Journal of Gastroenterology and Digestive Diseases

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Perspective - Journal of Gastroenterology and Digestive Diseases (2025) Volume 10, Issue 1

HPV and Gastrointestinal Tumors: Exploring the Viral-Oncogenic Nexus Beyond the Cervix

Tingting Yan*

Department of Anorectal Surgery, University of Chinese Medicine, China

*Corresponding Author:
Mbamalu ON
Department of Anorectal Surgery
University of Chinese Medicine, China
E-mail: yan.t@163.com

Received: 01-Jan-2025, Manuscript No. JGDD-25-167217; Editor assigned: 02-Jan-2025, Pre QC No. JGDD-25-167217 (PQ); Reviewed: 15-Jan-2025, QC No. JGDD-25-167217; Revised: 20-Jan-2025, Manuscript No. JGDD-25-167217 (R); Published: 27-Jan-2025, DOI: 10.35841/JGDD-10.1.250

Citation: Yan T. HPV and gastrointestinal tumors: Exploring the viral-oncogenic nexus beyond the cervix. J Gastroenterology Dig Dis. 2025;10(1):250

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Introduction

Human papillomavirus (HPV) is a double-stranded DNA virus known for its oncogenic potential, primarily in cervical and oropharyngeal cancers. However, growing evidence suggests that HPV may also play a role in the development of gastrointestinal tumors, including those of the esophagus, anus, and potentially the colon and rectum. While the association is not yet conclusive, the presence of high-risk HPV DNA in GI tissues and tumors raises important questions about its broader carcinogenic influence. Understanding this potential link could reshape screening practices, prevention strategies, and therapeutic options, especially in regions with high HPV prevalence and rising GI cancer rates.[1].

Human papillomavirus (HPV) encompasses over 200 types, with high-risk strains like HPV-16 and HPV-18 being strongly associated with cancer due to their integration into host DNA and the expression of oncoproteins E6 and E7, which respectively degrade p53 and inhibit retinoblastoma protein (pRb), thereby disrupting cell cycle regulation and promoting malignant transformation, particularly in cervical and oropharyngeal tissues. In the esophagus, HPV DNA has been found in esophageal squamous cell carcinomas (ESCC), especially in high-incidence areas such as China and Africa, with proposed oncogenic mechanisms including direct DNA integration and chronic inflammation.[2].

Anal squamous cell carcinoma (ASCC) is now firmly linked to HPV, especially type 16, with over 90% of cases testing positive, while the role of HPV in rectal adenocarcinoma remains inconclusive due to inconsistent findings and potential contamination. Similarly, HPV’s involvement in colorectal cancer (CRC) is debated, as studies show detection rates from 10% to 80%, but low viral loads, absence of viral mRNA, and inconsistent methodologies hinder definitive conclusions; if involved, HPV may act as a co-factor or via a transient “hit-and-run” mechanism in a carcinogenic environment. The mechanisms by which HPV may access and persist in gastrointestinal tissues include mucosal microabrasions during sexual contact, potential hematogenous spread, and possible latent infection within the gastrointestinal epithelium. [3].

If a clear causal role of HPV in gastrointestinal (GI) cancers is established, it could have significant implications for screening and vaccination. Expanded HPV screening, particularly in anal and esophageal cancers, may help identify at-risk populations, while HPV vaccination (targeting types 6, 11, 16, and 18) could potentially reduce GI cancer incidence over time [4].

Additionally, immunohistochemical and PCR-based diagnostics could stratify GI tumors based on viral status, influencing treatment decisions. However, research in this area faces key challenges, including the lack of standardized detection methods for viral DNA/RNA, confounding factors like tobacco, alcohol, and diet, and low viral gene expression in GI tissues compared to the cervix or oropharynx. Therefore, large-scale, prospective studies using consistent methodologies are essential to clarify HPV’s role in GI cancer development.[5].

Conclusion

The association between HPV and gastrointestinal tumors remains a frontier area in cancer research. While the oncogenic mechanisms of HPV are well understood in the cervix and anal canal, its role in other parts of the GI tract is still being unraveled. Current evidence suggests that high-risk HPV types may be involved in a subset of GI malignancies, particularly anal and possibly esophageal cancers.

References

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