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Cancers
Special Issues
Viral Oncogenes and Their Role in Cancer Pathogenesis
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Viral Oncogenes and Their Role in Cancer Pathogenesis

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

Deadline for manuscript submissions: 21 May 2025 | Viewed by 3395

Special Issue Editors

Dr. Ronen Borenstein

E-Mail Website
Guest Editor
The Program for Experimental and Theoretical Modeling Division of Hepatology, Department of Medicine Stritch School of Medicine, Loyola University Chicago, Maywood, IL 60153, USA
Interests: HBV; HDV; HSV; hRSV; coronavirus; EBV; ZIKV
Dr. Yosef Sabo

E-Mail Website
Guest Editor
Aaron Diamond AIDS Research Center, Columbia University Vagelos College of Physicians and Surgeons, New York, NY, USA
Interests: HRSV; HIV-1; virus

Special Issue Information

Dear Colleagues,

We are pleased to announce the call for submissions for a Special Issue of cancers focusing on the topic of "Viral Oncogenes and Their Role in Cancer Pathogenesis".

Viruses have long been recognized as significant contributors to cancer development. They achieve this by either expressing viral oncogenes or altering the cellular regulation of endogenous oncogenes. These oncogenes can modify host cell signaling pathways, leading to uncontrolled cell proliferation, evasion of apoptosis, and genomic instability. The study of viral oncogenes and the cellular regulation modifications that they induce has provided valuable insights into the molecular mechanisms underlying tumorigenesis, offering potential targets for therapeutic interventions. This Special Issue will explore the diverse array of viral strategies aimed at inducing oncogenesis identified across different viral families, their interactions with the host cellular machinery, and their impact on cancer pathogenesis. By elucidating the intricate relationship between viruses and cancer, this Special Issue will advance our understanding of oncogenic processes and pave the way for innovative antiviral and anticancer strategies.

All submitted articles will undergo a rigorous peer review process to ensure that they are of the highest scientific quality and are relevant to the field. We encourage contributions from researchers, clinicians, and experts in this field.

Should you have any questions, require further information, or need any assistance, please do not hesitate to reach out to us. We are here to support and facilitate your participation in this Special Issue

Thank you for your attention regarding this matter; we look forward to receiving your valuable submissions.

Dr. Ronen Borenstein
Dr. Yosef Sabo
Guest Editors

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 100 words) can be sent to the Editorial Office for announcement on this website.

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-blind 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

  • viral oncogenes
  • cancer pathogenesis
  • cellular regulation
  • tumorigenesis mechanisms
  • antiviral and anticancer strategies

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (2 papers)

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Research

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17 pages, 2379 KiB  
Article
A Novel Monoclonal Antibody against PD-1 for the Treatment of Viral Oncogene-Induced Tumors or Other Cancer
by Xu Xu, Shih-Long Yan, Yi-Te Yo, Peiyu Chiang, Chan-Yen Tsai, Lih-Ling Lin and Albert Qin
Cancers 2024, 16(17), 3052; https://doi.org/10.3390/cancers16173052 - 1 Sep 2024
Cited by 1 | Viewed by 2148
Abstract
Programmed cell death 1 (PD-1) and programmed death-ligand 1 (PD-L1) interact to form an immune checkpoint fostering viral infection and viral oncogene-induced tumorigenesis. We generated a novel anti-human PD-1, humanized monoclonal antibody P1801 and investigated its pharmacologic, pharmacokinetic (PK), and pharmacodynamic properties. In [...] Read more.
Programmed cell death 1 (PD-1) and programmed death-ligand 1 (PD-L1) interact to form an immune checkpoint fostering viral infection and viral oncogene-induced tumorigenesis. We generated a novel anti-human PD-1, humanized monoclonal antibody P1801 and investigated its pharmacologic, pharmacokinetic (PK), and pharmacodynamic properties. In vitro binding assays revealed that P1801 uniquely binds to human PD-1 and inhibits its interaction with PD-L1/2. It showed a minor effect on the induction of antibody-dependent cell-mediated cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC). P1801 significantly induced the release of IL-2 from activated T-cells but not from nonactivated T-cells. A dose-dependent linear PK profile was observed for the cynomolgus monkeys treated with repeated doses of P1801 at 5 mg/kg to 200 mg/kg once weekly. A four-week repeat-dose toxicity study revealed that P1801 given weekly was safe and well tolerated at doses ranging from 5 to 200 mg/kg/dose. No pathological abnormalities were noted. In humanized PD-1 mice harboring human PD-L1-expressing colon tumor cells, P1801 administered intraperitoneally twice per week at 12 mg/kg significantly inhibited tumor growth and prolonged mouse survival. P1801 displayed unique binding properties different from pembrolizumab and nivolumab. Therefore, it showed distinctive immunological reactions and significant antitumor activities. We are initiating a Phase 1 clinical study to test its combination use with ropeginterferon alfa-2b, which also has antiviral and antitumor activities, for the treatment of cancer. Full article
(This article belongs to the Special Issue Viral Oncogenes and Their Role in Cancer Pathogenesis)
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Review

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18 pages, 1028 KiB  
Review
Molecular Insights into HR-HPV and HCMV Co-Presence in Cervical Cancer Development
by Rancés Blanco and Juan P. Muñoz
Cancers 2025, 17(4), 582; https://doi.org/10.3390/cancers17040582 - 8 Feb 2025
Viewed by 741
Abstract
Background: Cervical cancer remains a significant health concern worldwide and the primary cause of cancerous cervical lesions is the infection with high-risk human papillomavirus (HR-HPV). However, emerging evidence suggests that HR-HPV infection alone is insufficient for cancer development, and other co-factors may contribute [...] Read more.
Background: Cervical cancer remains a significant health concern worldwide and the primary cause of cancerous cervical lesions is the infection with high-risk human papillomavirus (HR-HPV). However, emerging evidence suggests that HR-HPV infection alone is insufficient for cancer development, and other co-factors may contribute to cervical carcinogenesis. Human cytomegalovirus (HCMV), a common herpesvirus frequently detected in cervical cancer samples, has demonstrated oncogenic potential. Objectives: This review aims to explore the molecular interactions between HR-HPV and HCMV in promoting cervical cancer progression. Methods. A comprehensive search was conducted in PubMed and Google Scholar, focusing on articles examining the role of HCMV in cervical tissues and/or cells, selected based on relevance and significance. Results: The reviewed literature indicates that HCMV and HR-HPV share several oncogenic mechanisms that could drive cervical cell transformation. Conclusions. Both viruses may synergistically promote cervical epithelial transformation and tumor progression in multiple ways. HR-HPV may facilitate HCMV entry by increasing host cell receptors essential for viral attachment. Additionally, HR-HPV and HCMV may cooperatively disrupt cellular processes, enhancing carcinogenesis. Both viruses may also modulate the local immune environment, enabling immune evasion and lesion persistence. However, further in vitro and in vivo studies are required to validate these hypotheses. Full article
(This article belongs to the Special Issue Viral Oncogenes and Their Role in Cancer Pathogenesis)
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