HPV E6/E7 lead to overexpression of which biomarker?

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Multiple Choice

HPV E6/E7 lead to overexpression of which biomarker?

Explanation:
HPV oncoproteins E6 and E7 disrupt key cell cycle controls, with E7 inactivating the retinoblastoma protein (Rb). When Rb is blocked, E2F drives the cell into S phase, pushing proliferation forward. In response to this disruption, the cell increases production of p16INK4a, a CDK4/6 inhibitor, in an attempt to halt the cycle. Because Rb is already incapacitated by E7, this rise in p16 cannot restore the checkpoint, but p16 levels stay elevated. That pattern makes p16 overexpression a useful indirect marker of oncogenic HPV activity, particularly in cervical lesions and HPV-related cancers. The other markers aren’t as specific: Ki-67 reflects overall proliferation, not HPV-specific disruption; ER and CEA are unrelated to HPV-driven pathways.

HPV oncoproteins E6 and E7 disrupt key cell cycle controls, with E7 inactivating the retinoblastoma protein (Rb). When Rb is blocked, E2F drives the cell into S phase, pushing proliferation forward. In response to this disruption, the cell increases production of p16INK4a, a CDK4/6 inhibitor, in an attempt to halt the cycle. Because Rb is already incapacitated by E7, this rise in p16 cannot restore the checkpoint, but p16 levels stay elevated. That pattern makes p16 overexpression a useful indirect marker of oncogenic HPV activity, particularly in cervical lesions and HPV-related cancers. The other markers aren’t as specific: Ki-67 reflects overall proliferation, not HPV-specific disruption; ER and CEA are unrelated to HPV-driven pathways.

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