Hepatocellular carcinoma arising in regions with heavy dietary contamination by Aspergillus flavus characteristically harbors a specific molecular fingerprint. The signature alteration produced by this dietary carcinogen is:

• A KRAS codon 12 point mutation
• B Promoter methylation of CDKN2A
• C CTNNB1 exon 3 deletion affecting beta-catenin degradation
• D TP53 mutation at codon 249 resulting in arginine to serine substitution ✓

Explanation

Aflatoxin D1 forms adducts with guanine residues in DNA, producing a characteristic TP53 mutation at codon 249 that changes arginine to serine. This exact hotspot is found at high frequency in hepatocellular carcinoma in aflatoxin-endemic areas of sub-Saharan Africa and China and serves as a chemical fingerprint linking the carcinogen to the tumor. KRAS codon 12 is typical of pancreatic and colorectal cancer, while beta-catenin mutations occur independently of aflatoxin exposure.

Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.

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