p53 Mutations in nonmalignant human liver: Fingerprints of aflatoxins?

✍ Scribed by Mehmet Ozturk

• Book ID: 102238310
• Publisher: John Wiley and Sons
• Year: 1995
• Tongue: English
• Weight: 259 KB
• Volume: 21
• Category: Article
• ISSN: 0270-9139
• DOI: 10.1002/hep.1840210249

✦ Synopsis

Fifty-eight percent of hepatocellular carcinomas (HCCs) from Qidong, China, contain an AGG to AGT mutation at codon 249 of the p53 tumor suppressor gene, a mutation that is rarely seen in HCCs from Western countries. The population of Qidong is exposed to high levels of aflatoxin B1 (AFB,), a fungal toxin that has been shown to induce the same mutation in cultured human HCC cells. To investigate the role of AFBl and of these p53 mutations in hepatocarcinogenesis, normal liver samples from the United States, Thailand, and Qidong (where AFBl exposures are negligible, low, and high, respectively) were examined for p53 mutations. The frequency of the AGG to AGT mutation at codon 249 paralleled the level of AFBl exposure, which supports the hypothesis that this toxin has a causative-and probably early -role in hepatocarcinogenesis.