ArticleWorld journal of gastroenterology2004
Detection of point mutation in K-ras oncogene at codon 12 in pancreatic diseases.
Article in World journal of gastroenterology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 24 citations in OpenAlex.
- Molecular Targeted Intervention for Pancreatic Cancer.Cancers · 2015Review
- Metformin suppresses pancreatic tumor growth with inhibition of NFκB/STAT3 inflammatory signaling.Pancreas · 2015Article
- Endogenous n-3 polyunsaturated fatty acids delay progression of pancreatic ductal adenocarcinoma in Fat-1-p48(Cre/+)-LSL-Kras(G12D/+) mice.Neoplasia (New York, N.Y.) · 2012Article
- Atorvastatin delays progression of pancreatic lesions to carcinoma by regulating PI3/AKT signaling in p48Cre/+ LSL-KrasG12D/+ mice.International journal of cancer · 2012Article
- Inhibition of pancreatic intraepithelial neoplasia progression to carcinoma by nitric oxide-releasing aspirin in p48(Cre/+)-LSL-Kras(G12D/+) mice.Neoplasia (New York, N.Y.) · 2012Article
- Ras activity in acinar cells links chronic pancreatitis and pancreatic cancer.Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association · 2009Review
- Molecular analysis of the EGFR-RAS-RAF pathway in pancreatic ductal adenocarcinomas: lack of mutations in the BRAF and EGFR genes.Virchows Archiv : an international journal of pathology · 2006Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo investigate frequency and clinical significance of K-ras mutations in pancreatic diseases and to identify its diagnostic values in pancreatic carcinoma.
methods117 ductal lesions were identified in the available sections from pancreatic resection specimens of pancreatic ductal adenocarcinoma, comprising 24 pancreatic ductal adenocarcinoma, 19 peritumoral ductal atypical hyperplasia, 58 peritumoral ductal hyperplasia and 19 normal duct at the tumor free resection margin. 24 ductal lesions were got from 24 chronic pancreatitis. DNA was extracted. Codon 12 K-ras mutations were examined using the two-step polymerase chain reaction (PCR) combined with restriction enzyme digestion, followed by nonradioisotopic single-strand conformation polymorphism (SSCP) analysis and by means of automated DNA sequencing.
resultsK-ras mutation rate of the pancreatic carcinoma was 79%(19/24) which was significantly higher than that in the chronic pancreatitis 33%(8/24) (P<0.01). It was also found that K-ras mutation rate was progressively increased from normal duct at the tumor free resection margin, peritumoral ductal hyperplasia, peritumoral ductal atypical hyperplasia to pancreatic ductal adenocarcinoma. The mutation pattern of K-ras 12 codon of chronic pancreatitis was GGT-GAT, GGT and CGT, which is identical to that in pancreatic carcinoma.
conclusionK-ras mutation may play a role in the malignant transformation of pancreatic ductal cell. K-ras mutation was not specific enough to diagnose pancreatic carcinoma.
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