|Genetic alterations of K-ras, p53, c-erbB-2, and DPC4 in pancreatic ductal adenocarcinoma and their correlation with patient survival.|
|PMID: 23344532 Owner: NLM Status: MEDLINE|
|OBJECTIVES: The objective of this study was to evaluate genetic alterations of K-ras, p53, c-erbB-2, and deleted in pancreatic cancer, locus 4 (DPC4) genes in pancreatic ductal adenocarcinoma and correlate these changes with patients' overall survival.
METHODS: Between April 2004 and December 2008, 272 patients with pancreatic ductal adenocarcinoma underwent surgical resection at a single institute. Genetic analyses and immunohistochemical stains were reviewed retrospectively.
RESULTS: Alterational rates of each gene were as follows: K-ras, 53.8%; p53, 38.2%; c-erbB-2, 7.3%; DPC4, 81.6%. Subtypes of K-ras gene were as follows: GGT (wild type), 46.2%; GAT, 31.2%; GTT, 14.5%; CGT, 5.6%; TGT, 1.7%; CTG, 0.4%; AGT, 0.4%. K-ras mutation (especially GAT subtype) and DPC4 inactivation resulted in a reduction of postresection survival (P = 0.001 and P = 0.047). Univariate analysis revealed 8 factors affecting to the survival, and multivariate analysis revealed that 6 of them were independently responsible for poor survival of patients: presence of lymphovascular tumor emboli, DPC4 inactivation, poorly differentiated carcinoma, K-ras mutation, presence of lymph node metastasis, and elevated CA-19-9 (>37 U/mL).
CONCLUSIONS: This study may help to understand the genetic feature of pancreatic cancer and its survival effect in our population. This shows that additional genetic insights would contribute to the improvement of patients' prognosis.
|Sang Hyun Shin; Song Cheol Kim; Seung-Mo Hong; Young Hoon Kim; Ki-Byung Song; Kwang-Min Park; Young-Joo Lee|
|Type: Journal Article|
|Title: Pancreas Volume: 42 ISSN: 1536-4828 ISO Abbreviation: Pancreas Publication Date: 2013 Mar|
|Created Date: 2013-04-05 Completed Date: 2013-07-22 Revised Date: 2014-01-28|
Medline Journal Info:
|Nlm Unique ID: 8608542 Medline TA: Pancreas Country: United States|
|Languages: eng Pagination: 216-22 Citation Subset: IM|
|APA/MLA Format Download EndNote Download BibTex|
CA-19-9 Antigen / blood
Carcinoma, Pancreatic Ductal / blood, enzymology, genetics*, mortality, pathology, surgery
DNA Mutational Analysis
Genetic Predisposition to Disease
Pancreatic Neoplasms / blood, enzymology, genetics*, mortality, pathology, surgery
Polymerase Chain Reaction
Proportional Hazards Models
Proto-Oncogene Proteins / genetics*
Receptor, erbB-2 / analysis, genetics*
Republic of Korea / epidemiology
Smad4 Protein / analysis, genetics*
Tumor Markers, Biological / blood, genetics*
Tumor Suppressor Protein p53 / analysis, genetics*
ras Proteins / genetics*
|0/CA-19-9 Antigen; 0/KRAS protein, human; 0/Proto-Oncogene Proteins; 0/SMAD4 protein, human; 0/Smad4 Protein; 0/TP53 protein, human; 0/Tumor Markers, Biological; 0/Tumor Suppressor Protein p53; EC 22.214.171.124/ERBB2 protein, human; EC 126.96.36.199/Receptor, erbB-2; EC 188.8.131.52/ras Proteins|
|Pancreas. 2014 Jan;43(1):150-2
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: Acute Cholecystitis in the Late Phase of Severe Acute Pancreatitis: A Neglected Problem.
Next Document: Regulatory networks defining EMT during cancer initiation and progression.