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Genetic alterations in human pancreatic cancer
Author(s) -
Murakami Yoshinori
Publication year - 1997
Publication title -
journal of hepato‐biliary‐pancreatic surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.63
H-Index - 60
eISSN - 1868-6982
pISSN - 0944-1166
DOI - 10.1007/bf02489026
Subject(s) - pancreatic cancer , carcinogenesis , cancer research , gene , biology , germline , malignancy , germline mutation , point mutation , mutation , tumor suppressor gene , cancer , pancreas , genetics , endocrinology
Pancreatic cancers, like many other solid tumors in humans, develop and progress toward malignancy through accumulation of multiple genetic alterations. Previous studies demonstrated that point mutations of the c‐K‐ ras gene and inactivation of the p53 gene were frequent events in human pancreatic cancers. The high incidence of mutation at codon 12 of the c‐K‐ ras gene, which is detectable even in early stages of pancreatic tumors by means of the polymerase chain reaction, could make this codon an appropriate target for sensitive diagnosis. We now have evidence that inactivation of MTS1 (p16), DPC4 , and BRCA2 tumor suppressor genes, as well as amplification of the AKT2 gene, is also involved in human pancreatic cancers. Moreover, pancreatic cancers develop in some cancer‐prone individuals who carry germline mutations of the p53, MTS1 (p16) , or BRCA2 genes. Further elucidation of the molecular mechanism of each step of pancreatic carcinogenesis is essential for prevention, early diagnosis, and treatment of human pancreatic cancers.