Human papillomavirus (HPV) infection of the anogenital epithelium can result in a spectrum of changes referred to as squamous intraepithelial lesions (SILs), ranging from mild dysplasia to squamous cell carcinoma (SCC) in situ (SCCIS). Over time, these lesions can regress, persist, progress, or recur, in some cases to invasive SCC. Clinically, lesions appear as multifocal macules, papules, plaques on the external anogenital region. Lesions involving the cervix and anus have the highest risk for transformation to invasive SCC; however, lesions can transform at any site.
HPV-16 and -18 infected cells may not be able to differentiate fully as a result of either (a) functional interference of cell cycle-regulating proteins, caused by viral gene expression (e.g., interaction between HPV-16 E6 with cellular protein p53, interaction between HPV-16 E7 with cellular protein pRB) or (b) over-production of E5, E6, and E7. When this occurs, the host DNA synthesis continues unchecked and leads to rapidly dividing undifferentiated cells with morphologic characteristics of intraepithelial neoplasias. Accumulated chromosomal breakages, rearrangements, deletions, and other genomic mutations in these cells lead to cells with invasion capability and, ultimately, to cervical malignancy.
In situ SCC presents as one or more flat red scaly patches up to several centimetres wide, often found in large numbers on the lower legs. These patches are also known as ‘Bowen's disease'. ‘In situ' means the malignant cells are confined to the epidermis, the outside layer of the skin. In situ SCC can persist as such or develop into invasive SCC
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