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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.
Am J Pathol. 1993 Aug; 143(2):545-54.AJ

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.

Authors+Show Affiliations

Department of Pathology, Johns Hopkins Medical Institutions, Baltimore, Maryland.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

8342602

Citation

Hruban, R H., et al. "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, vol. 143, no. 2, 1993, pp. 545-54.
Hruban RH, van Mansfeld AD, Offerhaus GJ, et al. 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. Am J Pathol. 1993;143(2):545-54.
Hruban, R. H., van Mansfeld, A. D., Offerhaus, G. J., van Weering, D. H., Allison, D. C., Goodman, S. N., Kensler, T. W., Bose, K. K., Cameron, J. L., & Bos, J. L. (1993). 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, 143(2), 545-54.
Hruban RH, et al. 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. Am J Pathol. 1993;143(2):545-54. PubMed PMID: 8342602.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - 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. AU - Hruban,R H, AU - van Mansfeld,A D, AU - Offerhaus,G J, AU - van Weering,D H, AU - Allison,D C, AU - Goodman,S N, AU - Kensler,T W, AU - Bose,K K, AU - Cameron,J L, AU - Bos,J L, PY - 1993/8/1/pubmed PY - 1993/8/1/medline PY - 1993/8/1/entrez SP - 545 EP - 54 JF - The American journal of pathology JO - Am J Pathol VL - 143 IS - 2 N2 - 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. SN - 0002-9440 UR - https://www.unboundmedicine.com/medline/citation/8342602/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_ L2 - https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/8342602/ DB - PRIME DP - Unbound Medicine ER -