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P53 codon 249 mutation in hepatocellular carcinomas from Nigeria
D A Ndububa1, C M Yakicier, O S Ojo
1Laboratoire d'Oncologie Moléculaire, Centre Léon Bérard, 28, rue Laënnec, 69373 Lyon Cedex 08, France. dndububa@oauife.edu.ng
African Journal of Medicine and Medical Sciences
|September 27, 2003
Summary
Hepatocellular carcinoma (HCC) in Nigerian patients showed a low frequency (5.5%) of the p53 codon 249 mutation. This suggests aflatoxins may play a limited role in HCC development in this region.
Area of Science:
- Oncology
- Hepatology
- Molecular Biology
Background:
- The p53 tumor suppressor gene is frequently mutated in hepatocellular carcinoma (HCC).
- A specific p53 codon 249 mutation is common in HCC from regions with high aflatoxin exposure and hepatitis B virus endemicity.
- Hepatocellular carcinoma is a significant health concern in Nigeria.
Purpose of the Study:
- To determine the frequency of the p53 codon 249 mutation in Nigerian patients diagnosed with hepatocellular carcinoma.
- To investigate the potential role of aflatoxins in hepatocarcinogenesis in Nigeria.
Main Methods:
- Tumor samples were collected from 18 Nigerian patients with histologically confirmed HCC.
- DNA was extracted from tumor tissues, and exon 7 of the p53 gene was amplified using nested polymerase chain reaction.
- Restriction enzyme analysis was performed to detect the p53 codon 249 mutation.
Main Results:
- The p53 codon 249 mutation was detected in 1 out of 18 tumor samples, representing a frequency of 5.5%.
- Fourteen of the 18 patients had co-existing cirrhosis.
- The study included samples from autopsy (n=14), surgical resection (n=3), and liver biopsy (n=1).
Conclusions:
- The low frequency of the p53 codon 249 mutation in Nigerian HCC patients suggests a limited role for aflatoxins in hepatocarcinogenesis in this population, particularly in the Southwest region.
- Further research is needed to elucidate the specific etiological factors contributing to HCC in Nigeria.
- The findings contribute to understanding the geographical variations in HCC development and its molecular mechanisms.