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Cancers
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The Role of Viruses in the Development of Cancer
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The Role of Viruses in the Development of Cancer

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Infectious Agents and Cancer".

Deadline for manuscript submissions: closed (31 March 2026) | Viewed by 4088

Editor

Prof. Dr. George Eric Blair

E-Mail Website
Guest Editor
School of Molecular and Cellular Biology, University of Leeds, Leeds, UK
Interests: DNA viruses; HPV; adenovirus; viral vectors; cancer virotherapy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are pleased to invite you to contribute a paper for this Special Issue on “The Role of Viruses in the Development of Cancer”. Viruses have been studied as etiological agents in the development of animal and human cancers for more than a century. This work has aided the identification of oncogenes and tumour suppressor genes as well as highlighting viruses that play a crucial role in the development of human cancers, for example, the role of high-risk human papillomaviruses (HPVs) in ano-genital and oral cancers, and of the human retrovirus T-lymphotropic virus 1 (HTLV 1) in adult T-cell leukaemia (ATL). The field continues to be buoyant, with new tumour viruses such as the DNA viruses, Merkel Cell Polyomavirus (MCPyV) and Kaposi’s sarcoma herpesvirus (KSHV or HHV8) being discovered using DNA sequence and genomic analysis within the past two decades. While effective prophylactic vaccines have been developed against HPVs and Hepatitis B (HBV), there is still a requirement for novel therapeutic approaches to human cancers that are driven by tumour virus infection. 

Original research articles and reviews are welcome in this Special Issue. Research areas may include (but are not limited to) fundamental studies on the molecular mechanisms of cell transformation and oncogenesis by DNA and RNA tumour viruses; the immune response to tumour viruses; the immune evasion of cancers driven by tumour viruses; prophylactic and therapeutic vaccines against tumour viruses and the cancers that they cause; emerging tumour viruses; and global perspectives on tumour viruses and cancers.

We look forward to receiving your contributions.

Prof. Dr. George Eric Blair
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • DNA and RNA tumour viruses
  • HPV
  • EBV
  • KSHV
  • HCV
  • HBV
  • HTLV1
  • McPyV

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Published Papers (3 papers)

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Research

13 pages, 1777 KB  
Communication
Merkel Cell Polyomavirus and DNA Damage Response (DDR): Transcriptional Analysis of DDR Pathways in the Context of Merkel Cell Carcinoma
by Sara Messina, Domenico Mallardo, Amedeo Ferlosio, Lucia Festino, Claudia Trojaniello, Rossella Di Trolio, Marco Ciotti, Paolo Antonio Ascierto, Valeria Pietropaolo and Sara Passerini
Cancers 2026, 18(10), 1592; https://doi.org/10.3390/cancers18101592 - 14 May 2026
Viewed by 438
Abstract
Background/Objectives: Merkel cell polyomavirus (MCPyV) is a ubiquitous virus strictly associated with Merkel cell carcinoma (MCC), a rare and aggressive skin cancer. MCPyV oncogenic properties are associated mainly with early protein expression, integration, and LT truncation. MCPyV can also interact with DNA Damage [...] Read more.
Background/Objectives: Merkel cell polyomavirus (MCPyV) is a ubiquitous virus strictly associated with Merkel cell carcinoma (MCC), a rare and aggressive skin cancer. MCPyV oncogenic properties are associated mainly with early protein expression, integration, and LT truncation. MCPyV can also interact with DNA Damage Response (DDR) mechanisms, contributing to oncogenesis and tumor progression. In this work, we investigated the correlation between MCPyV and MCC and evaluated the mRNA expression profiles of DDR genes in virus-positive and -negative tumors. Methods: A total of 19 formalin-fixed paraffin-embedded biopsies were acquired from patients diagnosed with MCC. After DNA and RNA extraction, the DNA was used for MCPyV detection via qPCR and for sequencing analysis of the early, late, and non-coding control viral regions and the extracted RNA was used for MCPyV transcripts, miRNA detection and for the evaluation of several DDR genes expression such as ATM, ATR, CHK1, CHK2, H2AX, Rad51, p53, and p21, in MCPyV-positive and -negative samples via reverse transcription, PCR, and qPCR. Results: MCPyV presence was detected in 11/19 samples, all characterized by viral integration, LT truncation, and early region expression only. Furthermore, higher mRNA levels of DDR genes were observed in MCPyV-positive tumors compared with the negative ones. Conclusions: Our findings support the role of MCPyV in MCC formation and suggest its involvement in the transcriptional regulation of DDR genes, which may influence tumor progression. Understanding the molecular interplay between MCPyV and the DDR may guide future research into plausible novel diagnostic and therapeutic strategies for virus-induced tumors. Full article
(This article belongs to the Special Issue The Role of Viruses in the Development of Cancer)
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17 pages, 1145 KB  
Article
Valganciclovir Therapy Prevents Human Cytomegalovirus Reactivation in Glioblastoma Patients Undergoing Radiochemotherapy and Extends Time to Tumor Progression
by Mattia Russel Pantalone, Giuseppe Stragliotto, Nerea Martin-Almazan, Inti Peredo-Harvey, Jorge L. Jimenez-Macias, Afsar Rahbar, Sean Lawler, Jiri Bartek and Cecilia Söderberg-Naucler
Cancers 2026, 18(10), 1575; https://doi.org/10.3390/cancers18101575 - 12 May 2026
Viewed by 811
Abstract
Background: Emerging evidence suggests that antiviral treatment targeting human cytomegalovirus (HCMV) may improve outcomes in patients with glioblastoma (GBM). In this study, we analyzed serological data from the placebo-controlled VIGAS1 trial (Eudra number 2006-002022-29), which assessed the effect of valganciclovir (VGCV) on GBM [...] Read more.
Background: Emerging evidence suggests that antiviral treatment targeting human cytomegalovirus (HCMV) may improve outcomes in patients with glioblastoma (GBM). In this study, we analyzed serological data from the placebo-controlled VIGAS1 trial (Eudra number 2006-002022-29), which assessed the effect of valganciclovir (VGCV) on GBM progression in 42 patients, for impact of VGCV in preventing HCMV reactivation. Methods: VIGAS1 patients had undergone radical surgery and were randomized to receive either VGCV (n = 22) or placebo (n = 20) alongside standard radiochemotherapy. Blood was prospectively collected at baseline and 3-, 12- and 24-week follow-up visits. GBM cell lines and a cytomegalovirus-infected murine brain cancer model were used to validate the clinical findings. Results: Over the 24-week study period, we found that HCMV reactivation, as inferred from IgM seropositivity, occurred in 58.3% of patients in the placebo group, whereas this was completely prevented in the VGCV-treated group except for one patient with no treatment compliance (p = 0.0005). HCMV reactivation was linked to early recurrence. IgG-positive patients treated with VGCV showed a significantly longer time to progression (TTP) than those receiving placebo (6.7 vs. 3.7 months, p = 0.0408). We found a significant association between higher steroid doses and enhanced reactivation in the placebo group. In vitro and murine studies confirmed that corticosteroids, combined with radiation therapy, enhanced cytomegalovirus reactivation, which was mitigated by antiviral treatment. Conclusions: These findings suggest that preventing HCMV reactivation with antiviral therapy may improve patient outcomes, especially in HCMV-seropositive GBM patients, and further support the hypothesis that HCMV is a tumor-promoting virus. Full article
(This article belongs to the Special Issue The Role of Viruses in the Development of Cancer)
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19 pages, 11686 KB  
Article
Cross-Talk Between Tumor Cells and Stellate Cells Promotes Oncolytic VSV Activity in Intrahepatic Cholangiocarcinoma
by Victoria Neumeyer, Purva Chavan, Katja Steiger, Oliver Ebert and Jennifer Altomonte
Cancers 2025, 17(3), 514; https://doi.org/10.3390/cancers17030514 - 4 Feb 2025
Cited by 3 | Viewed by 1988
Abstract
As the mechanisms underlying tumorigenesis become better understood, the dynamic roles of cellular components of the tumor microenvironment, and their cross-talk with tumor cells, have come to light as key drivers of disease progression and have emerged as important targets of new cancer [...] Read more.
As the mechanisms underlying tumorigenesis become better understood, the dynamic roles of cellular components of the tumor microenvironment, and their cross-talk with tumor cells, have come to light as key drivers of disease progression and have emerged as important targets of new cancer therapies. In the field of oncolytic virus (OV) therapy, stromal cells have been considered as potential barriers to viral spread, thus limiting virus replication and therapeutic outcome. However, new evidence indicates that intratumoral fibroblasts could support virus replication. We have demonstrated in a rat model of stromal-rich intrahepatic cholangiocarcinoma (CCA) that vesicular stomatitis virus (VSV) can be localized within intratumoral hepatic stellate cells (HSCs), in addition to tumor cells, when the virus was applied via hepatic arterial infusion. Furthermore, VSV was shown to efficiently kill CCA cells and activated HSCs, and co-culture of CCA and HSCs increased viral titers. Interestingly, this effect is also observed when each cell type is cultured alone in a conditioned medium of the other cell type, indicating that secreted cell factors are at least partially responsible for this phenomenon. Partial reduction in sensitivity to type I interferons was observed in co-culture systems, providing a possible mechanism for the increased viral titers. Together, the results indicate that targeting activated HSCs with VSV could provide an additional mechanism of OV therapy, which, until now has not been considered. Furthermore, these findings suggest that VSV is a potentially powerful therapeutic agent for stromal-rich tumors, such as CCA and pancreatic cancer, both of which are very difficult to treat with conventional therapy and have a very poor prognosis. Full article
(This article belongs to the Special Issue The Role of Viruses in the Development of Cancer)
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