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Multiple Choice

Aflatoxin B1 increases hepatocellular carcinoma risk by mutating which gene?

Aflatoxin B1 promotes liver cancer mainly by disabling a key cellular safety switch: the p53 tumor suppressor gene. The toxin is metabolically activated to a reactive form that binds DNA and causes G to T transversions, with a well-known hotspot in p53. This specific mutation impairs p53’s ability to halt the cell cycle or trigger apoptosis in response to DNA damage, so damaged hepatocytes can survive, accumulate further mutations, and progress toward hepatocellular carcinoma. The other genes listed are not the characteristic targets of aflatoxin-driven carcinogenesis, making p53 the best answer.

Aflatoxin B1 promotes liver cancer mainly by disabling a key cellular safety switch: the p53 tumor suppressor gene. The toxin is metabolically activated to a reactive form that binds DNA and causes G to T transversions, with a well-known hotspot in p53. This specific mutation impairs p53’s ability to halt the cell cycle or trigger apoptosis in response to DNA damage, so damaged hepatocytes can survive, accumulate further mutations, and progress toward hepatocellular carcinoma. The other genes listed are not the characteristic targets of aflatoxin-driven carcinogenesis, making p53 the best answer.