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The Human Cytomegalovirus, from Oncomodulation to Oncogenesis

Georges Herbein

Viruses · 2018 · Review · CC BY

doi:10.3390/v10080408

Abstract

Besides its well-described impact in immunosuppressed patients, the role of human cytomegalovirus (HCMV) in the pathogenesis of cancer has been more recently investigated. In cancer, HCMV could favor the progression and the spread of the tumor, a paradigm named oncomodulation. Although oncomodulation could account for part of the protumoral effect of HCMV, it might not explain the whole impact of HCMV infection on the tumor and the tumoral microenvironment. On the contrary cases have been reported where HCMV infection slows down the progression and the spread of the tumor. In addition, HCMV proteins have oncogenic properties per se, HCMV activates pro-oncogenic pathways in infected cells, and recently the direct transformation of cells following HCMV infection has been described, which gave rise to tumors when injected in mice. Thus, beyond the oncomodulation model, this review will assess the direct transforming role of HMCV-infected cells and the potential classification of HCMV as an oncovirus.

Full text

From PubMed Central, U.S. National Library of Medicine, as current on Oct 25, 2026. Paragraph numbers are ours, so an answer can point at one.

1. Introduction

The human cytomegalovirus belongs to the Herpesviridae family with a double stranded DNA genome of 236 kbp in size. In contrast to previous predictions, the translated products from open reading frames (ORF) in human cytomegalovirus (HCMV) genome are much more numerous than previously believed because of the presence of viral short ORFs, alternative splicing, and translation on cytosolic transcripts outside of conserved reading frames. Several cellular functions involved in tumor development are targeted by HCMV gene products including cell cycle dysregulation, cellular immortalization, mutation and instability of the viral genome, enhanced cell survival, and immune escape with tumor spread. In addition, HCMV infects several cell types present in tumoral tissue and microenvironment.

Most organs and tissues of the human body can be infected by HCMV. Although the replication of highly passaged laboratory HCMV strains is limited to fibroblasts, HCMV low passage clinical isolates exhibit an extended cellular tropism for epithelial cells, endothelial cells, hepatocytes, fibroblasts, stromal cells, monocytes/macrophages, astrocytes, and neural stem/progenitor cells. Epithelial cells present in lung, breast, gastrointestinal tract, and kidney can be targeted by HCMV. HCMV infects human lung epithelial cells in vitro with release of newly produced virions up to eight weeks post-infection with a typical cytopathic effect. Human mammary epithelial cells (HMECs) are productively infected by HCMV clinical isolates with low levels of replication. HCMV also replicates in renal epithelial cells and hepatocytes are permissive for HCMV replication with a limited viral production. After prolonged infection in vitro of human embryonic fibroblasts, large syncytia appear in cultures with typical HCMV intranuclear inclusion bodies. In fact, low passage clinical HCMV strains have an intact ULb’ sequence, the region at the right end of the Unique Long region (UL) genome component, which is absent in laboratory adapted HCMV strains. The ULb’ sequence is critical for the viral tropism and favors the replication of HCMV in several primary cell types including epithelial cells, endothelial cells, and myeloid cells. On the contrary, laboratory adapted HCMV strains such as AD169 have lost fully or partially the ULb’ region and have a restricted tropism for fibroblasts. Besides epithelial cells and fibroblasts, HCMV infects persistently monocytes/macrophages, which behave like a viral reservoir and favor the viral spread through the body. Upon HCMV infection of monocytes, activation of NF–kB and PI3K pathways results in a M1/M2 phenotype with both inflammatory and immunosuppressive profiles. Inflammatory factors including Tumor Necrosis Factor (TNF)-alpha, interleukin-6 (IL-6), and nitric oxide synthase 2 are produced by M1 macrophages following HCMV infection. Similarly, an enhanced secretion of TNF-alpha, IL-6, and chemokines is detected in supernatants from CMV-stimulated purified microglial cell cultures. Increased production of proinflammatory cytokines could favor the development of cancer (reviewed in the work of). Infection of astrocytes with CMV results in the enhanced production of chemokines MCP-1 and IL-8, which attract macrophages/microglia in their vicinity. CMV infection of astrocytes turns on TGF-beta production, which exerts positive feedback on viral replication. Altogether, HCMV infects epithelial cells, myeloid cells, fibroblasts, and central nervous system (CNS) cells, all of which could participate to the tumor formation and the tumoral microenvironment.

HCMV may enhance the malignancy of cancer cells and/or tumor-associated cells, a paradigm named oncomodulation. Although HCMV-induced oncomodulation has been extensively studied so far, the direct involvement of HCMV in cell transformation and identifying viral genes favoring such a transformation could define HCMV as an oncovirus.

2.1. The Paradigm of Oncomodulation

On the one hand, the hypothesis of HCMV-induced oncomodulation is supported by the detection of viral proteins and DNA in cancer tissues including glioma, colorectal cancer, prostate cancer, breast cancer, mucoepidermoid carcinoma, medulloblastoma, and neuroblastoma. On the other hand, neither HCMV antigens nor HCMV genome were detected in high fractions of tumors. This apparent discrepancy could result from distinct sensitivity of biological assays used to detect HCMV in the tumor samples. Also, negative results could be due to the fact that the tumor harbors only part of the HCMV genome (similar to the detection of E6 and E7 HPV for cervical cancer), which is not targeted by the conventional HCMV assays that recognize well-known viral gene products (pUL123 (IE1), pUL122 (IE2), pUL83 (pp65)). On the contrary, positive results could result from the detection of HCMV in tumoral tissues like an “opportunistic infection” in already immunosuppressed cancerous patients and may have no direct link with tumor appearance and/or progression.

2.2. In Favor of Oncomodulation, HCMV Infection of Established Cancer Cells Favors Malignancy

As oncomodulation is defined as enhanced malignancy following viral infection, it is critical to show that HCMV infection of already transformed cells favors the development of oncogenesis and/or activates pathways implicated in transformation and/or oncogenesis (Figure 1). Thus, the HepG2 human liver cancer cell line with an epithelial morphology isolated from a patient with a hepatocellular carcinoma can be infected with HCMV. Secretion of IL-6 with autocrine/paracrine activation of the IL–6R–JAK–STAT3 pathway is observed in HCMV-infected HepG2 cells. Enhanced cell proliferation occurs in HCMV-infected HepG2 cells parallel to enhanced production of cyclin D1 and survivin. Enhanced production of tumorspheres is observed following HCMV infection of HepG2 cells compared with uninfected cultures. Altogether, HCMV infection of HepG2 liver cells enhances malignant properties of this established liver cancer cell line.

Neuroblastoma cell infected with HCMV are more prone to transendothelial penetration through downregulation of the Neural Cell Adhesion Molecule (NCAM) on tumor cells compared with uninfected cells. HCMV infection fuels the tumor formation in mice implanted with neurospheres compared with uninfected neurospheres. Interestingly, proliferation of patient-derived glioblastoma neurospheres was increased by HCMV. In addition, in patient-derived glioma stem-like cells (GSC) infected with HCMV the stemness properties were enhanced because of the expression of IE viral proteins. CMV infection of developing murine brain perturbates the mobility of virus-infected neuronal cells.

Following HCMV infection of the colorectal cancer (CRC) HT29 and SW480 ‘stem-like’ cells, both EMT and WNT pathways are activated resulting in enhanced cellular proliferation and mobility. In human CRC surgical specimen snail, EMT and CSC-like phenotype are linked to tumor spread. In addition, EMT and CSC-like phenotypes are observed in human CRC cells when twist is overexpressed resulting in increased invasion and tumorsphere formation abilities. We observed EMT features with enhanced snail and twist expression in CMV-transformed human mammary epithelial cells (CTH cells).

2.3. Against Oncomodulation, HCMV Infection of Established Cancer Cells Counteracts Malignancy

Besides a positive role for HCMV infection toward enhancement of malignancy, recent reports indicate that the virus can repress the transformation process in cancer cells (Figure 1). In the mesenchymal breast cancer lines MDA-MB-231 and SUM1315, HCMV induces a mesenchymal-to-epithelial transition (MET) with inhibition of their migratory capacity. In addition, in the HCMV infected MDA-MB-231 and SUM1315 cells, the viral replication is strongly inhibited. Similarly, we reported previously only limited tumor growth and even absence of tumor in mice xenografted with HCMV-infected HepG2 cells compared with unchecked tumor growth in mock-treated mice. Inhibition of tumor growth by HCMV resulted from restricted STAT3 activation and specific activation of the intrinsic apoptotic pathway. Recently, clearance of well-established tumors in a mouse melanoma model was obtained after injection of CMV into the growing tumor. Interestingly, the development of a liver lymphoma is controlled by distant murine CMV infection. Similarly, apoptosis is detected in lung tissues of xenografted mice injected subcutaneoulsy with HCMV-infected HepG2 cells. These results indicate that apoptosis induction occurs both at the site of HCMV infection and/or injection and in distant organs.

A reduced relapse rate occurs in patients who reactivate HCMV early after allogeneic stem cell transplantation as treatment for acute myeloid leukemia and non-Hodgkin lymphoma. The observed HCMV-induced immune modulating effects could result from increased activation of natural killer (NK) cells and CD8+ T cells, but also from HCMV-induced apoptosis of cancerous cells. Interestingly, HCMV genome is undetectable in tissues (tumor, liver and lung) of mice xenografted with HCMV-infected HepG2 cells several weeks post-infection, and a previous study reports undetectable CMV levels a few weeks post-infection in another murine model. Similar to the stalled HCMV replication cycle reported in infected MDA-MB-231 and SUM1315 cells, infection of HepG2 cells with HCMV results in restricted viral growth. Thus, HCMV cannot infect productively cancer cell lines in agreement with multiple restrictions to HCMV replication in cells expressing oncogenic alleles.

Altogether, the data presented above indicate that the oncomodulation paradigm cannot always apply to HCMV infection. Besides HCMV-induced oncomodulation, in several cases, the cytotoxic effect of HCMV on the tumor growth and/or expansion has been reported. Although oncomodulation by HCMV in tumor tissues has been extensively studied, the appearance of HCMV-transformed cells in culture which induce tumor formation in vivo could indicate that HCMV belongs to the group of human oncoviruses.

3.1. Human Oncoviruses

Among the 15–20% of human cancers caused by infections, several viruses have been named as human oncoviruses, including Epstein–Barr virus (EBV), hepatitis B virus (HBV), human T-lymphotropic virus-1 (HTLV-1), human papillomavirus (HPV), hepatitis C virus (HCV), Kaposi’s sarcoma associated herpesvirus (KSHV or HHV8), and Merkel cell polyomavirus. Among the seven human oncoviruses described so far, five are DNA oncoviruses and share some biological features. First, the tumor suppressor proteins p53 and Rb are typically inactivated by DNA oncoviruses. Second, by inactivating p53 function and Rb DNA oncoviruses overpass the G1/S check point and force the cell to enter into the S phase, which results in unregulated cell division and ultimately in tumor formation. Third, the viral integration, and to a lesser extent the viral episomes, characterize the cellular transformation by DNA oncoviruses. Although HCMV is a DNA virus, so far its role as a human oncovirus has not yet been demonstrated. We describe below several cellular and viral features that could define HCMV beyond oncomodulation close to the biological features of oncoviruses.

3.2. HCMV Expresses Viral Products with Potential Transforming Capacities

Transformation of NIH3T3 cells has been reported following stable expression of US28 gene and tumor growth occurred in mice injected with US28-expressing NIH3T3 cells. Activation of IL6–JAK–STAT3 axis by pUS28 could be one of the mechanisms involved in tumor development. Similarly, in primary human hepatocytes and HepG2 cells the IL-6/STAT3 axis is also activated upon HCMV infection and could favor sustained cellular transformation. Both pUS28 and phosphorylated STAT3 are detected in glioblastoma tumors (Table 1, Figure 2).

The entry into S phase is stimulated by the immediate early proteins pUL123 and pUL122. The proliferation of pUL123-expressing glioblastoma cells depends on p53 and Rb inhibition and PI3K/AKT activation. Both in CD133+ CSC from glioblastoma multiforme and in breast tumor tissue the pUL123 protein was detected (Table 1, Figure 2).

The viral cytokine cmvIL-10 is encoded by the UL111A gene, is secreted from infected cells and binds to the cellular IL-10 receptor like the natural IL-10 ligand. Activation of STAT3 results from the binding of cmvIL10 to the IL-10 receptor, and has been described in breast cancer, ovarian cancer with poor prognosis, and to increase the spread of glioma cancer stem cells in malignant glioma. In addition, exposure of MDA-MB-231 and MCF-7 cells to cmvIL-10 favors their proliferation, their migration and the metastatic spread due to cell surface expression of IL-10R (Table 1, Figure 2).

Chromosomal breaks are present in HCMV-infected primary human foreskin fibroblasts (HFF). In addition, chromosomal breaks are induced by UL76 gene stable expression in human glioblastoma cells. Parallel to chromosomal breaks, the DNA damage repair (DDR) is induced in cells infected with HCMV, as well as with other herpesviruses. In agreement with such a scenario, we observed the upregulation of the expression of the ataxia telangiectasia mutated (ATM) and human MutL homolog (MLH1) genes, both involved in DNA reparation, in human mammary epithelials cells (HMECs) infected with HCMV-DB. Recently, the detection of the HCMV long non-coding RNA4.9 (lncRNA4.9) in HCMV-transformed HMECs, namely CTH cells, could indicate that beyond a viral signature the lncRNA4.9 could directly participate to the transformation of epithelial cells infected with HCMV (Table 1, Figure 2).

3.3. HCMV Fullfills the Criteria of the Hallmarks of Cancer

Recently, the hallmarks of cancer have been updated by Hanahan and Weinberg to describe the essential alterations in cell physiology that lead to cancer especially following infection with human oncoviruses. HCMV infection fulfills the requirements of the hallmarks of cancer such as sustaining proliferative signals, evading growth suppressors, activating invasion and metastasis, enabling replicative immortality, inducing angiogenesis, resisting cell death, deregulating cellular energetics, avoiding immune destruction, genome instability and mutation, and tumor promoting inflammation. pUL123, pUL122, and pUL97 allow the evasion of tumor suppressors p53 and pRb. pUL122, pUL82, and pUL97 favor a sustained proliferative signal. The pUL123 protein favors immortality as measured by activation of telomerase. pUL123, pUL83, and pUL82 favor genome instability and mutation. The resistance to cell death results from the expression of pUL123, pUL122, vMIA (viral mitochondria-localized inhibitor of apoptosis also known as pUL37x1), and vICA (viral inhibitor of caspase-8 activation, pUL36). HCMV infection deregulates cellular energetics, changes glucose and glutamine utilization, and induces the Warburg effect. Several viral proteins including HCMV vIL-10 (pUL111A), pUS2, pUL16, pUL83, and pUL122 allow HCMV to avoid immune clearance. HCMV infection and especially pUS28 enhance tumor inflammation, for example, by induced production of IL-6, RANTES, MCP-1, and fraktaline. Angiogenesis is induced by pUL123 and pUS28. The pUS28 protein activates invasion and metastasis. Altogether, several HCMV proteins can potentially participate to cellular transformation in a context of genomic instability and favor the spread of the tumor.

3.4. HCMV Triggers Pro-Oncogenic Pathways in Infected Primary Cells

HCMV has been reported by several groups to trigger pro-oncogenic pathways in the infected cells. Although upregulation of p53 has been reported in fibroblasts, hepatocytes, and HMECs following HCMV infection, the pUL122 binding to p53 in HCMV-infected fibroblasts and HMECs decreased p53 binding to DNA with inhibition of p53 activity and increased cell cycle progression and unchecked cell division. Elevated levels of phosphoRb are observed in HCMV-infected fibroblasts and HMECs. HCMV pUL97 phosphorylates and inactivates proteins of the Rb family and favors cell cycle promotion. The pUL82 protein downregulates the Rb family proteins. In HCMV-infected HMECs, the decreased detection of the Rb protein is observed parallel to the enhanced presence of the UL82 transcript.

One of the main characteristics of transformed cells is the sustained cell growth without cellular senescence, which depends on enhanced telomerase activity. The enhancement of telomerase activity is observed in fibroblasts and HMECs infected with HCMV and leads to cell immortalization. Increased telomerase activity could be explained by STAT3 activation observed in HCMV-infected cells.

The up-regulation of c-Myc, Akt activation, STAT3 activation, and enhanced cyclin-D1 expression are reported in several cell types following HCMV infection. Previous reports indicate that HCMV upregulates c-Myc, c-Fos, and c-Jun in human embryo lung cells, as well as in macrophages and HMECs infected with HCMV. Besides the upregulation of gene expression of the oncogenes Myc (MYC), Fos (FOS), Jun (JUN), KRas (KRAS), HRas (HRAS), and NRas (NRAS), the upregulation of transcripts of numerous other oncogenes (KITLG, MCL1, MET, MYB, NFKBIA, PIK3CA, PML, PRKCA, RAF1, RARA, ROS1, RET, ABL1, ETS1, RUNX1, RUNX3) occurs in HCMV-infected HMECs compared with uninfected cells. In hepatocytes and HMECs infected with HCMV, the IL6/JAK/cyclin D1 pathway is activated with enhanced cell proliferation and upregulated transcripts of proliferation marker genes such as the Ki67 antigen gene (MKI67) and the topoisomerase 2 gene (TOPO2A).

The Akt pathway is activated in HMECs infected with HCMV and NF–kB activation is observed in HCMV-infected macrophages. In agreement with these findings, the expression of pro-survival genes (NFKB1, REL, AKT1, PIK3C2A, BCL-2) is increased in HCMV-DB infected HMECs compared with mock-infected cells, indicating a prosurvival signal in infected cells. In hepatocytes infected with HCMV, the expression of survivin is upregulated.

3.5. HCMV Transforms Epithelial Cells In Vitro and Leads to Tumorigenicity In Vivo

The most efficient assay to determine the malignancy of cells in vitro is the soft agar assay, a well-established method to measure anchorage-independent growth, the ability of transformed cells to growth independently of a solid surface, a hallmark of carcinogenesis. Although several groups reported the activation of pro-oncogenic pathways in cells infected with HCMV, only limited reports describe the appearance of colonies in soft agar seeded with HCMV-infected cells. The appearance of colonies in soft agar seeded with primary human hepatocytes infected with HCMV has been reported. In addition, our group observed following the infection of HMECs with the HCMV-DB strain the appearance of colonies in soft agar. Interestingly, following treatment of infected cells with UV and ganciclovir, no colonies were observed, indicating that the soft agar colony formation requires efficient viral replication, even during a limited period of time.

Although the appearance of colonies in soft agar seeded with HCMV-infected cells indicates cellular transformation, the tumor growth in xenografted mice following injection of HCMV-infected cells is required to directly assess the tumorigenic potential of HCMV. Recently, the injection of CMV-transformed HMECs (CTH cells), which were obtained after prolonged culture of HMECs infected with a clinical strain HCMV-DB in vitro, resulted in the development of tumors following their injection in NOD/SCID Gamma (NSG) mice. The tumor growth following injection of CTH cells in NSG mice was fast. In tumor biopies, a limited part of viral DNA was detected, namely the lncRNA.9 gene. The HCMV lncRNA4.9 gene is also detected in biopsies of patients with breast cancer. Thus, the HCMV-DB-infected HMEC model points toward a direct role for HMCV in oncogenesis, from viral proteins activating oncogenic pathways in infected cells to tumor growth in NSG mice xenografted with CTH cells (Figure 3).

3.6. HCMV Modifies the Tumorous Environment to Favor Tumor Formation

Besides a direct pro-oncogenic role of HCMV in tumor formation, the tumorous environment can be modulated by HCMV. Thus, tumor-associated macrophages (TAM), macrophages present within the tumorous environment, are present in several cancers where HCMV has been detected including breast cancer, prostate cancer, colon cancer, and glioblastoma. The TAM display a M2 phenotype and produce mostly cytokines such as IL-10 and TGF-beta, which favor immune evasion and, to a lesser extent, pro-inflammatory cytokines (reviewed in the work of). TAM with a M2 phenotype favors the establishment of a Th2 response, which promotes angiogenesis, tissue remodeling, and repair. High TAM density is a hallmark of poor prognosis in breast cancer, colorectal cancer, and glioblastoma. Within glioblastoma multiform, macrophages/microglia and glioma cancer stem cells can be infected with HCMV. Interestingly, only a limited copy number of the HCMV genome is detected in glioblastoma multiforme biopsies, indicating that non-viral biological effects may account for glioblastoma multiforme growth. HCMV vIL-10 is secreted by infected glioma cancer stem cells and favors the appearance of the M2 TAM phenotype. In addition, angiogenic factors such as VEGF, immunosuppressive cytokines such as TGF-beta, and enhanced migration of glioma cancer stem cells occur as a consequence of exposure of monocytes/macrophages to HCMV vIL10. Similarly, IL-10 and TGF-beta favor tumor migration and invasion in breast cancer and lung adenocarcinoma.

Among cell types present in breast tissue, HCMV can infect HMECs, macrophages, and fibroblasts. We observed that the clinical isolate HCMV-DB displays tropism for both macrophage and HMECs. In macrophage, HCMV-DB triggers an M2 activation state with enhanced upregulation of the proto-oncogene Bcl-3 parallel to limited viral growth. Similarly, in HCMV-DB-infected HMECs, the viral replication is contained. Thus, in HMECs and nearby tissue macrophages, a restricted viral replication could account for a specific tumor microenvironment, which might shape the viral fitness. Further, the tumoral microenvironment could be modulated by HCMV-infected HMECs with both up- and downregulation of genes involved in angiogenesis (upregulation: IL-6, SERPINE1, THBS1, S100A4, EGF; downregulation: ID1, SLIT2) and proteolysis (upregulation: MMP9; downregulation: CST6, CTSD). In addition, the presence of tumor cancer stem cells (CSCs) has been reported to favor the propagation and invasiveness of the tumor. The infection of HMECs with HCMV-DB triggers the appearance of mammospheres in culture and indicates that some HCMV strains could indeed induce CSCs expansion in breast tissue in vivo. In agreement with sustained STAT3 activation observed in breast cancer, unchecked cell division, resistance to cell apoptosis, as well as tumor growth in mice result from IL-6/STAT3 activation in mammary CSCs. Although some reports indicate that HCMV infection and/or viral proteins modulate STAT3 intracellular localization, IL-6 signaling, and NF-kB activation, altogether, HCMV participates to shape the tumorous environment and thereby could favor the development and spread of the tumor.

4. Conclusions

Although the paradigm of oncomodulation can be applied to some of the tumors infected with HCMV, oncomodulation cannot account for all the biological observations made in HCMV-infected tumors. The pro-oncogenic potential of HCMV proteins per se, the activation of pro-oncogenic pathways in HCMV-infected cells, the transformation of HCMV-infected cells in vitro, the sustained growth of CTH cells with a HCMV signature, the tumorigenicity of CTH cells injected in NSG mice, and the fulfillment of the requirement of the hallmarks of cancer all point toward the inclusion of HCMV in the list of human oncoviruses.

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    Not in our library

  30. 30.

    Baryawno N., Rahbar A., Wolmer-Solberg N., Taher C., Odeberg J., Darabi A., Khan Z., Sveinbjörnsson B., FuskevÅg O.-M., Segerström L., et al. Detection of human cytomegalovirus in medulloblastomas reveals a potential therapeutic target. J. Clin. Investig. 2011;121:4043-4055.

    Not in our library10.1172/jci57147

  31. 31.

    Dziurzynski K., Chang S.M., Heimberger A.B., Kalejta R.F., McGregor Dallas S.R., Smit M., Soroceanu L., Cobbs C.S. HCMV and gliomas symposium consensus on the role of human cytomegalovirus in glioblastoma. Neuro Oncol. 2012;14:246-255.

    Not in our library10.1093/neuonc/nor227

  32. 32.

    Johnsen J.I., Baryawno N., Söderberg-Nauclér C. Is human cytomegalovirus a target in cancer therapy? Oncotarget. 2011;2:1329-1338.

    Not in our library10.18632/oncotarget.383

  33. 33.

    Soroceanu L., Cobbs C.S. Is HCMV a tumor promoter? Virus Res. 2011;157:193-203.

    Not in our library10.1016/j.virusres.2010.10.026

  34. 34.

    Wolmer-Solberg N., Baryawno N., Rahbar A., Fuchs D., Odeberg J., Taher C., Wilhelmi V., Milosevic J., Mohammad A.-A., Martinsson T., et al. Frequent detection of human cytomegalovirus in neuroblastoma: A novel therapeutic target? Int. J. Cancer. 2013;133:2351-2361.

    Not in our library10.1002/ijc.28265

  35. 35.

    Melnick M., Sedghizadeh P.P., Allen C.M., Jaskoll T. Human cytomegalovirus and mucoepidermoid carcinoma of salivary glands: Cell-specific localization of active viral and oncogenic signaling proteins is confirmatory of a causal relationship. Exp. Mol. Pathol. 2012;92:118-125.

    Not in our library10.1016/j.yexmp.2011.10.011

  36. 36.

    Knösel T., Schewe C., Dietel M., Petersen I. Cytomegalovirus is not associated with progression and metastasis of colorectal cancer. Cancer Lett. 2004;211:243-247.

    Not in our library10.1016/j.canlet.2004.02.011

  37. 37.

    Cosset É., Petty T.J., Dutoit V., Cordey S., Padioleau I., Otten-Hernandez P., Farinelli L., Kaiser L., Bruyère-Cerdan P., Tirefort D., et al. Comprehensive metagenomic analysis of glioblastoma reveals absence of known virus despite antiviral-like type I interferon gene response. Int. J. Cancer. 2014;135:1381-1389.

    Not in our library10.1002/ijc.28670

  38. 38.

    Lau S.K., Chen Y.-Y., Chen W.-G., Diamond D.J., Mamelak A.N., Zaia J.A., Weiss L.M. Lack of association of cytomegalovirus with human brain tumors. Mod. Pathol. 2005;18:838-843.

    Not in our library10.1038/modpathol.3800352

  39. 39.

    Sabatier J., Uro-Coste E., Pommepuy I., Labrousse F., Allart S., Trémoulet M., Delisle M.B., Brousset P. Detection of human cytomegalovirus genome and gene products in central nervous system tumours. Br. J. Cancer. 2005;92:747-750.

    Not in our library10.1038/sj.bjc.6602339

  40. 40.

    Sehic D., Forslund O., Sandén E., Mengelbier L.H., Karlsson J., Bzhalava D., Ekström J., Warenholt J., Darabi A., Dillner J., et al. Absence of Epstein-Barr and cytomegalovirus infection in neuroblastoma cells by standard detection methodologies. Pediatr. Blood Cancer. 2013;60:E91-E93.

    Not in our library10.1002/pbc.24535

  41. 41.

    Tang K.-W., Alaei-Mahabadi B., Samuelsson T., Lindh M., Larsson E. The landscape of viral expression and host gene fusion and adaptation in human cancer. Nat. Commun. 2013;4.

    Not in our library10.1038/ncomms3513

  42. 42.

    Yamashita Y., Ito Y., Isomura H., Takemura N., Okamoto A., Motomura K., Tsujiuchi T., Natsume A., Wakabayashi T., Toyokuni S., et al. Lack of presence of the human cytomegalovirus in human glioblastoma. Mod. Pathol. 2014;27:922-929.

    Not in our library10.1038/modpathol.2013.219

  43. 43.

    Baumgarten P., Michaelis M., Rothweiler F., Starzetz T., Rabenau H.F., Berger A., Jennewein L., Braczynski A.K., Franz K., Seifert V., et al. Human cytomegalovirus infection in tumor cells of the nervous system is not detectable with standardized pathologico-virological diagnostics. Neuro Oncol. 2014;16:1469-1477.

    Not in our library10.1093/neuonc/nou167

  44. 44.

    Scholz M., Blaheta R.A., Wittig B., Cinatl J., Vogel J.U., Doerr H.W., Cinatl J. Cytomegalovirus-infected neuroblastoma cells exhibit augmented invasiveness mediated by beta1alpha5 integrin (VLA-5). Tissue Antigens. 2000;55:412-421.

    Not in our library10.1034/j.1399-0039.2000.550503.x

  45. 45.

    Blaheta R.A., Beecken W.-D., Engl T., Jonas D., Oppermann E., Hundemer M., Doerr H.W., Scholz M., Cinatl J. Human cytomegalovirus infection of tumor cells downregulates NCAM (CD56): A novel mechanism for virus-induced tumor invasiveness. Neoplasia. 2004;6:323-331.

    Not in our library10.1593/neo.03418

  46. 46.

    Price R.L., Song J., Bingmer K., Kim T.H., Yi J.-Y., Nowicki M.O., Mo X., Hollon T., Murnan E., Alvarez-Breckenridge C., et al. Cytomegalovirus contributes to glioblastoma in the context of tumor suppressor mutations. Cancer Res. 2013;73:3441-3450.

    Not in our library10.1158/0008-5472.can-12-3846

  47. 47.

    Soroceanu L., Matlaf L., Khan S., Akhavan A., Singer E., Bezrookove V., Decker S., Ghanny S., Hadaczek P., Bengtsson H., et al. Cytomegalovirus immediate-early proteins promote stemness properties in glioblastoma. Cancer Res. 2015;75:3065-3076.

    Not in our library10.1158/0008-5472.can-14-3307

  48. 48.

    Shinmura Y., Kosugi I., Kaneta M., Tsutsui Y. Migration of virus-infected neuronal cells in cerebral slice cultures of developing mouse brains after in vitro infection with murine cytomegalovirus. Acta Neuropathol. 1999;98:590-596.

    Not in our library10.1007/s004010051123

  49. 49.

    Shinmura Y., Kosugi I., Aiba-Masago S., Baba S., Yong L.R., Tsutsui Y. Disordered migration and loss of virus-infected neuronal cells in developing mouse brains infected with murine cytomegalovirus. Acta Neuropathol. 1997;93:551-557.

    Not in our library10.1007/s004010050651

  50. 50.

    Teo W.H., Chen H.-P., Huang J.C., Chan Y.-J. Human cytomegalovirus infection enhances cell proliferation, migration and upregulation of EMT markers in colorectal cancer-derived stem cell-like cells. Int. J. Oncol. 2017;51:1415-1426.

    Not in our library10.3892/ijo.2017.4135

  51. 51.
    Overexpression of Snail induces epithelial–mesenchymal transition and a cancer stem cell–like phenotype in human colorectal cancer cells · 2012
    No notice
  52. 52.

    Deng J.-J., Zhang W., Xu X.-M., Zhang F., Tao W.-P., Ye J.-J., Ge W. Twist mediates an aggressive phenotype in human colorectal cancer cells. Int. J. Oncol. 2016;48:1117-1124.

    Not in our library10.3892/ijo.2016.3342

  53. 53.

    Oberstein A., Shenk T. Cellular responses to human cytomegalovirus infection: Induction of a mesenchymal-to-epithelial transition (MET) phenotype. PNAS. 2017;114:E8244-E8253.

    Not in our library10.1073/pnas.1710799114

  54. 54.

    Kumar A., Coquard L., Pasquereau S., Russo L., Valmary-Degano S., Borg C., Pothier P., Herbein G. Tumor control by human cytomegalovirus in a murine model of hepatocellular carcinoma. Mol. Ther. Oncolytics. 2016;3.

    Not in our library10.1038/mto.2016.12

  55. 55.

    Jurak I., Brune W. Induction of apoptosis limits cytomegalovirus cross-species infection. EMBO J. 2006;25:2634-2642.

    Not in our library10.1038/sj.emboj.7601133

  56. 56.

    Erkes D.A., Wilski N.A., Snyder C.M. Intratumoral infection by CMV may change the tumor environment by directly interacting with tumor-associated macrophages to promote cancer immunity. Hum. Vaccin. Immunother. 2017;13:1778-1785.

    Not in our library10.1080/21645515.2017.1331795

  57. 57.

    Erlach K.C., Böhm V., Seckert C.K., Reddehase M.J., Podlech J. Lymphoma cell apoptosis in the liver induced by distant murine cytomegalovirus infection. J. Virol. 2006;80:4801-4819.

    Not in our library10.1128/jvi.80.10.4801-4819.2006

  58. 58.

    Elmaagacli A.H., Steckel N.K., Koldehoff M., Hegerfeldt Y., Trenschel R., Ditschkowski M., Christoph S., Gromke T., Kordelas L., Ottinger H.D., et al. Early human cytomegalovirus replication after transplantation is associated with a decreased relapse risk: Evidence for a putative virus-versus-leukemia effect in acute myeloid leukemia patients. Blood. 2011;118:1402-1412.

    Not in our library10.1182/blood-2010-08-304121

  59. 59.

    Green M.L., Leisenring W.M., Xie H., Walter R.B., Mielcarek M., Sandmaier B.M., Riddell S.R., Boeckh M. CMV reactivation after allogeneic HCT and relapse risk: evidence for early protection in acute myeloid leukemia. Blood. 2013;122:1316-1324.

    Not in our library10.1182/blood-2013-02-487074

  60. 60.

    Koldehoff M., Ross S.R., Dührsen U., Beelen D.W., Elmaagacli A.H. Early CMV-replication after allogeneic stem cell transplantation is associated with a reduced relapse risk in lymphoma. Leuk. Lymphoma. 2017;58:822-833.

    Not in our library10.1080/10428194.2016.1217524

  61. 61.

    Koldehoff M., Lindemann M., Opalka B., Bauer S., Ross R.S., Elmaagacli A.H. Cytomegalovirus induces apoptosis in acute leukemia cells as a virus-versus-leukemia function. Leuk. Lymphoma. 2015;56:3189-3197.

    Not in our library10.3109/10428194.2015.1032968

  62. 62.

    Bidanset D.J., Rybak R.J., Hartline C.B., Kern E.R. Replication of human cytomegalovirus in severe combined immunodeficient mice implanted with human retinal tissue. J. Infect. Dis. 2001;184:192-195.

    Not in our library10.1086/322015

  63. 63.

    Xu S., Schafer X., Munger J. Expression of oncogenic alleles induces multiple blocks to human cytomegalovirus infection. J. Virol. 2016;90:4346-4356.

    Not in our library10.1128/jvi.00179-16

  64. 64.

    Cao J., Li D. Searching for human oncoviruses: Histories, challenges, and opportunities. J. Cell. Biochem. 2018;119:4897-4906.

    Not in our library10.1002/jcb.26717

  65. 65.

    Mesri E.A., Feitelson M.A., Munger K. Human viral oncogenesis: A cancer hallmarks analysis. Cell Host Microbe. 2014;15:266-282.

    Not in our library10.1016/j.chom.2014.02.011

  66. 66.

    Maussang D., Verzijl D., van Walsum M., Leurs R., Holl J., Pleskoff O., Michel D., van Dongen G.A.M.S., Smit M.J. Human cytomegalovirus-encoded chemokine receptor US28 promotes tumorigenesis. Proc. Natl. Acad. Sci. USA. 2006;103:13068-13073.

    Not in our library10.1073/pnas.0604433103

  67. 67.

    Slinger E., Maussang D., Schreiber A., Siderius M., Rahbar A., Fraile-Ramos A., Lira S.A., Söderberg-Nauclér C., Smit M.J. HCMV-encoded chemokine receptor US28 mediates proliferative signaling through the IL-6-STAT3 axis. Sci. Signal. 2010;3.

    Not in our library10.1126/scisignal.2001180

  68. 68.

    Soroceanu L., Matlaf L., Bezrookove V., Harkins L., Martinez R., Greene M., Soteropoulos P., Cobbs C.S. Human cytomegalovirus US28 found in glioblastoma promotes an invasive and angiogenic phenotype. Cancer Res. 2011;71:6643-6653.

    Not in our library10.1158/0008-5472.can-11-0744

  69. 69.

    Castillo J.P., Yurochko A.D., Kowalik T.F. Role of human cytomegalovirus immediate-early proteins in cell growth control. J. Virol. 2000;74:8028-8037.

    Not in our library10.1128/jvi.74.17.8028-8037.2000

  70. 70.

    Castillo J.P., Kowalik T.F. Human cytomegalovirus immediate early proteins and cell growth control. Gene. 2002;290:19-34.

    Not in our library10.1016/s0378-1119(02)00566-8

  71. 71.

    Cobbs C.S., Soroceanu L., Denham S., Zhang W., Kraus M.H. Modulation of oncogenic phenotype in human glioma cells by cytomegalovirus IE1-mediated mitogenicity. Cancer Res. 2008;68:724-730.

    Not in our library10.1158/0008-5472.can-07-2291

  72. 72.
    High Prevalence of Human Cytomegalovirus Proteins and Nucleic Acids in Primary Breast Cancer and Metastatic Sentinel Lymph Nodes · 2013
    No notice
  73. 73.

    Jones B.C., Logsdon N.J., Josephson K., Cook J., Barry P.A., Walter M.R. Crystal structure of human cytomegalovirus IL-10 bound to soluble human IL-10R1. Proc. Natl. Acad. Sci. USA. 2002;99:9404-9409.

    Not in our library10.1073/pnas.152147499

  74. 74.

    Gruber S.G., Gloria Luciani M., Grundtner P., Zdanov A., Gasche C. Differential signaling of cmvIL-10 through common variants of the IL-10 receptor 1. Eur. J. Immunol. 2008;38:3365-3375.

    Not in our library10.1002/eji.200837718

  75. 75.

    Raftery M.J., Wieland D., Gronewald S., Kraus A.A., Giese T., Schönrich G. Shaping phenotype, function, and survival of dendritic cells by cytomegalovirus-encoded IL-10. J. Immunol. 2004;173:3383-3391.

    Not in our library10.4049/jimmunol.173.5.3383

  76. 76.

    Spencer J.V. The cytomegalovirus homolog of interleukin-10 requires phosphatidylinositol 3-kinase activity for inhibition of cytokine synthesis in monocytes. J. Virol. 2007;81:2083-2086.

    Not in our library10.1128/jvi.01655-06

  77. 77.

    Lin Y.-L., Chang P.-C., Wang Y., Li M. Identification of novel viral interleukin-10 isoforms of human cytomegalovirus AD169. Virus Res. 2008;131:213-223.

    Not in our library10.1016/j.virusres.2007.09.011

  78. 78.

    Banerjee K., Resat H. Constitutive activation of STAT3 in breast cancer cells: A review. Int. J. Cancer. 2016;138:2570-2578.

    Not in our library10.1002/ijc.29923

  79. 79.

    Dziurzynski K., Wei J., Qiao W., Hatiboglu M.A., Kong L.-Y., Wu A., Wang Y., Cahill D., Levine N., Prabhu S., et al. Glioma-associated cytomegalovirus mediates subversion of the monocyte lineage to a tumor propagating phenotype. Clin. Cancer Res. 2011;17:4642-4649.

    Not in our library10.1158/1078-0432.ccr-11-0414

  80. 80.

    Zhang X., Liu P., Zhang B., Wang A., Yang M. Role of STAT3 decoy oligodeoxynucleotides on cell invasion and chemosensitivity in human epithelial ovarian cancer cells. Cancer Genet. Cytogenet. 2010;197:46-53.

    Not in our library10.1016/j.cancergencyto.2009.10.004

  81. 81.

    Valle Oseguera C.A., Spencer J.V. Cmvil-10 stimulates the invasive potential of MDA-MB-231 breast cancer cells. PLoS ONE. 2014;9.

    Not in our library10.1371/journal.pone.0088708

  82. 82.

    Bishop R.K., Valle Oseguera C.A., Spencer J.V. Human cytomegalovirus interleukin-10 promotes proliferation and migration of MCF-7 breast cancer cells. Cancer Cell Microenviron. 2015;2.

    Not in our library10.14800/ccm.678

  83. 83.

    Valle Oseguera C.A., Spencer J.V. Human cytomegalovirus interleukin-10 enhances matrigel invasion of MDA-MB-231 breast cancer cells. Cancer Cell Int. 2017;17.

    Not in our library10.1186/s12935-017-0399-5

  84. 84.
    Specific chromosome 1 breaks induced by human cytomegalovirus · 2000
    Not checked
  85. 85.

    Siew V.-K., Duh C.-Y., Wang S.-K. Human cytomegalovirus UL76 induces chromosome aberrations. J. Biomed. Sci. 2009;16.

    Not in our library10.1186/1423-0127-16-107

  86. 86.

    Li R., Zhu J., Xie Z., Liao G., Liu J., Chen M.-R., Hu S., Woodard C., Lin J., Taverna S.D., et al. Conserved herpesvirus kinases target the DNA damage response pathway and TIP60 histone acetyltransferase to promote virus replication. Cell Host Microbe. 2011;10:390-400.

    Not in our library10.1016/j.chom.2011.08.013

  87. 87.

    Al Moussawi F., Kumar A., Pasquereau S., Tripathy M.K., Karam W., Diab Assaf M., Herbein G. The transcriptome of human mammary epithelial cells infected with the HCMV-DB strain displays an oncogenic profile. Sci. Rep. 2018.

    Not in our library10.1038/s41598-018-30109-1

  88. 88.

    Hanahan D., Weinberg R.A. Hallmarks of cancer: the next generation. Cell. 2011;144:646-674.

    Not in our library10.1016/j.cell.2011.02.013

  89. 89.

    Chen Z., Knutson E., Kurosky A., Albrecht T. Degradation of p21cip1 in cells productively infected with human cytomegalovirus. J. Virol. 2001;75:3613-3625.

    Not in our library10.1128/jvi.75.8.3613-3625.2001

  90. 90.

    Song Y.-J., Stinski M.F. Effect of the human cytomegalovirus IE86 protein on expression of E2F-responsive genes: A DNA microarray analysis. Proc. Natl. Acad. Sci. USA. 2002;99:2836-2841.

    Not in our library10.1073/pnas.052010099

  91. 91.

    Kalejta R.F., Shenk T. Proteasome-dependent, ubiquitin-independent degradation of the Rb family of tumor suppressors by the human cytomegalovirus pp71 protein. Proc. Natl. Acad. Sci. USA. 2003;100:3263-3268.

    Not in our library10.1073/pnas.0538058100

  92. 92.

    Hume A.J., Finkel J.S., Kamil J.P., Coen D.M., Culbertson M.R., Kalejta R.F. Phosphorylation of retinoblastoma protein by viral protein with cyclin-dependent kinase function. Science. 2008;320:797-799.

    Not in our library10.1126/science.1152095

  93. 93.

    Murphy E.A., Streblow D.N., Nelson J.A., Stinski M.F. The human cytomegalovirus IE86 protein can block cell cycle progression after inducing transition into the S phase of permissive cells. J. Virol. 2000;74:7108-7118.

    Not in our library10.1128/jvi.74.15.7108-7118.2000

  94. 94.

    Strååt K., Liu C., Rahbar A., Zhu Q., Liu L., Wolmer-Solberg N., Lou F., Liu Z., Shen J., Jia J., et al. Activation of telomerase by human cytomegalovirus. J. Natl. Cancer Inst. 2009;101:488-497.

    Not in our library10.1093/jnci/djp031

  95. 95.

    Gaspar M., Shenk T. Human cytomegalovirus inhibits a DNA damage response by mislocalizing checkpoint proteins. Proc. Natl. Acad. Sci. USA. 2006;103:2821-2826.

    Not in our library10.1073/pnas.0511148103

  96. 96.

    Castillo J.P., Frame F.M., Rogoff H.A., Pickering M.T., Yurochko A.D., Kowalik T.F. Human cytomegalovirus IE1-72 activates ataxia telangiectasia mutated kinase and a p53/p21-mediated growth arrest response. J. Virol. 2005;79:11467-11475.

    Not in our library10.1128/jvi.79.17.11467-11475.2005

  97. 97.

    Luo M.H., Rosenke K., Czornak K., Fortunato E.A. Human cytomegalovirus disrupts both ataxia telangiectasia mutated protein (ATM)- and ATM-Rad3-related kinase-mediated DNA damage responses during lytic infection. J. Virol. 2007;81:1934-1950.

    Not in our library10.1128/jvi.01670-06

  98. 98.

    Xiaofei E., Pickering M.T., Debatis M., Castillo J., Lagadinos A., Wang S., Lu S., Kowalik T.F. An E2F1-mediated DNA damage response contributes to the replication of human cytomegalovirus. PLoS Pathog. 2011;7.

    Not in our library10.1371/journal.ppat.1001342

  99. 99.

    Yu Y., Alwine J.C. Human cytomegalovirus major immediate-early proteins and simian virus 40 large T antigen can inhibit apoptosis through activation of the phosphatidylinositide 3′-OH kinase pathway and the cellular kinase Akt. J. Virol. 2002;76:3731-3738.

    Not in our library10.1128/jvi.76.8.3731-3738.2002

  100. 100.

    McCormick A.L., Roback L., Livingston-Rosanoff D., St Clair C. The human cytomegalovirus UL36 gene controls caspase-dependent and -independent cell death programs activated by infection of monocytes differentiating to macrophages. J. Virol. 2010;84:5108-5123.

    Not in our library10.1128/jvi.01345-09

  101. 101.

    Goldmacher V.S. vMIA, a viral inhibitor of apoptosis targeting mitochondria. Biochimie. 2002;84:177-185.

    Not in our library10.1016/s0300-9084(02)01367-6

  102. 102.

    Yu Y., Clippinger A.J., Alwine J.C. Viral effects on metabolism: changes in glucose and glutamine utilization during human cytomegalovirus infection. Trends Microbiol. 2011;19:360-367.

    Not in our library10.1016/j.tim.2011.04.002

  103. 103.

    Spencer J.V., Lockridge K.M., Barry P.A., Lin G., Tsang M., Penfold M.E.T., Schall T.J. Potent immunosuppressive activities of cytomegalovirus-encoded interleukin-10. J. Virol. 2002;76:1285-1292.

    Not in our library10.1128/jvi.76.3.1285-1292.2002

  104. 104.

    Yoo Y.D., Chiou C.J., Choi K.S., Yi Y., Michelson S., Kim S., Hayward G.S., Kim S.J. The IE2 regulatory protein of human cytomegalovirus induces expression of the human transforming growth factor beta1 gene through an Egr-1 binding site. J. Virol. 1996;70:7062-7070.

    Not in our library10.1128/jvi.70.10.7062-7070.1996

  105. 105.

    Kotenko S.V., Saccani S., Izotova L.S., Mirochnitchenko O.V., Pestka S. Human cytomegalovirus harbors its own unique IL-10 homolog (cmvIL-10). Proc. Natl. Acad. Sci. USA. 2000;97:1695-1700.

    Not in our library10.1073/pnas.97.4.1695

  106. 106.

    Rölle A., Mousavi-Jazi M., Eriksson M., Odeberg J., Söderberg-Nauclér C., Cosman D., Kärre K., Cerboni C. Effects of human cytomegalovirus infection on ligands for the activating NKG2D receptor of NK cells: Up-regulation of UL16-binding protein (ULBP)1 and ULBP2 is counteracted by the viral UL16 protein. J. Immunol. 2003;171:902-908.

    Not in our library10.4049/jimmunol.171.2.902

  107. 107.

    Lepiller Q., Aziz Khan K., Di Martino V., Herbein G. Cytomegalovirus and tumors: Two players for one goal-immune escape. Open Virol. J. 2011;5:60-69.

    Not in our library10.2174/1874357901105010060

  108. 108.

    Arnon T.I., Achdout H., Levi O., Markel G., Saleh N., Katz G., Gazit R., Gonen-Gross T., Hanna J., Nahari E., et al. Inhibition of the NKp30 activating receptor by pp65 of human cytomegalovirus. Nat. Immunol. 2005;6:515-523.

    Not in our library10.1038/ni1190

  109. 109.

    Rölle A., Brodin P. Immune adaptation to environmental influence: The case of NK cells and HCMV. Trends Immunol. 2016;37:233-243.

    Not in our library10.1016/j.it.2016.01.005

  110. 110.

    Casarosa P., Bakker R.A., Verzijl D., Navis M., Timmerman H., Leurs R., Smit M.J. Constitutive signaling of the human cytomegalovirus-encoded chemokine receptor US28. J. Biol. Chem. 2001;276:1133-1137.

    Not in our library10.1074/jbc.m008965200

  111. 111.

    Murayama T., Mukaida N., Sadanari H., Yamaguchi N., Khabar K.S., Tanaka J., Matsushima K., Mori S., Eizuru Y. The immediate early gene 1 product of human cytomegalovirus is sufficient for up-regulation of interleukin-8 gene expression. Biochem. Biophys. Res. Commun. 2000;279:298-304.

    Not in our library10.1006/bbrc.2000.3923

  112. 112.

    Maussang D., Langemeijer E., Fitzsimons C.P., Stigter-van Walsum M., Dijkman R., Borg M.K., Slinger E., Schreiber A., Michel D., Tensen C.P., et al. The human cytomegalovirus-encoded chemokine receptor US28 promotes angiogenesis and tumor formation via cyclooxygenase-2. Cancer Res. 2009;69:2861-2869.

    Not in our library10.1158/0008-5472.can-08-2487

  113. 113.

    Melnychuk R.M., Streblow D.N., Smith P.P., Hirsch A.J., Pancheva D., Nelson J.A. Human cytomegalovirus-encoded G protein-coupled receptor US28 mediates smooth muscle cell migration through Galpha12. J. Virol. 2004;78:8382-8391.

    Not in our library10.1128/jvi.78.15.8382-8391.2004

  114. 114.

    Vomaske J., Varnum S., Melnychuk R., Smith P., Pasa-Tolic L., Shutthanandan J.I., Streblow D.N. HCMV pUS28 initiates pro-migratory signaling via activation of Pyk2 kinase. Herpesviridae. 2010;1.

    Not in our library10.1186/2042-4280-1-2

  115. 115.

    Muganda P., Mendoza O., Hernandez J., Qian Q. Human cytomegalovirus elevates levels of the cellular protein p53 in infected fibroblasts. J. Virol. 1994;68:8028-8034.

    Not in our library10.1128/jvi.68.12.8028-8034.1994

  116. 116.

    Hannemann H., Rosenke K., O’Dowd J.M., Fortunato E.A. The presence of p53 influences the expression of multiple human cytomegalovirus genes at early times postinfection. J. Virol. 2009;83:4316-4325.

    Not in our library10.1128/jvi.02075-08

  117. 117.

    Hsu C.-H., Chang M.D.T., Tai K.-Y., Yang Y.-T., Wang P.-S., Chen C.-J., Wang Y.-H., Lee S.-C., Wu C.-W., Juan L.-J. HCMV IE2-mediated inhibition of HAT activity downregulates p53 function. EMBO J. 2004;23:2269-2280.

    Not in our library10.1038/sj.emboj.7600239

  118. 118.

    Iwahori S., Umaña A.C., VanDeusen H.R., Kalejta R.F. Human cytomegalovirus-encoded viral cyclin-dependent kinase (v-CDK) UL97 phosphorylates and inactivates the retinoblastoma protein-related p107 and p130 proteins. J. Biol. Chem. 2017;292:6583-6599.

    Not in our library10.1074/jbc.m116.773150

  119. 119.

    Hahn W.C., Meyerson M. Telomerase activation, cellular immortalization and cancer. Ann. Med. 2001;33:123-129.

    Not in our library10.3109/07853890109002067

  120. 120.

    Chung S.S., Aroh C., Vadgama J.V. Constitutive activation of STAT3 signaling regulates hTERT and promotes stem cell-like traits in human breast cancer cells. PLoS ONE. 2013;8:e83971.

    Not in our library10.1371/journal.pone.0083971

  121. 121.

    Boldogh I., AbuBakar S., Albrecht T. Activation of proto-oncogenes: An immediate early event in human cytomegalovirus infection. Science. 1990;247:561-564.

    Not in our library10.1126/science.1689075

  122. 122.

    Boldogh I., AbuBakar S., Deng C.Z., Albrecht T. Transcriptional activation of cellular oncogenes fos, jun, and myc by human cytomegalovirus. J. Virol. 1991;65:1568-1571.

    Not in our library10.1128/jvi.65.3.1568-1571.1991

  123. 123.

    Hagemeier C., Walker S.M., Sissons P.J., Sinclair J.H. The 72K IE1 and 80K IE2 proteins of human cytomegalovirus independently trans-activate the c-fos, c-myc and HSP 70 promoters via basal promoter elements. J. Gen. Virol. 1992;73:2385-2393.

    Not in our library10.1099/0022-1317-73-9-2385

  124. 124.

    Gilmore T.D., Cormier C., Jean-Jacques J., Gapuzan M.E. Malignant transformation of primary chicken spleen cells by human transcription factor c-Rel. Oncogene. 2001;20:7098-7103.

    Not in our library10.1038/sj.onc.1204898

  125. 125.

    Banerjee S., Wei Z., Tan F., Peck K.N., Shih N., Feldman M., Rebbeck T.R., Alwine J.C., Robertson E.S. Distinct microbiological signatures associated with triple negative breast cancer. Sci. Rep. 2015;5.

    Not in our library10.1038/srep15162

  126. 126.

    Mantovani A., Marchesi F., Malesci A., Laghi L., Allavena P. Tumour-associated macrophages as treatment targets in oncology. Nat. Rev. Clin. Oncol. 2017;14:399-416.

    Not in our library10.1038/nrclinonc.2016.217

  127. 127.

    Tang X. Tumor-associated macrophages as potential diagnostic and prognostic biomarkers in breast cancer. Cancer Lett. 2013;332:3-10.

    Not in our library10.1016/j.canlet.2013.01.024

  128. 128.

    Bacman D., Merkel S., Croner R., Papadopoulos T., Brueckl W., Dimmler A. TGF-beta receptor 2 downregulation in tumour-associated stroma worsens prognosis and high-grade tumours show more tumour-associated macrophages and lower TGF-beta1 expression in colon carcinoma: A retrospective study. BMC Cancer. 2007;7.

    Not in our library10.1186/1471-2407-7-156

  129. 129.

    Chen Z., Feng X., Herting C.J., Garcia V.A., Nie K., Pong W.W., Rasmussen R., Dwivedi B., Seby S., Wolf S.A., et al. Cellular and molecular identity of tumor-associated macrophages in glioblastoma. Cancer Res. 2017;77:2266-2278.

    Not in our library10.1158/0008-5472.can-16-2310

  130. 130.

    Ranganathan P., Clark P.A., Kuo J.S., Salamat M.S., Kalejta R.F. Significant association of multiple human cytomegalovirus genomic loci with glioblastoma multiforme samples. J. Virol. 2012;86:854-864.

    Not in our library10.1128/jvi.06097-11

  131. 131.

    Singh R., Shankar B.S., Sainis K.B. TGF-β1-ROS-ATM-CREB signaling axis in macrophage mediated migration of human breast cancer MCF7 cells. Cell Signal. 2014;26:1604-1615.

    Not in our library10.1016/j.cellsig.2014.03.028

  132. 132.

    Sung W.-W., Wang Y.-C., Lin P.-L., Cheng Y.-W., Chen C.-Y., Wu T.-C., Lee H. IL-10 promotes tumor aggressiveness via upregulation of CIP2A transcription in lung adenocarcinoma. Clin. Cancer Res. 2013;19:4092-4103.

    Not in our library10.1158/1078-0432.ccr-12-3439

  133. 133.

    Browne E.P., Wing B., Coleman D., Shenk T. Altered cellular mRNA levels in human cytomegalovirus-infected fibroblasts: Viral block to the accumulation of antiviral mRNAs. J. Virol. 2001;75:12319-12330.

    Not in our library10.1128/jvi.75.24.12319-12330.2001

  134. 134.
    Rapid Intrahost Evolution of Human Cytomegalovirus Is Shaped by Demography and Positive Selection · 2013
    No notice
  135. 135.

    Batlle E., Clevers H. Cancer stem cells revisited. Nat. Med. 2017;23:1124-1134.

    Not in our library10.1038/nm.4409

  136. 136.

    Lombardo Y., de Giorgio A., Coombes C.R., Stebbing J., Castellano L. Mammosphere formation assay from human breast cancer tissues and cell lines. J. Vis. Exp. 2015;97.

    Not in our library10.3791/52671

  137. 137.

    Reitsma J.M., Sato H., Nevels M., Terhune S.S., Paulus C. Human cytomegalovirus IE1 protein disrupts interleukin-6 signaling by sequestering STAT3 in the nucleus. J. Virol. 2013;87:10763-10776.

    Not in our library10.1128/jvi.01197-13

  138. 138.

    Mathers C., Schafer X., Martinez-Sobrido L., Munger J. The human cytomegalovirus UL26 protein antagonizes NF-κB activation. J. Virol. 2014;88:14289-14300.

    Not in our library10.1128/jvi.02552-14

  139. 139.

    Parkin D.M. The global health burden of infection-associated cancers in the year 2002. Int. J. Cancer. 2006;118:3030-3044.

    Not in our library10.1002/ijc.21731

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