ArticleWorld journal of gastroenterology2004
Potential role of p53 mutation in chemical hepatocarcinogenesis of rats.
Article in World journal of gastroenterology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 11 citations in OpenAlex.
- Gallic Acid and Taurine Attenuate Thiamethoxam-Induced Hepatotoxicity in Rats by Modulating SIRT-1/PGC-1α, NF-κB/iNOS, and p53/Bax/Caspase-3 Pathways.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Abnormal expression of HNRNPA3 in multistep hepatocarcinogenesis.Oncology letters · 2021Article
- Discrimination of carcinogens by hepatic transcript profiling in rats following 28-day administration.Cancer informatics · 2009Article
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4 authors at 3 institutions in 3 countries.
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No grant is acknowledged in the PubMed record.
Abstract
aimInactivation of p53 gene is one of the most frequent genetic alterations in carcinogenesis. The mutation status of p53 gene was analyzed, in order to understand the effect of p53 mutation on chemical hepatocarcinogenesis of rats.
methodsDuring hepatocarcinogenesis of rats induced by 3'-methyl-4- dimethylaminoazobenzene (3'-Me-DAB), prehepatocarcinoma and hepatocarcinoma foci were collected by laser capture microdissection (LCM), and quantitatively analyzed for levels of p53 mRNA by LightCycler(TM) real-time RT-PCR and for mutations in p53 gene exons 5-8 by direct sequencing.
resultsSamples consisting of 44 precancerous foci and 24 cancerous foci were collected by LCM. A quantitative analysis of p53 mRNA showed that p53 mRNA peaked at an early stage (week 6) in the prehepatocarcinoma lesion, more than ten times that of adjacent normal tissue, and gradually decreased from week 6 to week 24. The expression of p53 mRNA in adjacent normal tissue was significantly lower than that in prehepatocarcinoma. Similar to prehepatocarcinoma, p53 mRNA in cancer was markedly higher than that in adjacent normal tissue at week 12, and was closer to normal at week 24. Direct p53 gene sequencing showed that 35.3% (24/68) (9 precancer, 15 cancer) LCM samples exhibited point mutations, 20.5% of prehepatocarcinoma LCM samples presented missense mutations at exon 6/7 or/and 8, and was markedly lower than 62.5% of hepatocarcinoma ones (P<0.01). Mutation of p53 gene formed the mutant hot spots at 5 codons. Positive immunostaining for p53 protein could be seen in prehepatocarcinoma and hepatocarcinoma foci at 24 weeks.
conclusionp53 gene mutation is present in initial chemical hepatocarcinogenesis, and the mutation of p53 gene induced by 3'-Me-DAB is an important factor of hepatocarcinogenesis.
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