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Patterns of genetic alterations in pancreatic cancer: a pooled analysis.
Environ Mol Mutagen 1999; 33(2):111-22EM

Abstract

Both K-ras and p53 gene mutations are found commonly in pancreatic tumors. Analysis of the mutational patterns may provide insight into disease etiology. To further describe the mutational patterns of pancreatic cancer and to assess the evidence to date, we performed a pooled analysis of the published data on genetic mutations associated with pancreatic ductal adenocarcinoma. We included data from studies that evaluated point mutations in the two genes most studied in pancreatic cancer, K-ras and p53. A majority of the 204 tumors had mutations in at least one gene, with 29% having both K-ras and p53 mutations, 39% with K-ras mutation alone, and 16% having p53 mutation alone. Sixteen percent of tumors lacked mutation in either gene. K-ras mutations were present in high frequencies in all tumor grades (>69%). A statistically significant trend was observed for p53 mutation with higher tumor grade (P = 0.04). For K-ras, G2 and G3 grades, combined, had notably higher prevalences of mutation than G1 (P = 0.004). CGT mutations in K-ras codon 12 were marginally associated with lower tumor grade (P for trend = 0.09), and these tumors were somewhat less likely to have a p53 mutation than tumors with other K-ras mutations (P = 0.06). In the 59 K-ras+/p53+ tumors, 64% had the same type of mutation (transition or transversion) in both genes, suggesting a common mechanism. The mutational pattern of p53 in pancreatic cancer is similar to bladder cancer, another smoking-related cancer, but not to lung cancer. Analyses of molecular data, such as that performed here, present new avenues for epidemiologists in the study of the etiology of specific cancers.

Authors+Show Affiliations

Division of Biological and Biomedical Sciences, Emory University, Atlanta, Georgia 30322, USA.

Pub Type(s)

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

Language

eng

PubMed ID

10217065

Citation

Blanck, H M., et al. "Patterns of Genetic Alterations in Pancreatic Cancer: a Pooled Analysis." Environmental and Molecular Mutagenesis, vol. 33, no. 2, 1999, pp. 111-22.
Blanck HM, Tolbert PE, Hoppin JA. Patterns of genetic alterations in pancreatic cancer: a pooled analysis. Environ Mol Mutagen. 1999;33(2):111-22.
Blanck, H. M., Tolbert, P. E., & Hoppin, J. A. (1999). Patterns of genetic alterations in pancreatic cancer: a pooled analysis. Environmental and Molecular Mutagenesis, 33(2), pp. 111-22.
Blanck HM, Tolbert PE, Hoppin JA. Patterns of Genetic Alterations in Pancreatic Cancer: a Pooled Analysis. Environ Mol Mutagen. 1999;33(2):111-22. PubMed PMID: 10217065.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Patterns of genetic alterations in pancreatic cancer: a pooled analysis. AU - Blanck,H M, AU - Tolbert,P E, AU - Hoppin,J A, PY - 1999/4/27/pubmed PY - 1999/4/27/medline PY - 1999/4/27/entrez SP - 111 EP - 22 JF - Environmental and molecular mutagenesis JO - Environ. Mol. Mutagen. VL - 33 IS - 2 N2 - Both K-ras and p53 gene mutations are found commonly in pancreatic tumors. Analysis of the mutational patterns may provide insight into disease etiology. To further describe the mutational patterns of pancreatic cancer and to assess the evidence to date, we performed a pooled analysis of the published data on genetic mutations associated with pancreatic ductal adenocarcinoma. We included data from studies that evaluated point mutations in the two genes most studied in pancreatic cancer, K-ras and p53. A majority of the 204 tumors had mutations in at least one gene, with 29% having both K-ras and p53 mutations, 39% with K-ras mutation alone, and 16% having p53 mutation alone. Sixteen percent of tumors lacked mutation in either gene. K-ras mutations were present in high frequencies in all tumor grades (>69%). A statistically significant trend was observed for p53 mutation with higher tumor grade (P = 0.04). For K-ras, G2 and G3 grades, combined, had notably higher prevalences of mutation than G1 (P = 0.004). CGT mutations in K-ras codon 12 were marginally associated with lower tumor grade (P for trend = 0.09), and these tumors were somewhat less likely to have a p53 mutation than tumors with other K-ras mutations (P = 0.06). In the 59 K-ras+/p53+ tumors, 64% had the same type of mutation (transition or transversion) in both genes, suggesting a common mechanism. The mutational pattern of p53 in pancreatic cancer is similar to bladder cancer, another smoking-related cancer, but not to lung cancer. Analyses of molecular data, such as that performed here, present new avenues for epidemiologists in the study of the etiology of specific cancers. SN - 0893-6692 UR - https://www.unboundmedicine.com/medline/citation/10217065/Patterns_of_genetic_alterations_in_pancreatic_cancer:_a_pooled_analysis_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0893-6692&date=1999&volume=33&issue=2&spage=111 DB - PRIME DP - Unbound Medicine ER -