<![CDATA[Cervical cancer is the fourth most common cancer in women globally, with the majority of deaths occurring in developing countries. This disease is mostly associated with high-risk Human Papillomavirus (HPV) infection, especially types 16 and 18, which trigger the development of abnormal cells or precancerous lesions (SIL/CIN). A deep understanding of the mechanisms of precancerous lesion progression is crucial for improving early detection and increasing the chances of recovery. This literature review was compiled using 18 relevant reference articles, such as journals, book, and official websites. Cervical cancer occurs through a progressive change from low-grade lesions (LSIL/CIN 1) to high-grade lesions (HSIL/CIN 2 and 3). The process of carcinogenesis is driven by the entry of HPV DNA into the basal cells within the transformation zone (SCJ), which triggers the production of viral oncoproteins E6 and E7. The E6 and E7 proteins interfere with the cell cycle and the regulation of apoptosis, consequently causing dysplasia and increases the progression to malignancy. A comprehensive understanding of the mechanism of precancerous lesion progression can improve and enhance the system for early detection and diagnosis enforcement to prevent the spread of cancer cells and increase the chances of recovery. In-depth molecular research is required to support the development of a therapeutic HPV vaccine, which may prevent recurrence and promote the regression of low-grade lesions.]]>
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