Publications by authors named "V Antonio-Vejar"

Human papillomaviruses (HPVs) and, specifically, high-risk HPVs (HR-HPVs) are identified as necessary factors in the development of cancer of the lower genital tract, with CaCU standing out as the most prevalent tumor. This review summarizes ten mechanisms activated by HR-HPVs during cervical carcinogenesis, which are broadly associated with at least seven of the fourteen distinctive physiological capacities of cancer in the newly established model by Hanahan in 2022. These mechanisms involve infection by human papillomavirus, cellular tropism, genetic predisposition to uterine cervical cancer (CaCU), viral load, viral physical state, regulation of epigenetic mechanisms, loss of function of the E2 protein, deregulated expression of E6/E7 oncogenes, regulation of host cell protein function, and acquisition of the mesenchymal phenotype.

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DNA methylation is an epigenetic mechanism involving the transfer of a methyl group onto the C5 position of the cytosine to form 5-methylcytosine (5mC). In general, DNA methylation in cancer is associated with the repression of the expression of tumor suppressor genes (TSG) and the demethylation with the overexpression of oncogenes. DNA methylation was considered a stable modification for a long time, but in 2009, it was reported that DNA methylation is a dynamic modification.

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Breast Cancer (BC) was the most common female cancer in incidence and mortality worldwide in 2020. Similarly, BC was the top female cancer in the USA in 2022. Risk factors include earlier age at menarche, oral contraceptive use, hormone replacement therapy, high body mass index, and mutations in 1/2 genes, among others.

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Background: Cervical cancer (CC) is the fourth most common malignancy of the female genital tract. Human Papillomavirus (HPV) is the main cause of precancerous lesions and CC cases worldwide.

Objective: We assessed the prevalence and distribution of HPV types and association with precancerous lesions and CC.

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Article Synopsis
  • The study investigates how HPV-16 E6 splice variant isoforms (E6, E6*I, and E6*II) affect p53 and its isoforms, particularly in relation to apoptosis in cervical cancer cells.
  • Results show that E6 and E6*II can significantly reduce p53 levels, with E6 specifically decreasing Δ40p53, while E6*I has no impact.
  • Combining p53 or Δ40p53 with the chemotherapy drug cisplatin enhanced apoptosis in cancer cells, suggesting a potential therapeutic strategy for treating cancers linked to high-risk HPV.
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