A 30-year-old man with xeroderma pigmentosum (XP) has extreme ultraviolet radiation sensitivity and multiple skin cancers. The molecular mechanism underlying XP most commonly involves a defect in:

• A Nucleotide excision repair ✓
• B Base excision repair
• C Mismatch repair
• D Homologous recombination repair

Explanation

UV radiation generates pyrimidine dimers (cyclobutane pyrimidine dimers and 6-4 photoproducts) that are recognized and repaired by the nucleotide excision repair (NER) pathway. XP results from mutations in any of the XPC/XPA/XPB/XPD/XPG proteins involved in NER, impairing recognition and excision of UV-induced bulky adducts. Unrepaired pyrimidine dimers cause C-to-T and CC-to-TT transition mutations in proto-oncogenes and tumor suppressor genes, leading to skin cancer.

Reference: Harper's Illustrated Biochemistry, 32nd ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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