RESUMO
Cervical cancer is a potentially preventable disease; however, it remains the second most common malignancy in women worldwide. The human papillomavirus (HPV) is the single most important etiological agent in cervical cancer. HPV contributes to neoplastic progression through the action of two viral oncoproteins E6 and E7, which interfere with critical cell cycle pathways, tumor protein p53, and retinoblastoma protein. However, evidence suggests that HPV infection alone is insufficient to induce malignant changes, and other host genetic variations are important in the development of cervical cancer. Advances in molecular biology and high throughput technologies have heralded a new era in biomarker discovery and identification of molecular targets related to carcinogenesis. These advancements have improved our understanding of carcinogenesis and will facilitate screening, early detection, management, and personalized targeted therapy. A number of these developments and molecular targets associated with cervical cancer will be addressed in this review.
