Abstract
Colorectal cancer (CRC) is a common malignancy with a high mortality rate worldwide. It is a complex, multifactorial disease that is strongly impacted by both hereditary and environmental factors. The role of microbes (e.g., viruses) in the pathogenesis of CRC is poorly understood. In the current study, we explored the status of high-risk human papillomaviruses (HPV) and Epstein–Barr virus (EBV) in a well-defined CRC cohort using immunohistochemistry and polymerase chain reaction assays. Our data showed that high-risk HPVs were common (~80%) and EBV had a low presence (14–25%) in the CRC samples. The most common high-risk HPVs are HPV16, 31, 18, 51, 52 and 45 genotypes. The co-presence of high-risk HPV and EBV was observed in ~16% of the sample population without any significant association with the clinicopathological variables. We conclude that high-risk HPVs are very prevalent in CRC samples while EBV positivity is relatively low. The co-expression of the two viruses was observed in a minority of cases and without any correlation with the studied parameters. Further studies are necessary to confirm the clinical relevance and potential therapeutic (preventive) effects of the observations reported herein.
Highlights
Colorectal cancer (CRC) is the third most common cancer reported worldwide, and corresponds to about 10% of all cancer cases [1]
We explored the co-presence of high-risk human papillomaviruses (HPV) and Epstein–Barr virus (EBV) in a well-defined rectal cancer cohort
PCR and IHC data were in good concordance for HPV analysis while discrepant data were observed in EBV assessment; the inter-reliability rating between PCR and IHC was fair (Kappa = 0.31; p = 0.005)
Summary
Colorectal cancer (CRC) is the third most common cancer reported worldwide, and corresponds to about 10% of all cancer cases [1]. The L region takes part in virus assembly by encoding the structural proteins (L1-L2) [10], whereas the high-risk HPV early proteins (E5, E6 and E7) act as oncogenes, working closely together through molecular mechanisms involved in the epithelial–mesenchymal transition (EMT) [11,12]. These proteins deregulate cell cycle progression, immortalize epithelial cells, which leads to their neoplastic transformation in cooperation with other oncogenes and/or oncoviruses [8,13,14]. We explored the co-presence of high-risk HPVs and EBV in a well-defined rectal cancer cohort
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