Human Papillomaviruses and Epstein–Barr Virus Interactions in Colorectal Cancer: A Brief Review

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Abstract

Human papillomaviruses (HPVs) and the Epstein–Barr virus (EBV) are the most common oncoviruses, contributing to approximately 10%–15% of all malignancies. Oncoproteins of high-risk HPVs (E5 and E6/E7), as well as EBV (LMP1, LMP2A and EBNA1), play a principal role in the onset and progression of several human carcinomas, including head and neck, cervical and colorectal. Oncoproteins of high-risk HPVs and EBV can cooperate to initiate and/or enhance epithelial-mesenchymal transition (EMT) events, which represents one of the hallmarks of cancer progression and metastasis. Although the role of these oncoviruses in several cancers is well established, their role in the pathogenesis of colorectal cancer is still nascent. This review presents an overview of the most recent advances related to the presence and role of high-risk HPVs and EBV in colorectal cancer, with an emphasis on their cooperation in colorectal carcinogenesis.

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Most cited references 166

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Colorectal cancer epidemiology: incidence, mortality, survival, and risk factors.

Fatima Haggar, Robin P Boushey (2009)

In this article, the incidence, mortality, and survival rates for colorectal cancer are reviewed, with attention paid to regional variations and changes over time. A concise overview of known risk factors associated with colorectal cancer is provided, including familial and hereditary factors, as well as environmental lifestyle-related risk factors such as physical inactivity, obesity, smoking, and alcohol consumption.

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The SWI/SNF complex and cancer.

D Reisman, S Glaros, E. Thompson (2009)

The mammalian SWI/SNF complexes mediate ATP-dependent chromatin remodeling processes that are critical for differentiation and proliferation. Not surprisingly, loss of SWI/SNF function has been associated with malignant transformation, and a substantial body of evidence indicates that several components of the SWI/SNF complexes function as tumor suppressors. This review summarizes the evidence that underlies this conclusion, with particular emphasis upon the two catalytic subunits of the SWI/SNF complexes, BRM, the mammalian ortholog of SWI2/SNF2 in yeast and brahma in Drosophila, and Brahma-related gene-1 (BRG1).

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Human papillomavirus, smoking, and sexual practices in the etiology of anal cancer.

Janet R Daling, Margaret Madeleine, Lisa Johnson … (2004)

The incidence of anal cancer has increased among both men (160%) and women (78%) from 1973 to 2000 in the U.S. The authors conducted a population-based case-control study of anal cancer to examine factors that may account for this increase. Men (n = 119 patients) and women (n = 187 patients) who were diagnosed with anal cancer between 1986 and 1998 in the Seattle area were ascertained through the local Surveillance, Epidemiology, and End Results registry. Control participants (n = 1700) were ascertained through random-digit telephone dialing. Participants were interviewed in person and provided blood samples. Archival tumor tissue was tested for human papilloma virus (HPV) DNA, and serum samples were tested for HPV type 16 (HPV-16). Overall, 88% of tumors (all histologies) in the study were found to be positive for HPV. HPV-16 was the most frequent HPV type detected (73% of all tumors), followed by HPV-18 (6.9%), regardless of gender. However, 97.7% of tumors from men who were not exclusively heterosexual contained HPV DNA. The risk of anal cancer increased among men (odds ratio [OR], 5.3; 95% confidence interval [95% CI], 2.4-12.0) and women (OR, 11.0; 95% CI, 5.5-22.1) who had > or = 15 sexual partners during their lifetime. Among men who were not exclusively heterosexual and women, receptive anal intercourse was related strongly to the risk of anal cancer (OR, 6.8 [95% CI, 1.4-33.8] and OR, 2.2 [95% CI, 1.4-3.3], respectively). Current smokers among men and women were at particularly high risk for anal cancer, independent of age and other risk factors (OR, 3.9 [95% CI, 1.9-8.0] and OR, 3.8 [95% CI, 2.4-6.2], respectively). The high proportion of tumors with detectable HPV suggests that infection with HPV is a necessary cause of anal cancer, similar to that of cervical cancer. Increases in the prevalence of exposures, such as cigarette smoking, anal intercourse, HPV infection, and the number of lifetime sexual partners, may account for the increasing incidence of anal cancer in men and women. Copyright 2004 American Cancer Society.

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Author and article information

Journal

Journal ID (nlm-ta): Pathogens

Journal ID (iso-abbrev): Pathogens

Journal ID (publisher-id): pathogens

Title: Pathogens

Publisher: MDPI

ISSN (Electronic): 2076-0817

Publication date (Electronic): 20 April 2020

Publication date Collection: April 2020

Volume: 9

Issue: 4

Electronic Location Identifier: 300

Affiliations

[1 ]College of Medicine, QU Health, Qatar University, Doha 2713, Qatar; queenie.fernandez@ 123456gmail.com (Q.F.); ishita.gupta@ 123456qu.edu.qa (I.G.)

[2 ]Biomedical Research Centre, Qatar University, Doha 2713, Qatar

Author notes

[* ]Correspondence: svranic@ 123456qu.edu.qa (S.V.); aalmoustafa@ 123456qu.edu.qa (A.-E.A.M.); Tel.:+974-4403-7873 (S.V.); +974-4403-7817 (A.-E.A.M.)

[†]

Both authors contributed equally to this review.

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Semir Vranic https://orcid.org/0000-0001-9743-7265

Ala-Eddin Al Moustafa https://orcid.org/0000-0003-4452-3439

Article

Publisher ID: pathogens-09-00300

DOI: 10.3390/pathogens9040300

PMC ID: 7238043

PubMed ID: 32325943

SO-VID: a33bf15e-f513-41f3-a205-1802e25cebf8

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Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

Human Papillomaviruses and Epstein–Barr Virus Interactions in Colorectal Cancer: A Brief Review

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Karger: Oncology

Most cited references 166

Colorectal cancer epidemiology: incidence, mortality, survival, and risk factors.

The SWI/SNF complex and cancer.

Human papillomavirus, smoking, and sexual practices in the etiology of anal cancer.

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