Journal ArticleDOI
Selective G to T mutations of p53 gene in hepatocellular carcinoma from southern Africa
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TLDR
Allelic deletions from chromosome 17p and mutations of the p53 gene found in 50% of primary HCCs from southern Africa are reported, with four of five mutations detected were G → T substitutions, with clusters at codon 249.Abstract:
Hepatocellular carcinoma (HCC) is a prevalent cancer in sub-Saharan Africa and eastern Asia. Hepatitis B virus and aflatoxins are risk factors for HCC, but the molecular mechanism of human hepatocellular carcinogenesis is largely unknown. Abnormalities in the structure and expression of the tumour-suppressor gene p53 are frequent in HCC cell lines, and allelic losses from chromosome 17p have been found in HCCs from China and Japan. Here we report on allelic deletions from chromosome 17p and mutations of the p53 gene found in 50% of primary HCCs from southern Africa. Four of five mutations detected were G----T substitutions, with clustering at codon 249. This mutation specificity could reflect exposure to a specific carcinogen, one candidate being aflatoxin B1 (ref. 7), a food contaminant in Africa, which is both a mutagen that induces G to T substitution and a liver-specific carcinogen.read more
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p53 mutations in human cancers
TL;DR: The p53 mutational spectrum differs among cancers of the colon, lung, esophagus, breast, liver, brain, reticuloendothelial tissues, and hemopoietic tissues as mentioned in this paper.
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Damage to DNA by reactive oxygen and nitrogen species: role in inflammatory disease and progression to cancer.
Helen Wiseman,Barry Halliwell +1 more
TL;DR: ROS and RNS could contribute to the initiation of cancer, in addition to being important in the promotion and progression phases, as evidence is growing that antioxidants may prevent or delay the onset of some types of cancer.
References
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Randall Keichi Saiki,David H. Gelfand,Susanne Stoffel,Stephen J. Scharf,Russell Higuchi,Glenn Thomas Horn,Kary B. Mullis,Henry A. Erlich +7 more
TL;DR: A thermostable DNA polymerase was used in an in vitro DNA amplification procedure, the polymerase chain reaction, which significantly improves the specificity, yield, sensitivity, and length of products that can be amplified.
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Germ line p53 mutations in a familial syndrome of breast cancer, sarcomas, and other neoplasms
David Malkin,Frederick P. Li,Frederick P. Li,Louise C. Strong,Joseph F. Fraumeni,Camille E. Nelson,Camille E. Nelson,David H. Kim,Jayne Kassel,Magdalena A. Gryka,Farideh Z. Bischoff,Michael A. Tainsky,Stephen H. Friend +12 more
TL;DR: Germ line p53 mutations have been detected in all five LFS families analyzed and can now be examined in additional families with LFS, and in other cancer patients and families with clinical features that might be attributed to the mutation.
Journal ArticleDOI
Mutations in the p53 gene occur in diverse human tumour types
Janice M. Nigro,Suzanne J. Baker,Antonette C. Preisinger,J M Jessup,R. Hostetter,Karen R. Cleary,S H Bigner,Nancy E. Davidson,Stephen B. Baylin,Peter Devilee +9 more
TL;DR: It is suggested that most tumours with allelic deletions of chromosome 17p contain p53 point mutations resulting in amino-acid substitutions, and p53 gene mutations are clustered in four 'hot-spots' which exactly coincide with the four most highly conserved regions of the gene.
Journal ArticleDOI
Carcinogens are Mutagens: A Simple Test System Combining Liver Homogenates for Activation and Bacteria for Detection
TL;DR: It is proposed that a ring system sufficiently planar for a stacking interaction with DNA base pairs and a part of the molecule capable of being metabolized to a reactive group are discussed in terms of the theory of frameshift mutagenesis.
Journal ArticleDOI
Chromosome 17 deletions and p53 gene mutations in colorectal carcinomas
Suzanne J. Baker,Eric R. Fearon,Janice M. Nigro,Stanley R. Hamilton,Ann C. Preisinger,J. Milburn Jessup,P vanTuinen,David H. Ledbetter,David F. Barker,Yusuke Nakamura,Ray White,Bert Vogelstein +11 more
TL;DR: The data suggest that p53 gene mutations may be involved in colorectal neoplasia, perhaps through inactivation of a tumor suppressor function of the wild-type p53 genes.