Dados do Resumo

Título

NEOPLASTIC PATHOPHYSIOLOGY OF HPV PROGRESSION: A REVIEW OF THE LITERATURE

Introdução

The neoplastic progression associated with the Human Papillomavirus (HPV) can lead to the development of cervical and oropharyngeal cancers. These are DNA viruses, oncogenic by types 16 and 18, promoting malignancy, resulting in the deregulated expression of the E6 and E7 oncoproteins, which inactivate the tumor suppressors p53 and pRb. This disruptive process compromises cell control mechanisms leading to malignant neoplasia. The incipience regarding the mechanisms that act in HPV cancer is highlighted.

Objetivo

This study aims to assess the relationship between psychological stress and the progression of HPV associated cervical lesions, by investigating how stress modulates the immune response. The findings will contribute to the enhancement of clinical prevention strategies.

Métodos

This summary was constructed through a literature review conducted by searching for publications in the PUBMED and LILACS databases from 2015 to 2024, using the terms “HPV progression” and “neoplastic pathophysiology”, written in english. Inclusion criteria were articles related to the neoplastic pathophysiology of HPV progression, and reviews were also analyzed. Exclusion criteria were articles that did not meet the inclusion criteria and duplicate articles. Seven articles were found on each platform, and after applying the criteria, only four studies were selected for this review.

Resultados

A new deterministic model assesses HPV progression rates and cervical cancer risk, providing a faster alternative for early detection. Healthy vaginal microbiota maintains an acidic pH, protecting against HPV infections. When the microbiota is compromised and the vaginal pH becomes alkaline, carcinogenesis is favored. Chronic stress can elevate cortisol levels, which reactivates HPV and contributes to cervical neoplasms. Elevated cortisol levels impair apoptosis and the local immune response. Persistent HPV infection is associated with cervical cancer and an inflammatory environment with protumorigenic T-helper-17 (Th17) cells. CCL20, expressed in the stroma of cervical squamous cell carcinomas, is correlated with CD4(+)/IL17(+) cell infiltration and FIGO stage advancement. CCL20 is induced by cancer cells and attracts CD4/IL17/CCR6 cells. IL6 regulates CCL20 via C/EBPβ, sustaining Th17 infiltration and cancer progression.

Conclusões

This review highlights the complex interplay between HPV infection, immune response, and the role of stress and microbiota in neoplastic progression. Understanding these mechanisms is crucial for developing more effective prevention and early detection strategies, potentially reducing the incidence of HPV-related cancers. Further research is needed to explore these pathways and their implications for targeted therapies.

Palavras Chave

HPV Progression; Neoplastic Pathophysiology; Literature Review