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[Genetics of pancreatic cancer: recent advances in molecular diagnosis].
Nihon Geka Gakkai Zasshi 2002; 103(6):476-81NG

Abstract

Pancreatic cancer is an important cause of death from cancer throughout the world. Until recently, pancreatic cancer was a poorly understood disease. Research in the past decade has shown conclusively, however, that pancreatic cancer is primarily genetic in nature. Inactivation with a variety of tumor-suppressor genes such as p53, p16, and DPC4, and genome-maintenance genes such as BRCA2, coupled with the activation of oncogenes such as K-ras, are a few of the mutations that trigger the growth of cancerous cells. The genetic profile of pancreatic cancer has reshaped the nomenclature describing histological progression in pancreatic ductal tumorigenesis. K-ras mutations frequently occur early, whereas changes in the expression and genetic integrity of the p16 gene appear in intermediate lesions, and the inactivation of the p53 and DPC4 genes and activation of telomerase occur late in the neoplastic progression. Although the majority of pancreatic cancers occur sporadically, a minority has been shown to aggregate in families and has aided our understanding of pancreatic tumorigenesis. An improved understanding of the genetics of pancreatic cancer should lead to the development of gene-based screening tests and novel rational therapies.

Authors+Show Affiliations

Department of Surgery II, Kumamoto University Medical School, Kumamoto, Japan.No affiliation info availableNo affiliation info available

Pub Type(s)

English Abstract
Journal Article

Language

jpn

PubMed ID

12094699

Citation

Hayashi, Naoko, et al. "[Genetics of Pancreatic Cancer: Recent Advances in Molecular Diagnosis]." Nihon Geka Gakkai Zasshi, vol. 103, no. 6, 2002, pp. 476-81.
Hayashi N, Egami H, Ogawa M. [Genetics of pancreatic cancer: recent advances in molecular diagnosis]. Nihon Geka Gakkai Zasshi. 2002;103(6):476-81.
Hayashi, N., Egami, H., & Ogawa, M. (2002). [Genetics of pancreatic cancer: recent advances in molecular diagnosis]. Nihon Geka Gakkai Zasshi, 103(6), pp. 476-81.
Hayashi N, Egami H, Ogawa M. [Genetics of Pancreatic Cancer: Recent Advances in Molecular Diagnosis]. Nihon Geka Gakkai Zasshi. 2002;103(6):476-81. PubMed PMID: 12094699.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [Genetics of pancreatic cancer: recent advances in molecular diagnosis]. AU - Hayashi,Naoko, AU - Egami,Hiroshi, AU - Ogawa,Michio, PY - 2002/7/4/pubmed PY - 2002/7/18/medline PY - 2002/7/4/entrez SP - 476 EP - 81 JF - Nihon Geka Gakkai zasshi JO - Nihon Geka Gakkai Zasshi VL - 103 IS - 6 N2 - Pancreatic cancer is an important cause of death from cancer throughout the world. Until recently, pancreatic cancer was a poorly understood disease. Research in the past decade has shown conclusively, however, that pancreatic cancer is primarily genetic in nature. Inactivation with a variety of tumor-suppressor genes such as p53, p16, and DPC4, and genome-maintenance genes such as BRCA2, coupled with the activation of oncogenes such as K-ras, are a few of the mutations that trigger the growth of cancerous cells. The genetic profile of pancreatic cancer has reshaped the nomenclature describing histological progression in pancreatic ductal tumorigenesis. K-ras mutations frequently occur early, whereas changes in the expression and genetic integrity of the p16 gene appear in intermediate lesions, and the inactivation of the p53 and DPC4 genes and activation of telomerase occur late in the neoplastic progression. Although the majority of pancreatic cancers occur sporadically, a minority has been shown to aggregate in families and has aided our understanding of pancreatic tumorigenesis. An improved understanding of the genetics of pancreatic cancer should lead to the development of gene-based screening tests and novel rational therapies. SN - 0301-4894 UR - https://www.unboundmedicine.com/medline/citation/12094699/[Genetics_of_pancreatic_cancer:_recent_advances_in_molecular_diagnosis]_ L2 - http://www.diseaseinfosearch.org/result/5551 DB - PRIME DP - Unbound Medicine ER -