دورية أكاديمية

Distinct pattern of p53 mutations in bladder cancer: relationship to tobacco usage.

التفاصيل البيبلوغرافية
العنوان: Distinct pattern of p53 mutations in bladder cancer: relationship to tobacco usage.
المؤلفون: Spruck CH 3rd; Kenneth Norris Jr. Comprehensive Cancer Center, Urologic Cancer Research Laboratory, University of Southern California, Los Angeles 90033., Rideout WM 3rd, Olumi AF, Ohneseit PF, Yang AS, Tsai YC, Nichols PW, Horn T, Hermann GG, Steven K, et. al.
المصدر: Cancer research [Cancer Res] 1993 Mar 01; Vol. 53 (5), pp. 1162-6.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
اللغة: English
بيانات الدورية: Publisher: American Association for Cancer Research Country of Publication: United States NLM ID: 2984705R Publication Model: Print Cited Medium: Print ISSN: 0008-5472 (Print) Linking ISSN: 00085472 NLM ISO Abbreviation: Cancer Res Subsets: MEDLINE
أسماء مطبوعة: Publication: Baltimore, Md. : American Association for Cancer Research
Original Publication: Chicago [etc.]
مواضيع طبية MeSH: Mutation*, Genes, p53/*genetics , Smoking/*genetics , Urinary Bladder Neoplasms/*genetics, Base Sequence ; Free Radicals ; Humans ; Molecular Sequence Data
مستخلص: A distinct mutational spectrum for the p53 tumor suppressor gene in bladder carcinomas was established in patients with known exposures to cigarette smoke. Single-strand conformational polymorphism analysis of exons 5 through 8 of the p53 gene showed inactivating mutations in 16 of 40 (40%) bladder tumors from smokers and 13 of 40 (33%) tumors from lifetime nonsmokers. Overall, 13 of the 50 (26%) total point mutations discovered in this and previous work were G:C-->C:G transversions, a relatively rare mutational type in human tumors. In six tumors, identical AGA (Arg)-->ACA (Thr) point mutations at codon 280 were observed, suggesting a mutational hotspot in these tumors. Comparison of the mutational spectra from smokers and nonsmokers revealed no obvious differences in the types or positions of inactivating mutations; however, 5 of 15 tumors containing point mutations from cigarette smokers had double mutations, four of which were tandem mutations on the same allele. No double mutations were found in tumors from nonsmoking patients. None of the mutations in smokers were G:C-->T:A transversions, which would be anticipated for exposure to the suspected cigarette smoke carcinogen 4-aminobiphenyl. The results suggest that, although cigarette smoke exposure may not significantly alter the kinds of mutations sustained in the p53 gene, it may act to increase the extent of DNA damage per mutagenic event.
التعليقات: Erratum in: Cancer Res 1993 May 15;53(10 Suppl):2427.
معلومات مُعتمدة: R01 CA40468 United States CA NCI NIH HHS; R35 CA49758 United States CA NCI NIH HHS
Gene Symbol: p53
المشرفين على المادة: 0 (Free Radicals)
تواريخ الأحداث: Date Created: 19930301 Date Completed: 19930401 Latest Revision: 20220410
رمز التحديث: 20231215
PMID: 8439962
قاعدة البيانات: MEDLINE