Article: K-ras oncogene activation in adenocarcinoma of the human pancreas. A study of 82 carcinomas using a combination of mutant-enriched polymerase chain reaction analysis and allele-specific oligonucleotide hybridization.
The American journal of pathology
1993 Volume 143, Issue 2, Page(s) 545–554
Abstract: ... This combination of mutant-enriched polymerase chain reaction-restriction fragment length polymorphism analysis and ... Mutations were detected using primer-mediated, mutant-enriched, polymerase chain reaction ... polymerase chain reaction-restriction fragment length polymorphism analysis combined with allele-specific oligonucleotide ...
| Abstract | We examined 82 surgically resected or biopsied, formalin-fixed, paraffin-embedded primary adenocarcinomas of the pancreas for the presence of activating point mutations in codon 12 of the K-ras oncogene. Mutations were detected using primer-mediated, mutant-enriched, polymerase chain reaction-restriction fragment length polymorphism analysis and characterized further by allele-specific oligonucleotide hybridization. This combination of mutant-enriched polymerase chain reaction-restriction fragment length polymorphism analysis and allele-specific oligonucleotide hybridization results in a rapid and sensitive characterization of the mutations in codon 12 of K-ras. Sixty-eight (83%) of the 82 carcinomas examined harbored a point mutation. Of the 68 mutations, 33 (49%) were guanine to adenine transitions, 27 (39%) were guanine to thymine transversions, and eight (12%) were guanine to cytosine transversions. Mutations were found in carcinomas of the head (61 of 75, 81%) as well as in carcinomas of the body or tail (seven of seven, 100%) of the pancreas. The overall prevalence of K-ras point mutations in adenocarcinomas of the pancreas obtained from patients who smoked cigarettes at some point during their lives (88%; 86% in current smokers and 89% in ex-smokers) was greater than that seen in pancreatic adenocarcinomas from patients who never smoked cigarettes (68%, P = 0.046). The presence of K-ras point mutations did not correlate with tumor ploidy, tumor proliferating index, or patient survival. These results demonstrate that primer-mediated, mutant-enriched polymerase chain reaction-restriction fragment length polymorphism analysis combined with allele-specific oligonucleotide hybridization can be used to detect and characterize mutations in codon 12 of the K-ras oncogene in formalin-fixed, paraffin-embedded tissues, and the results confirm that activating point mutations in codon 12 of the K-ras oncogene occur frequently in adenocarcinomas of the pancreas. |
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| MeSH term(s) | Adenocarcinoma/genetics ; Adenocarcinoma/pathology ; Adult ; Aged ; Aged, 80 and over ; Alleles ; Base Sequence ; Codon ; Female ; Follow-Up Studies ; Gene Expression Regulation, Neoplastic ; Genes, ras ; Humans ; Male ; Middle Aged ; Molecular Sequence Data ; Oligonucleotide Probes ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/pathology ; Point Mutation ; Polymerase Chain Reaction ; Survival Rate | |||||
| Chemical Substances | Codon ; Oligonucleotide Probes | |||||
| Language | English | |||||
| Publishing date | 1993-08 | |||||
| Publishing country | United States | |||||
| Document type | Journal Article ; Research Support, Non-U.S. Gov't ; Review | |||||
| ZDB-ID | 2943-9 | |||||
| ISSN | 1525-2191 ; 0002-9440 | |||||
| ISSN (online) | 1525-2191 | |||||
| ISSN | 0002-9440 | |||||
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| Database | MEDical Literature Analysis and Retrieval System OnLINE |
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