Among women who are already infected with high-risk HPV, cigarette smoking increases the risk of progression to cervical carcinoma primarily through which mechanism?
- A Systemic elevation of oestrogen leading to increased HPV replication
- B Direct induction of HPV DNA integration into the host genome
- C Local immunosuppression within cervical tissues favouring viral persistence ✓
- D Somatic mutation of the TP53 gene in cervical epithelial cells
Explanation
Robbins describes smoking as a cofactor that roughly doubles the risk of cervical cancer in HPV-infected women. Carcinogenic nicotine derivatives concentrate in cervical mucus and produce a localised immunosuppressive effect, impairing clearance of the virus and permitting persistence. TP53 mutation is characteristic of HPV-negative tumours driven by E6-independent pathways, and HPV integration is a viral event, not something tobacco induces directly.
Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.