anti-tumour immunity. Apoptosis (2010 ) 15(9):1050–71.

    Not in our library10.1007/s10495-010-0479-7 (opens in a new tab)

  64. 64.

    Suzuki S Kulkarni AB. Extracellular heat shock protein HSP90beta secreted by MG63 osteosarcoma cells inhibits activation of latent TGF-beta1. Biochem Biophys Res Commun (2010 ) 398(3):525–31.

    Not in our library10.1016/j.bbrc.2010.06.112 (opens in a new tab)

  65. 65.

    Korbelik M Sun J Cecic I. Photodynamic therapy-induced cell surface expression and release of heat shock proteins: relevance for tumor response. Cancer Res (2005 ) 65(3):1018–26.

    Not in our library

  66. 66.

    Cirone M Di Renzo L Lotti LV Conte V Trivedi P Santarelli R Primary effusion lymphoma cell death induced by bortezomib and AG 490 activates dendritic cells through CD91. PLoS One (2012 ) 7(3):e31732.

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  67. 67.

    Zunino B Rubio-Patino C Villa E Meynet O Proics E Cornille A Hyperthermic intraperitoneal chemotherapy leads to an anticancer immune response via exposure of cell surface heat shock protein 90. Oncogene (2015 ).

    Not in our library10.1038/onc.2015.82 (opens in a new tab)

  68. 68.

    Zhou Z Yamamoto Y Sugai F Yoshida K Kishima Y Sumi H Hepatoma-derived growth factor is a neurotrophic factor harbored in the nucleus. J Biol Chem (2004 ) 279(26):27320–6.

    Not in our library10.1074/jbc.m308650200 (opens in a new tab)

  69. 69.
    Endogenous histones function as alarmins in sterile inflammatory liver injury through Toll-like receptor 9 in mice · 2011
    No notice
  70. 70.

    Apetoh L Ghiringhelli F Tesniere A Obeid M Ortiz C Criollo A Toll-like receptor 4-dependent contribution of the immune system to anticancer chemotherapy and radiotherapy. Nat Med (2007 ) 13(9):1050–9.

    Not in our library10.1038/nm1622 (opens in a new tab)

  71. 71.

    Semino C Angelini G Poggi A Rubartelli A. NK/iDC interaction results in IL-18 secretion by DCs at the synaptic cleft followed by NK cell activation and release of the DC maturation factor HMGB1. Blood (2005 ) 106(2):609–16.

    Not in our library10.1182/blood-2004-10-3906 (opens in a new tab)

  72. 72.

    Scaffidi P Misteli T Bianchi ME. Release of chromatin protein HMGB1 by necrotic cells triggers inflammation. Nature (2002 ) 418(6894):191–5.

    Not in our library10.1038/nature00858 (opens in a new tab)

  73. 73.

    Thorburn J Horita H Redzic J Hansen K Frankel AE Thorburn A. Autophagy regulates selective HMGB1 release in tumor cells that are destined to die. Cell Death Differ (2009 ) 16(1):175–83.

    Not in our library10.1038/cdd.2008.143 (opens in a new tab)

  74. 74.

    Yang D Postnikov YV Li Y Tewary P de la Rosa G Wei F. High-mobility group nucleosome-binding protein 1 acts as an alarmin and is critical for lipopolysaccharide-induced immune responses. J Exp Med (2012 ) 209(1):157–71.

    Not in our library10.1084/jem.20101354 (opens in a new tab)

  75. 75.

    Cohen I Rider P Carmi Y Braiman A Dotan S White MR Differential release of chromatin-bound IL-1alpha discriminates between necrotic and apoptotic cell death by the ability to induce sterile inflammation. Proc Natl Acad Sci U S A (2010 ) 107(6):2574–9.

    Not in our library10.1073/pnas.0915018107 (opens in a new tab)

  76. 76.

    Vanden Berghe T Kalai M Denecker G Meeus A Saelens X Vandenabeele P. Necrosis is associated with IL-6 production but apoptosis is not. Cell Signal (2006 ) 18(3):328–35.

    Not in our library10.1016/j.cellsig.2005.05.003 (opens in a new tab)

  77. 77.

    Lauber K Bohn E Krober SM Xiao YJ Blumenthal SG Lindemann RK Apoptotic cells induce migration of phagocytes via caspase-3-mediated release of a lipid attraction signal. Cell (2003 ) 113:717–30.

    Not in our library10.1016/s0092-8674(03)00422-7 (opens in a new tab)

  78. 78.

    Zhang Q Raoof M Chen Y Sumi Y Sursal T Junger W Circulating mitochondrial DAMPs cause inflammatory responses to injury. Nature (2010 ) 464(7285):104–7.

    Not in our library10.1038/nature08780 (opens in a new tab)

  79. 79.

    Collins LV Hajizadeh S Holme E Jonsson IM Tarkowski A. Endogenously oxidized mitochondrial DNA induces in vivo and in vitro inflammatory responses. J Leukoc Biol (2004 ) 75(6):995–1000.

    Not in our library10.1189/jlb.0703328 (opens in a new tab)

  80. 80.

    Galluzzi L Kepp O Kroemer G. Mitochondria: master regulators of danger signalling. Nat Rev Mol Cell Biol (2012 ) 13(12):780–8.

    Not in our library10.1038/nrm3479 (opens in a new tab)

  81. 81.

    Shi Y Evans JE Rock KL. Molecular identification of a danger signal that alerts the immune system to dying cells. Nature (2003 ) 425(6957):516–21.

    Not in our library10.1038/nature01991 (opens in a new tab)

  82. 82.

    Carp H. Mitochondrial N-formylmethionyl proteins as chemoattractants for neutrophils. J Exp Med (1982 ) 155(1):264–75.

    Not in our library10.1084/jem.155.1.264 (opens in a new tab)

  83. 83.

    Rabiet MJ Huet E Boulay F. The N-formyl peptide receptors and the anaphylatoxin C5a receptors: an overview. Biochimie (2007 ) 89(9):1089–106.

    Not in our library10.1016/j.biochi.2007.02.015 (opens in a new tab)

  84. 84.

    Czapiga M Gao JL Kirk A Lekstrom-Himes J. Human platelets exhibit chemotaxis using functional N-formyl peptide receptors. Exp Hematol (2005 ) 33(1):73–84.

    Not in our library10.1016/j.exphem.2004.09.010 (opens in a new tab)

  85. 85.

    Moghaddam AE Gartlan KH Kong L Sattentau QJ. Reactive carbonyls are a major Th2-inducing damage-associated molecular pattern generated by oxidative stress. J Immunol (2011 ) 187(4):1626–33.

    Not in our library10.4049/jimmunol.1003906 (opens in a new tab)

  86. 86.

    Miller YI Choi SH Wiesner P Fang L Harkewicz R Hartvigsen K Oxidation-specific epitopes are danger-associated molecular patterns recognized by pattern recognition receptors of innate immunity. Circ Res (2011 ) 108(2):235–48.

    Not in our library10.1161/circresaha.110.223875 (opens in a new tab)

  87. 87.

    Vandenberk L Garg AD Verschuere T Koks C Belmans J Beullens M Irradiation of necrotic cancer cells employed for pulsing dendritic cells (DCs), potentiates DC vaccine-induced antitumor immunity against high-grade glioma. Oncoimmunology (2015 ).

    Not in our library10.1080/2162402x.2015.1083669 (opens in a new tab)

  88. 88.

    Riddell JR Wang XY Minderman H Gollnick SO. Peroxiredoxin 1 stimulates secretion of proinflammatory cytokines by binding to TLR4. J Immunol (2010 ) 184(2):1022–30.

    Not in our library10.4049/jimmunol.0901945 (opens in a new tab)

  89. 89.

    Franz S Herrmann K Furnrohr BG Sheriff A Frey B Gaipl US After shrinkage apoptotic cells expose internal membrane-derived epitopes on their plasma membranes. Cell Death Differ (2007 ) 14(4):733–42.

    Not in our library10.1038/sj.cdd.4402066 (opens in a new tab)

  90. 90.

    Petrovski G Zahuczky G Katona K Vereb G Martinet W Nemes Z Clearance of dying autophagic cells of different origin by professional and non-professional phagocytes. Cell Death Differ (2007 ) 14(6):1117–28.

    Not in our library10.1038/sj.cdd.4402112 (opens in a new tab)

  91. 91.

    Bratton DL Fadok VA Richter DA Kailey JM Guthrie LA Henson PM. Appearance of phosphatidylserine on apoptotic cells requires calcium-mediated nonspecific flip-flop and is enhanced by loss of the aminophospholipid translocase. J Biol Chem (1997 ) 272(42):26159–65.

    Not in our library10.1074/jbc.272.42.26159 (opens in a new tab)

  92. 92.

    Martin SJ Reutelingsperger CP McGahon AJ Rader JA van Schie RC LaFace DM Early redistribution of plasma membrane phosphatidylserine is a general feature of apoptosis regardless of the initiating stimulus: inhibition by overexpression of Bcl-2 and Abl. J Exp Med (1995 ) 182(5):1545–56.

    Not in our library10.1084/jem.182.5.1545 (opens in a new tab)

  93. 93.

    Brouckaert G Kalai M Krysko DV Saelens X Vercammen D Ndlovu MN Phagocytosis of necrotic cells by macrophages is phosphatidylserine dependent and does not induce inflammatory cytokine production. Mol Biol Cell (2004 ) 15(3):1089–100.

    Not in our library10.1091/mbc.e03-09-0668 (opens in a new tab)

  94. 94.

    Donato R. RAGE: a single receptor for several ligands and different cellular responses: the case of certain S100 proteins. Curr Mol Med (2007 ) 7(8):711–24.

    Not in our library10.2174/156652407783220688 (opens in a new tab)

  95. 95.

    Goh FG Piccinini AM Krausgruber T Udalova IA Midwood KS. Transcriptional regulation of the endogenous danger signal tenascin-C: a novel autocrine loop in inflammation. J Immunol (2010 ) 184(5):2655–62.

    Not in our library10.4049/jimmunol.0903359 (opens in a new tab)

  96. 96.

    Krispin A Bledi Y Atallah M Trahtemberg U Verbovetski I Nahari E Apoptotic cell thrombospondin-1 and heparin-binding domain lead to dendritic-cell phagocytic and tolerizing states. Blood (2006 ) 108(10):3580–9.

    Not in our library10.1182/blood-2006-03-013334 (opens in a new tab)

  97. 97.
    Essential versus accessory aspects of cell death: recommendations of the NCCD 2015 · 2014
    No notice
  98. 98.

    Melcher A Todryk S Hardwick N Ford M Jacobson M Vile RG. Tumor immunogenicity is determined by the mechanism of cell death via induction of heat shock protein expression. Nat Med (1998 ) 4(5):581–7.

    Not in our library10.1038/nm0598-581 (opens in a new tab)

  99. 99.

    Gough MJ Melcher AA Crittenden MR Sanchez-Perez L Voellmy R Vile RG. Induction of cell stress through gene transfer of an engineered heat shock transcription factor enhances tumor immunogenicity. Gene Ther (2004 ) 11(13):1099–104.

    Not in our library10.1038/sj.gt.3302274 (opens in a new tab)

  100. 100.

    Spisek R Charalambous A Mazumder A Vesole DH Jagannath S Dhodapkar MV. Bortezomib enhances dendritic cell (DC)-mediated induction of immunity to human myeloma via exposure of cell surface heat shock protein 90 on dying tumor cells: therapeutic implications. Blood (2007 ) 109(11):4839–45.

    Not in our library10.1182/blood-2006-10-054221 (opens in a new tab)

  101. 101.

    Casares N Pequignot MO Tesniere A Ghiringhelli F Roux S Chaput N Caspase-dependent immunogenicity of doxorubicin-induced tumor cell death. J Exp Med (2005 ) 202(12):1691–701.

    Not in our library10.1084/jem.20050915 (opens in a new tab)

  102. 102.

    Kroemer G Galluzzi L Kepp O Zitvogel L Immunogenic cell death in cancer therapy. Annu Rev Immunol (2013 ) 31:51–72.

    Not in our library10.1146/annurev-immunol-032712-100008 (opens in a new tab)

  103. 103.

    Garg AD Dudek-Peric AM Romano E Agostinis P. Immunogenic cell death. Int J Dev Biol (2015 ) 59:131–40.

    Not in our library10.1387/ijdb.150061pa (opens in a new tab)

  104. 104.

    Kepp O Senovilla L Vitale I Vacchelli E Adjemian S Agostinis P Consensus guidelines for the detection of immunogenic cell death. Oncoimmunology (2014 ) 3(9):e955691.

    Not in our library10.4161/21624011.2014.955691 (opens in a new tab)

  105. 105.
    Immature, Semi-Mature, and Fully Mature Dendritic Cells: Toward a DC-Cancer Cells Interface That Augments Anticancer Immunity · 2013
    No notice
  106. 106.

    Ma Y Adjemian S Mattarollo SR Yamazaki T Aymeric L Yang H Anticancer chemotherapy-induced intratumoral recruitment and differentiation of antigen-presenting cells. Immunity (2013 ) 38(4):729–41.

    Not in our library10.1016/j.immuni.2013.03.003 (opens in a new tab)

  107. 107.

    Zhang JG Czabotar PE Policheni AN Caminschi I Wan SS Kitsoulis S The dendritic cell receptor Clec9A binds damaged cells via exposed actin filaments. Immunity (2012 ) 36(4):646–57.

    Not in our library10.1016/j.immuni.2012.03.009 (opens in a new tab)

  108. 108.

    Garnett CT Palena C Chakraborty M Tsang KY Schlom J Hodge JW. Sublethal irradiation of human tumor cells modulates phenotype resulting in enhanced killing by cytotoxic T lymphocytes. Cancer Res (2004 ) 64(21):7985–94.

    Not in our library10.1158/0008-5472.can-04-1525 (opens in a new tab)

  109. 109.

    Hodge JW Garnett CT Farsaci B Palena C Tsang KY Ferrone S Chemotherapy-induced immunogenic modulation of tumor cells enhances killing by cytotoxic T lymphocytes and is distinct from immunogenic cell death. Int J Cancer (2013 ) 133(3):624–36.

    Not in our library10.1002/ijc.28070 (opens in a new tab)

  110. 110.
    Radiation-induced immunogenic modulation of tumor enhances antigen processing and calreticulin exposure, resulting in enhanced T-cell killing · 2013
    No notice
  111. 111.

    Michaud M Martins I Sukkurwala AQ Adjemian S Ma Y Pellegatti P Autophagy-dependent anticancer immune responses induced by chemotherapeutic agents in mice. Science (2011 ) 334(6062):1573–7.

    Not in our library10.1126/science.1208347 (opens in a new tab)

  112. 112.

    Garg AD Dudek AM Agostinis P Calreticulin surface exposure is abrogated in cells lacking, chaperone-mediated autophagy-essential gene, LAMP2A. Cell Death Dis (2013 ) 4:e826

    Not in our library10.1038/cddis.2013.372 (opens in a new tab)

  113. 113.

    Martins I Wang Y Michaud M Ma Y Sukkurwala AQ Shen S Molecular mechanisms of ATP secretion during immunogenic cell death. Cell Death Differ (2014 ) 21(1):79–91.

    Not in our library10.1038/cdd.2013.75 (opens in a new tab)

  114. 114.

    Kazama H Ricci JE Herndon JM Hoppe G Green DR Ferguson TA. Induction of immunological tolerance by apoptotic cells requires caspase-dependent oxidation of high-mobility group box-1 protein. Immunity (2008 ) 29(1):21–32.

    Not in our library10.1016/j.immuni.2008.05.013 (opens in a new tab)

  115. 115.

    Jube S Rivera Z Bianchi ME Powers A Wang E Pagano IS Cancer cell secretion of the DAMP protein HMGB1 supports progression in malignant mesothelioma. Cancer Res (2012 ) 72(13):3290–301.

    Not in our library10.1158/0008-5472.can-11-3481 (opens in a new tab)

  116. 116.

    Garg AD Krysko DV Vandenabeele P Agostinis P. Hypericin-based photodynamic therapy induces surface exposure of damage-associated molecular patterns like HSP70 and calreticulin. Cancer Immunol Immunother (2012 ) 61(2):215–21.

    Not in our library10.1007/s00262-011-1184-2 (opens in a new tab)

  117. 117.

    Lancaster GI Febbraio MA. Exosome-dependent trafficking of HSP70: a novel secretory pathway for cellular stress proteins. J Biol Chem (2005 ) 280(24):23349–55.

    Not in our library10.1074/jbc.m502017200 (opens in a new tab)

  118. 118.

    Mambula SS Calderwood SK. Heat shock protein 70 is secreted from tumor cells by a nonclassical pathway involving lysosomal endosomes. J Immunol (2006 ) 177(11):7849–57.

    Not in our library10.4049/jimmunol.177.11.7849 (opens in a new tab)

  119. 119.

    Vega VL Rodriguez-Silva M Frey T Gehrmann M Diaz JC Steinem C Hsp70 translocates into the plasma membrane after stress and is released into the extracellular environment in a membrane-associated form that activates macrophages. J Immunol (2008 ) 180(6):4299–307.

    Not in our library10.4049/jimmunol.180.6.4299 (opens in a new tab)

  120. 120.

    Kotter B Frey B Winderl M Rubner Y Scheithauer H Sieber R The in vitro immunogenic potential of caspase-3 proficient breast cancer cells with basal low immunogenicity is increased by hypofractionated irradiation. Radiat Oncol (2015 ) 10(1):197.

    Not in our library10.1186/s13014-015-0506-5 (opens in a new tab)

  121. 121.

    Multhoff G Botzler C Wiesnet M Muller E Meier T Wilmanns W A stress-inducible 72-kDa heat-shock protein (HSP72) is expressed on the surface of human tumor cells, but not on normal cells. Int J Cancer (1995 ) 61(2):272–9.

    Not in our library10.1002/ijc.2910610222 (opens in a new tab)

  122. 122.

    Gastpar R Gehrmann M Bausero MA Asea A Gross C Schroeder JA Heat shock protein 70 surface-positive tumor exosomes stimulate migratory and cytolytic activity of natural killer cells. Cancer Res (2005 ) 65(12):5238–47.

    Not in our library10.1158/0008-5472.can-04-3804 (opens in a new tab)

  123. 123.

    Panaretakis T Kepp O Brockmeier U Tesniere A Bjorklund AC Chapman DC Mechanisms of pre-apoptotic calreticulin exposure in immunogenic cell death. EMBO J (2009 ) 28(5):578–90.

    Not in our library10.1038/emboj.2009.1 (opens in a new tab)

  124. 124.

    Madeo F Durchschlag M Kepp O Panaretakis T Zitvogel L Frohlich KU Phylogenetic conservation of the preapoptotic calreticulin exposure pathway from yeast to mammals. Cell Cycle (2009 ) 8(4):639–42.

    Not in our library10.4161/cc.8.4.7794 (opens in a new tab)

  125. 125.

    Martin S Dudek-Peric AM Maes H Garg AD Gabrysiak M Demirsoy S Concurrent MEK and autophagy inhibition is required to restore cell death associated danger-signalling in vemurafenib-resistant melanoma cells. Biochem Pharmacol (2015 ) 93(3):290–304.

    Not in our library10.1016/j.bcp.2014.12.003 (opens in a new tab)

  126. 126.
    STRING v10: protein–protein interaction networks, integrated over the tree of life · 2014
    No notice
  127. 127.

    Dudek AM Garg AD Krysko DV De Ruysscher D Agostinis P. Inducers of immunogenic cancer cell death. Cytokine Growth Factor Rev (2013 ) 24(4):319–33.

    Not in our library10.1016/j.cytogfr.2013.01.005 (opens in a new tab)

  128. 128.
    Combinatorial Strategies for the Induction of Immunogenic Cell Death · 2015
    No notice
  129. 129.

    Siurala M Bramante S Vassilev L Hirvinen M Parviainen S Tahtinen S Oncolytic adenovirus and doxorubicin-based chemotherapy results in synergistic antitumor activity against soft-tissue sarcoma. Int J Cancer (2015 ) 136(4):945–54.

    Not in our library10.1002/ijc.29048 (opens in a new tab)

  130. 130.

    Menger L Vacchelli E Adjemian S Martins I Ma Y Shen S Cardiac glycosides exert anticancer effects by inducing immunogenic cell death. Sci Transl Med (2012 ) 4(143):143ra99.

    Not in our library10.1126/scitranslmed.3003807 (opens in a new tab)

  131. 131.

    Panaretakis T Joza N Modjtahedi N Tesniere A Vitale I Durchschlag M The co-translocation of ERp57 and calreticulin determines the immunogenicity of cell death. Cell Death Differ (2008 ) 15(9):1499–509.

    Not in our library10.1038/cdd.2008.67 (opens in a new tab)

  132. 132.

    Tufi R Panaretakis T Bianchi K Criollo A Fazi B Di Sano F Reduction of endoplasmic reticulum Ca2+ levels favors plasma membrane surface exposure of calreticulin. Cell Death Differ (2008 ) 15(2):274–82.

    Not in our library10.1038/sj.cdd.4402275 (opens in a new tab)

  133. 133.

    Martins I Kepp O Schlemmer F Adjemian S Tailler M Shen S Restoration of the immunogenicity of cisplatin-induced cancer cell death by endoplasmic reticulum stress. Oncogene (2011 ) 30(10):1147–58.

    Not in our library10.1038/onc.2010.500 (opens in a new tab)

  134. 134.

    Verfaillie T Rubio N Garg AD Bultynck G Rizzuto R Decuypere JP PERK is required at the ER-mitochondrial contact sites to convey apoptosis after ROS-based ER stress. Cell Death Differ (2012 ) 19(11):1880–91.

    Not in our library10.1038/cdd.2012.74 (opens in a new tab)

  135. 135.

    Galluzzi L Bravo-San Pedro JM Kroemer G. Organelle-specific initiation of cell death. Nat Cell Biol (2014 ) 16(8):728–36.

    Not in our library10.1038/ncb3005 (opens in a new tab)

  136. 136.

    Chaurio RA Munoz LE Maueroder C Janko C Harrer T Furnrohr BG The progression of cell death affects the rejection of allogeneic tumors in immune-competent mice – implications for cancer therapy. Front Immunol (2014 ) 5:560.

    Not in our library10.3389/fimmu.2014.00560 (opens in a new tab)

  137. 137.

    Garg AD Maes H van Vliet AR Agostinis P Targeting the hallmarks of cancer with therapy-induced endoplasmic reticulum (ER) stress. Mol Cell Oncol (2015 ) 2(1):e975089

    Not in our library10.4161/23723556.2014.975089 (opens in a new tab)

  138. 138.

    van Vliet AR Martin S Garg AD Agostinis P. The PERKs of damage-associated molecular patterns mediating cancer immunogenicity: from sensor to the plasma membrane and beyond. Semin Cancer Biol (2015 ) 33:74–85.

    Not in our library10.1016/j.semcancer.2015.03.010 (opens in a new tab)

  139. 139.

    Sukkurwala AQ Adjemian S Senovilla L Michaud M Spaggiari S Vacchelli E Screening of novel immunogenic cell death inducers within the NCI mechanistic diversity set. Oncoimmunology (2014 ) 3:e28473.

    Not in our library10.4161/onci.28473 (opens in a new tab)

  140. 140.

    Wong DY Ong WW Ang WH. Induction of immunogenic cell death by chemotherapeutic platinum complexes. Angew Chem Int Ed Engl (2015 ) 54(22):6483–7.

    Not in our library10.1002/anie.201500934 (opens in a new tab)

  141. 141.

    Sistigu A Yamazaki T Vacchelli E Chaba K Enot DP Adam J Cancer cell-autonomous contribution of type I interferon signaling to the efficacy of chemotherapy. Nat Med (2014 ) 20(11):1301–9.

    Not in our library10.1038/nm.3708 (opens in a new tab)

  142. 142.

    Ramakrishnan R Gabrilovich DI. The role of mannose-6-phosphate receptor and autophagy in influencing the outcome of combination therapy. Autophagy (2013 ) 9(4):615–6.

    Not in our library10.4161/auto.23485 (opens in a new tab)

  143. 143.

    Kaminski JM Shinohara E Summers JB Niermann KJ Morimoto A Brousal J. The controversial abscopal effect. Cancer Treat Rev (2005 ) 31(3):159–72.

    Not in our library10.1016/j.ctrv.2005.03.004 (opens in a new tab)

  144. 144.

    Golden EB Frances D Pellicciotta I Demaria S Helen Barcellos-Hoff M Formenti SC. Radiation fosters dose-dependent and chemotherapy-induced immunogenic cell death. Oncoimmunology (2014 ) 3:e28518.

    Not in our library10.4161/onci.28518 (opens in a new tab)

  145. 145.

    Garrido G Rabasa A Sanchez B Lopez MV Blanco R Lopez A Induction of immunogenic apoptosis by blockade of epidermal growth factor receptor activation with a specific antibody. J Immunol (2011 ) 187(10):4954–66.

    Not in our library10.4049/jimmunol.1003477 (opens in a new tab)

  146. 146.

    Bugaut H Bruchard M Berger H Derangere V Odoul L Euvrard R Bleomycin exerts ambivalent antitumor immune effect by triggering both immunogenic cell death and proliferation of regulatory T cells. PLoS One (2013 ) 8(6):e65181.

    Not in our library10.1371/journal.pone.0065181 (opens in a new tab)

  147. 147.

    Diaconu I Cerullo V Hirvinen ML Escutenaire S Ugolini M Pesonen SK Immune response is an important aspect of the antitumor effect produced by a CD40L-encoding oncolytic adenovirus. Cancer Res (2012 ) 72(9):2327–38.

    Not in our library10.1158/0008-5472.can-11-2975 (opens in a new tab)

  148. 148.

    Hemminki O Parviainen S Juhila J Turkki R Linder N Lundin J Immunological data from cancer patients treated with Ad5/3-E2F-Delta24-GMCSF suggests utility for tumor immunotherapy. Oncotarget (2015 ) 6(6):4467–81.

    Not in our library10.18632/oncotarget.2901 (opens in a new tab)

  149. 149.

    Sun C Wang H Mao S Liu J Li S Wang J. Reactive oxygen species involved in CT26 immunogenic cell death induced by Clostridium difficile toxin B. Immunol Lett (2015 ) 164(2):65–71.

    Not in our library10.1016/j.imlet.2015.02.007 (opens in a new tab)

  150. 150.

    Miyamoto S Inoue H Nakamura T Yamada M Sakamoto C Urata Y Coxsackievirus B3 Is an oncolytic virus with immunostimulatory properties that is active against lung Adenocarcinoma. Cancer Res (2012 ) 72(10):2609–21.

    Not in our library10.1158/0008-5472.can-11-3185 (opens in a new tab)

  151. 151.

    Vacchelli E Eggermont A Sautes-Fridman C Galon J Zitvogel L Kroemer G Trial watch: oncolytic viruses for cancer therapy. Oncoimmunology (2013 ) 2(6):e24612.

    Not in our library10.4161/onci.22789 (opens in a new tab)

  152. 152.

    Schiavoni G Sistigu A Valentini M Mattei F Sestili P Spadaro F Cyclophosphamide synergizes with type I interferons through systemic dendritic cell reactivation and induction of immunogenic tumor apoptosis. Cancer Res (2011 ) 71(3):768–78.

    Not in our library10.1158/0008-5472.can-10-2788 (opens in a new tab)

  153. 153.

    Viaud S Saccheri F Mignot G Yamazaki T Daillere R Hannani D The intestinal microbiota modulates the anticancer immune effects of cyclophosphamide. Science (2013 ) 342(6161):971–6.

    Not in our library10.1126/science.1240537 (opens in a new tab)

  154. 154.

    Fucikova J Moserova I Truxova I Hermanova I Vancurova I Partlova S High hydrostatic pressure induces immunogenic cell death in human tumor cells. Int J Cancer (2014 ) 135(5):1165–77.

    Not in our library10.1002/ijc.28766 (opens in a new tab)

  155. 155.
    Physical modalities inducing immunogenic tumor cell death for cancer immunotherapy · 2014
    No notice
  156. 156.

    Weiss EM Meister S Janko C Ebel N Schlucker E Meyer-Pittroff R High hydrostatic pressure treatment generates inactivated mammalian tumor cells with immunogeneic features. J Immunotoxicol (2010 ) 7(3):194–204.

    Not in our library10.3109/15476911003657414 (opens in a new tab)

  157. 157.

    Garg AD Agostinis P. ER stress, autophagy and immunogenic cell death in photodynamic therapy-induced anti-cancer immune responses. Photochem Photobiol Sci (2014 ) 13(3):474–87.

    Not in our library10.1039/c3pp50333j (opens in a new tab)

  158. 158.

    Yu Z Geng J Zhang M Zhou Y Fan Q Chen J. Treatment of osteosarcoma with microwave thermal ablation to induce immunogenic cell death. Oncotarget (2014 ) 5(15):6526–39.

    Not in our library10.18632/oncotarget.2310 (opens in a new tab)

  159. 159.

    Zamarin D Holmgaard RB Subudhi SK Park JS Mansour M Palese P Localized oncolytic virotherapy overcomes systemic tumor resistance to immune checkpoint blockade immunotherapy. Sci Transl Med (2014 ) 6(226):226ra32.

    Not in our library10.1126/scitranslmed.3008095 (opens in a new tab)

  160. 160.

    Chen HM Wang PH Chen SS Wen CC Chen YH Yang WC Shikonin induces immunogenic cell death in tumor cells and enhances dendritic cell-based cancer vaccine. Cancer Immunol Immunother (2012 ) 61(11):1989–2002.

    Not in our library10.1007/s00262-012-1258-9 (opens in a new tab)

  161. 161.

    Korbelik M Dougherty GJ. Photodynamic therapy-mediated immune response against subcutaneous mouse tumors. Cancer Res (1999 ) 59(8):1941–6.

    Not in our library

  162. 162.
    Induction of immune cell infiltration into murine SCCVII tumour by photofrin-based photodynamic therapy · 1995
    No notice
  163. 163.

    Korbelik M Stott B Sun J. Photodynamic therapy-generated vaccines: relevance of tumour cell death expression. Br J Cancer (2007 ) 97(10):1381–7.

    Not in our library10.1038/sj.bjc.6604059 (opens in a new tab)

  164. 164.

    Korbelik M Zhang W Merchant S. Involvement of damage-associated molecular patterns in tumor response to photodynamic therapy: surface expression of calreticulin and high-mobility group box-1 release. Cancer Immunol Immunother (2011 ) 60(10):1431–7.

    Not in our library10.1007/s00262-011-1047-x (opens in a new tab)

  165. 165.

    Duewell P Steger A Lohr H Bourhis H Hoelz H Kirchleitner SV RIG-I-like helicases induce immunogenic cell death of pancreatic cancer cells and sensitize tumors toward killing by CD8 T cells. Cell Death Differ (2014 ) 21(12):1825–37.

    Not in our library10.1038/cdd.2014.96 (opens in a new tab)

  166. 166.

    West AC Mattarollo SR Shortt J Cluse LA Christiansen AJ Smyth MJ An intact immune system is required for the anticancer activities of histone deacetylase inhibitors. Cancer Res (2013 ) 73(24):7265–76.

    Not in our library10.1158/0008-5472.can-13-0890 (opens in a new tab)

  167. 167.

    Yang Y Li XJ Chen Z Zhu XX Wang J Zhang LB Wogonin induced calreticulin/annexin A1 exposure dictates the immunogenicity of cancer cells in a PERK/AKT dependent manner. PLoS One (2012 ) 7(12):e50811.

    Not in our library10.1371/journal.pone.0050811 (opens in a new tab)

  168. 168.

    Panzarini E Inguscio V Fimia GM Dini L. Rose Bengal acetate photodynamic therapy (RBAc-PDT) induces exposure and release of damage-associated molecular patterns (DAMPs) in human HeLa cells. PLoS One (2014 ) 9(8):e105778.

    Not in our library10.1371/journal.pone.0105778 (opens in a new tab)

  169. 169.

    Molinari R D’Eliseo D Manzi L Zolla L Velotti F Merendino N. The n3-polyunsaturated fatty acid docosahexaenoic acid induces immunogenic cell death in human cancer cell lines via pre-apoptotic calreticulin exposure. Cancer Immunol Immunother (2011 ) 60(10):1503–7.

    Not in our library10.1007/s00262-011-1074-7 (opens in a new tab)

  170. 170.

    D’Eliseo D Manzi L Velotti F. Capsaicin as an inducer of damage-associated molecular patterns (DAMPs) of immunogenic cell death (ICD) in human bladder cancer cells. Cell Stress Chaperones (2013 ) 18(6):801–8.

    Not in our library10.1007/s12192-013-0422-2 (opens in a new tab)

  171. 171.

    Gilardini Montani MS D’Eliseo D Cirone M Di Renzo L Faggioni A Santoni A Capsaicin-mediated apoptosis of human bladder cancer cells activates dendritic cells via CD91. Nutrition (2015 ) 31(4):578–81.

    Not in our library10.1016/j.nut.2014.05.005 (opens in a new tab)

  172. 172.

    Janeway C Immunobiology: The Immune System in Health and Disease. 6th ed New York, NY: Garland Science (2005 ). 823 p.

    Not in our library

  173. 173.

    Fucikova J Kralikova P Fialova A Brtnicky T Rob L Bartunkova J Human tumor cells killed by anthracyclines induce a tumor-specific immune response. Cancer Res (2011 ) 71(14):4821–33.

    Not in our library10.1158/0008-5472.can-11-0950 (opens in a new tab)

  174. 174.

    Krysko DV Kaczmarek A Krysko O Heyndrickx L Woznicki J Bogaert P TLR-2 and TLR-9 are sensors of apoptosis in a mouse model of doxorubicin-induced acute inflammation. Cell Death Differ (2011 ) 18(8):1316–25.

    Not in our library10.1038/cdd.2011.4 (opens in a new tab)

  175. 175.

    Tseng LM Liu CY Chang KC Chu PY Shiau CW Chen KF. CIP2A is a target of bortezomib in human triple negative breast cancer cells. Breast Cancer Res (2012 ) 14(2):R68.

    Not in our library10.1186/bcr3175 (opens in a new tab)

  176. 176.

    Davies AM Lara PN Jr Mack PC Gandara DR. Incorporating bortezomib into the treatment of lung cancer. Clin Cancer Res (2007 ) 13(15 Pt 2):s4647–51.

    Not in our library10.1158/1078-0432.ccr-07-0334 (opens in a new tab)

  177. 177.

    Huang T Li S Li G Tian Y Wang H Shi L Utility of Clostridium difficile toxin B for inducing anti-tumor immunity. PLoS One (2014 ) 9(10):e110826.

    Not in our library10.1371/journal.pone.0110826 (opens in a new tab)

  178. 178.

    Bravim F de Freitas JM Fernandes AA Fernandes PM. High hydrostatic pressure and the cell membrane: stress response of Saccharomyces cerevisiae. Ann N Y Acad Sci (2010 ) 1189:127–32.

    Not in our library10.1111/j.1749-6632.2009.05182.x (opens in a new tab)

  179. 179.

    Senovilla L Vitale I Martins I Tailler M Pailleret C Michaud M An immunosurveillance mechanism controls cancer cell ploidy. Science (2012 ) 337(6102):1678–84.

    Not in our library10.1126/science.1224922 (opens in a new tab)

  180. 180.

    Korbelik M. Cancer vaccines generated by photodynamic therapy. Photochem Photobiol Sci (2011 ) 10(5):664–9.

    Not in our library10.1039/c0pp00343c (opens in a new tab)

  181. 181.

    Garg AD Krysko DV Vandenabeele P Agostinis P. DAMPs and PDT-mediated photo-oxidative stress: exploring the unknown. Photochem Photobiol Sci (2011 ) 10(5):670–80.

    Not in our library10.1039/c0pp00294a (opens in a new tab)

  182. 182.

    Chen J Xie J Jiang Z Wang B Wang Y Hu X. Shikonin and its analogs inhibit cancer cell glycolysis by targeting tumor pyruvate kinase-M2. Oncogene (2011 ) 30(42):4297–306.

    Not in our library10.1038/onc.2011.137 (opens in a new tab)

  183. 183.

    Tsai CF Yeh WL Huang SM Tan TW Lu DY. Wogonin induces reactive oxygen species production and cell apoptosis in human glioma cancer cells. Int J Mol Sci (2012 ) 13(8):9877–92.

    Not in our library10.3390/ijms13089877 (opens in a new tab)

  184. 184.

    Sanovic R Verwanger T Hartl A Krammer B. Low dose hypericin-PDT induces complete tumor regression in BALB/c mice bearing CT26 colon carcinoma. Photodiagnosis Photodyn Ther (2011 ) 8(4):291–6.

    Not in our library10.1016/j.pdpdt.2011.04.003 (opens in a new tab)

  185. 185.

    Garg AD Krysko DV Vandenabeele P Agostinis P. The emergence of phox-ER stress induced immunogenic apoptosis. OncoImmunology (2012 ) 1(5):787–9.

    Not in our library10.4161/onci.19750 (opens in a new tab)

  186. 186.

    Liu Z Zhang HM Yuan J Ye X Taylor GA Yang D. The immunity-related GTPase Irgm3 relieves endoplasmic reticulum stress response during Coxsackievirus B3 infection via a PI3K/Akt dependent pathway. Cell Microbiol (2012 ) 14(1):133–46.

    Not in our library10.1111/j.1462-5822.2011.01708.x (opens in a new tab)

  187. 187.

    Bian J Wang K Kong X Liu H Chen F Hu M Caspase- and p38-MAPK-dependent induction of apoptosis in A549 lung cancer cells by Newcastle disease virus. Arch Virol (2011 ) 156(8):1335–44.

    Not in our library10.1007/s00705-011-0987-y (opens in a new tab)

  188. 188.

    Garg AD De Ruysscher D Agostinis P Immunological metagene signatures derived from immunogenic cancer cell death associate with improved survival of patients with lung, breast or ovarian malignancies: a large-scale meta-analysis. Oncoimmunology (2015 ).

    Not in our library10.1080/2162402x.2015.1069938 (opens in a new tab)

  189. 189.

    Galluzzi L Kepp O Kroemer G Enlightening the impact of immunogenic cell death in photodynamic cancer therapy. EMBO J (2012 ) 31(5):1055–7.

    Not in our library10.1038/emboj.2012.2 (opens in a new tab)

  190. 190.

    Galluzzi L Pietrocola F Bravo-San Pedro JM Amaravadi RK Baehrecke EH Cecconi F Autophagy in malignant transformation and cancer progression. EMBO J (2015 ) 34(7):856–80.

    Not in our library10.15252/embj.201490784 (opens in a new tab)

  191. 191.

    Mattarollo SR Loi S Duret H Ma Y Zitvogel L Smyth MJ. Pivotal role of innate and adaptive immunity in anthracycline chemotherapy of established tumors. Cancer Res (2011 ) 71(14):4809–20.

    Not in our library10.1158/0008-5472.can-11-0753 (opens in a new tab)

  192. 192.

    Lin TJ Lin HT Chang WT Mitapalli SP Hsiao PW Yin SY Shikonin-enhanced cell immunogenicity of tumor vaccine is mediated by the differential effects of DAMP components. Mol Cancer (2015 ) 14:174.

    Not in our library10.1186/s12943-015-0435-9 (opens in a new tab)

  193. 193.

    Ma Y Aymeric L Locher C Mattarollo SR Delahaye NF Pereira P Contribution of IL-17-producing gamma delta T cells to the efficacy of anticancer chemotherapy. J Exp Med (2011 ) 208(3):491–503.

    Not in our library10.1084/jem.20100269 (opens in a new tab)

  194. 194.

    Yang H Yamazaki T Pietrocola F Zhou H Zitvogel L Ma Y STAT3 inhibition enhances the therapeutic efficacy of immunogenic chemotherapy by stimulating type 1 interferon production by cancer cells. Cancer Res (2015 ) 75(18):3812–22.

    Not in our library10.1158/0008-5472.can-15-1122 (opens in a new tab)

  195. 195.

    Ciampricotti M Hau CS Doornebal CW Jonkers J de Visser KE Chemotherapy response of spontaneous mammary tumors is independent of the adaptive immune system. Nat Med (2012 ) 18(3):344–6.

    Not in our library10.1038/nm.2652 (opens in a new tab)

  196. 196.

    Gould SE Junttila MR de Sauvage FJ. Translational value of mouse models in oncology drug development. Nat Med (2015 ) 21(5):431–9.

    Not in our library10.1038/nm.3853 (opens in a new tab)

  197. 197.

    Tesniere A Schlemmer F Boige V Kepp O Martins I Ghiringhelli F Immunogenic death of colon cancer cells treated with oxaliplatin. Oncogene (2010 ) 29(4):482–91.

    Not in our library10.1038/onc.2009.356 (opens in a new tab)

  198. 198.

    Hannesdottir L Tymoszuk P Parajuli N Wasmer MH Philipp S Daschil N Lapatinib and doxorubicin enhance the Stat1-dependent antitumor immune response. Eur J Immunol (2013 ) 43(10):2718–29.

    Not in our library10.1002/eji.201242505 (opens in a new tab)

  199. 199.

    Michaud M Xie X Bravo-San Pedro JM Zitvogel L White E Kroemer G. An autophagy-dependent anticancer immune response determines the efficacy of melanoma chemotherapy. Oncoimmunology (2014 ) 3(7):e944047.

    Not in our library10.4161/21624011.2014.944047 (opens in a new tab)

  200. 200.

    Demaria S Santori FR Ng B Liebes L Formenti SC Vukmanovic S. Select forms of tumor cell apoptosis induce dendritic cell maturation. J Leukoc Biol (2005 ) 77(3):361–8.

    Not in our library10.1189/jlb.0804478 (opens in a new tab)

  201. 201.

    Schumacher LY Vo DD Garban HJ Comin-Anduix B Owens SK Dissette VB Immunosensitization of tumor cells to dendritic cell-activated immune responses with the proteasome inhibitor bortezomib (PS-341, Velcade). J Immunol (2006 ) 176(8):4757–65.

    Not in our library10.4049/jimmunol.176.8.4757 (opens in a new tab)

  202. 202.

    Chang CL Hsu YT Wu CC Yang YC Wang C Wu TC Immune mechanism of the antitumor effects generated by bortezomib. J Immunol (2012 ) 189(6):3209–20.

    Not in our library10.4049/jimmunol.1103826 (opens in a new tab)

  203. 203.

    van der Most RG Currie AJ Mahendran S Prosser A Darabi A Robinson BW Tumor eradication after cyclophosphamide depends on concurrent depletion of regulatory T cells: a role for cycling TNFR2-expressing effector-suppressor T cells in limiting effective chemotherapy. Cancer Immunol Immunother (2009 ) 58(8):1219–28.

    Not in our library10.1007/s00262-008-0628-9 (opens in a new tab)

  204. 204.

    Obeid M Panaretakis T Joza N Tufi R Tesniere A van Endert P Calreticulin exposure is required for the immunogenicity of gamma-irradiation and UVC light-induced apoptosis. Cell Death Differ (2007 ) 14(10):1848–50.

    Not in our library10.1038/sj.cdd.4402201 (opens in a new tab)

  205. 205.

    Carr-Brendel V Markovic D Smith M Taylor-Papadimitriou J Cohen EP. Immunity to breast cancer in mice immunized with X-irradiated breast cancer cells modified to secrete IL-12. J Immunother (1999 ) 22(5):415–22.

    Not in our library10.1097/00002371-199909000-00005 (opens in a new tab)

  206. 206.

    Strome SE Voss S Wilcox R Wakefield TL Tamada K Flies D Strategies for antigen loading of dendritic cells to enhance the antitumor immune response. Cancer Res (2002 ) 62(6):1884–9.

    Not in our library

  207. 207.

    Prasad SJ Farrand KJ Matthews SA Chang JH McHugh RS Ronchese F. Dendritic cells loaded with stressed tumor cells elicit long-lasting protective tumor immunity in mice depleted of CD4+CD25+ regulatory T cells. J Immunol (2005 ) 174(1):90–8.

    Not in our library10.4049/jimmunol.174.1.90 (opens in a new tab)

  208. 208.

    Yang H Zhou P Huang H Chen D Ma N Cui QC Shikonin exerts antitumor activity via proteasome inhibition and cell death induction in vitro and in vivo. Int J Cancer (2009 ) 124(10):2450–9.

    Not in our library10.1002/ijc.24195 (opens in a new tab)

  209. 209.

    Sharma P Allison JP. The future of immune checkpoint therapy. Science (2015 ) 348(6230):56–61.

    Not in our library10.1126/science.aaa8172 (opens in a new tab)

  210. 210.

    Viney M Lazarou L Abolins S. The laboratory mouse and wild immunology. Parasite Immunol (2015 ) 37(5):267–73.

    Not in our library10.1111/pim.12150 (opens in a new tab)

  211. 211.

    Davis MM. A prescription for human immunology. Immunity (2008 ) 29(6):835–8.

    Not in our library10.1016/j.immuni.2008.12.003 (opens in a new tab)

  212. 212.

    Mestas J Hughes CC. Of mice and not men: differences between mouse and human immunology. J Immunol (2004 ) 172(5):2731–8.

    Not in our library10.4049/jimmunol.172.5.2731 (opens in a new tab)

  213. 213.

    Tubiana M. Klaas Breur medal lecture 1985. The growth and progression of human tumors: implications for management strategy. Radiother Oncol (1986 ) 6(3):167–84.

    Not in our library10.1016/s0167-8140(86)80151-7 (opens in a new tab)

  214. 214.

    Klein CA. Parallel progression of primary tumours and metastases. Nat Rev Cancer (2009 ) 9(4):302–12.

    Not in our library10.1038/nrc2627 (opens in a new tab)

  215. 215.

    Yamazaki T Hannani D Poirier-Colame V Ladoire S Locher C Sistigu A Defective immunogenic cell death of HMGB1-deficient tumors: compensatory therapy with TLR4 agonists. Cell Death Differ (2014 ) 21(1):69–78.

    Not in our library10.1038/cdd.2013.72 (opens in a new tab)

  216. 216.

    Loi S Pommey S Haibe-Kains B Beavis PA Darcy PK Smyth MJ CD73 promotes anthracycline resistance and poor prognosis in triple negative breast cancer. Proc Natl Acad Sci U S A (2013 ) 110(27):11091–6.

    Not in our library10.1073/pnas.1222251110 (opens in a new tab)

  217. 217.

    Shalapour S Font-Burgada J Di Caro G Zhong Z Sanchez-Lopez E Dhar D Immunosuppressive plasma cells impede T-cell-dependent immunogenic chemotherapy. Nature (2015 ) 521(7550):94–8.

    Not in our library10.1038/nature14395 (opens in a new tab)

  218. 218.

    De Boo S Kopecka J Brusa D Gazzano E Matera L Ghigo D iNOS activity is necessary for the cytotoxic and immunogenic effects of doxorubicin in human colon cancer cells. Mol Cancer (2009 ) 8:108.

    Not in our library10.1186/1476-4598-8-108 (opens in a new tab)

  219. 219.
    Zoledronic acid restores doxorubicin chemosensitivity and immunogenic cell death in multidrug-resistant human cancer cells. · 2013
    Not checked
  220. 220.

    Stoll G Enot D Mlecnik B Galon J Zitvogel L Kroemer G. Immune-related gene signatures predict the outcome of neoadjuvant chemotherapy. Oncoimmunology (2014 ) 3(1):e27884.

    Not in our library10.4161/onci.27884 (opens in a new tab)

  221. 221.

    Pardoll DM. The blockade of immune checkpoints in cancer immunotherapy. Nat Rev Cancer (2012 ) 12(4):252–64.

    Not in our library10.1038/nrc3239 (opens in a new tab)

  222. 222.

    Galon J Angell HK Bedognetti D Marincola FM. The continuum of cancer immunosurveillance: prognostic, predictive, and mechanistic signatures. Immunity (2013 ) 39(1):11–26.

    Not in our library10.1016/j.immuni.2013.07.008 (opens in a new tab)

  223. 223.

    Fridman WH Pages F Sautes-Fridman C Galon J. The immune contexture in human tumours: impact on clinical outcome. Nat Rev Cancer (2012 ) 12(4):298–306.

    Not in our library10.1038/nrc3245 (opens in a new tab)

  224. 224.

    Zitvogel L Tesniere A Kroemer G. Cancer despite immunosurveillance: immunoselection and immunosubversion. Nat Rev Immunol (2006 ) 6(10):715–27.

    Not in our library10.1038/nri1936 (opens in a new tab)

  225. 225.

    Ladoire S Penault-Llorca F Senovilla L Dalban C Enot D Locher C Combined evaluation of LC3B puncta and HMGB1 expression predicts residual risk of relapse after adjuvant chemotherapy in breast cancer. Autophagy (2015 ) 11(10):1878–90.

    Not in our library10.1080/15548627.2015.1082022 (opens in a new tab)

  226. 226.

    Kacerovska D Pizinger K Majer F Smid F. Photodynamic therapy of nonmelanoma skin cancer with topical Hypericum perforatum extract – a pilot study. Photochem Photobiol (2008 ) 84(3):779–85.

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  227. 227.

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