Cervical cancer is the main cause of mortality among women in populations with low and medium human development index. The infection with 14 genotypes of the high-risk human papillomavirus (HR-HPV) is the main cause of this cancer. Prophylactic vaccines prevent this infection if they are applied before the onset of sexual activity. Unvaccinated women should be screened with the HR-HPV test and receive the histopathological diagnosis and timely treatment. About 20% of women are HR-HPV positive, but very few have potentially malignant lesions. Women infected with HPV16 or 18 genotypes or women with European ancestry infected with Native American variants of HPV 16 have a higher risk of cancer. Also, those with a history of use of hormonal contraceptives and cigarette smoking. These factors seem to contribute to an increase in the expression of the HR-HPV oncoproteins E6 and E7, which leads to the deregulation of cell cycle control and finally to cancer. We present here the state of the art of the carcinogenic mechanisms of HPV-AR emphasizing the role of the E6 and E7 proteins, as well as the results of our study on the HPV16 or 18 genotyping, the positivity rate of the p16 and ki67 proteins, and the bioinformatic evaluation of the aberrant expression of miRNAs and their correlation with the degree of cervical lesions. These data contribute to validate the clinical potential of these biomarkers for the detection of potentially malignant lesions of the cervix.

Triple-negative breast cancer (TNBC) is an aggressive, heterogeneous subtype of breast cancer. miRNAs play an essential role in TNBC pathogenesis and prognosis. Obesity is linked with an increased risk for several cancers, including breast cancer. Obesity is also related to the dysregulation of miRNA expression in adipose tissues. However, there is limited knowledge about race- and obesity-specific differential miRNA expression in TNBC. We performed miRNA sequencing of 48 samples (24 tumor and 24 adjacent non-tumor tissues) and RNA sequencing of 24 tumors samples from Black (AA) and White (EA) TNBC patients with or without obesity. We identified 55 miRNAs exclusively associated with tumors in obese EA patients and 33 miRNAs in obese AA patients, each capable of distinguishing tumor tissues from obese from lean individuals within their respective racial groups. In EA, we detected 41 significant miRNA–mRNA correlations. Notably, miR-181b-5p and miR-877-5p acted as negative regulators of tumor-suppressor genes (e.g., HEY2, MCL2, HAND2), while miR-204-5p and miR-143-3p appeared to indirectly target oncogenes (e.g., RAB10, DR1, PTBP3, NCBP1). Among AA patients, we found 28 significant miRNA–mRNA interactions. miR-195-5p, miR-130a-3p, miR-130a-5p, miR-424-5p, miR-148a-3p, miR-374-5p, and miR-30a-5p each potentially downregulated two or more genes (e.g., CLCN4, PLCB1, CDC25B, AEBP2, ERBB4). Pathway enrichment analysis highlighted KRAS, ESR1, ESR2, RAB10, TNRC6C, and NCAN as the most commonly differentially expressed in EA, whereas ERBB4, PLCB1, and SERPINE1 were most frequently in AA. These findings highlight the importance of considering race-specific miRNA–mRNA signatures in understanding TNBC in the context of obesity, offering insights into biomarker-driven patient stratification for targeted therapeutic strategies.