pubmed-article:9641496 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:9641496 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
pubmed-article:9641496 | lifeskim:mentions | umls-concept:C0030274 | lld:lifeskim |
pubmed-article:9641496 | lifeskim:mentions | umls-concept:C0026882 | lld:lifeskim |
pubmed-article:9641496 | lifeskim:mentions | umls-concept:C0221198 | lld:lifeskim |
pubmed-article:9641496 | lifeskim:mentions | umls-concept:C0334094 | lld:lifeskim |
pubmed-article:9641496 | lifeskim:mentions | umls-concept:C0205234 | lld:lifeskim |
pubmed-article:9641496 | pubmed:issue | 6 | lld:pubmed |
pubmed-article:9641496 | pubmed:dateCreated | 1998-8-31 | lld:pubmed |
pubmed-article:9641496 | pubmed:abstractText | The K-ras gene is mutated in > or =75% of human pancreatic adenocarcinomas and in a number of hyperplastic ductal lesions from noncarcinoma patients. In this study, the incidence of K-ras mutation was determined in a spectrum of focal proliferative pancreatic lesions to evaluate their preneoplastic significance. PCR-based mutation-enriched RFLP analysis was used to identify mutations in codon 12. Immunostaining for Ki67 and p53 was also performed. Forty-seven % of intraductal nonpapillary hyperplasias (8 of 17) contained codon 12 mutations, as did 55% of adenomatoid hyperplasias (6 of 11). This rate increased to 61% in papillary hyperplasias (27 of 44) and to 78% when there was severe dysplasia (7 of 9). The fraction of cells staining for the Ki67 proliferation marker showed a general correlation with the rate of K-ras mutation. Nuclear staining for p53 protein was seen only in two ductal lesions with severe dysplasia. No mutations were found in normal acinar tissue (n = 38), squamous metaplasia (n = 13), ductal complexes (n = 8), or focal acinar cell dysplasia (n = 5). There seemed to be a general correlation of proliferative potential with the presence of K-ras mutation in ductal lesions. However, because of the high prevalence of lesions with K-ras mutations, we conclude that this mutation alone cannot be taken as proof of significant risk for progression to carcinoma. Efforts to use the presence of K-ras mutations in DNA harvested from pancreatic juice or duodenal aspirates as an approach for diagnosis of occult pancreatic carcinoma seem vulnerable to a high false-positive rate. | lld:pubmed |
pubmed-article:9641496 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9641496 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9641496 | pubmed:language | eng | lld:pubmed |
pubmed-article:9641496 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9641496 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:9641496 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9641496 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9641496 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:9641496 | pubmed:month | Jun | lld:pubmed |
pubmed-article:9641496 | pubmed:issn | 1055-9965 | lld:pubmed |
pubmed-article:9641496 | pubmed:author | pubmed-author:LongneckerD... | lld:pubmed |
pubmed-article:9641496 | pubmed:author | pubmed-author:TostesonT DTD | lld:pubmed |
pubmed-article:9641496 | pubmed:author | pubmed-author:TerhuneP GPG | lld:pubmed |
pubmed-article:9641496 | pubmed:author | pubmed-author:PhiferD MDM | lld:pubmed |
pubmed-article:9641496 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:9641496 | pubmed:volume | 7 | lld:pubmed |
pubmed-article:9641496 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:9641496 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:9641496 | pubmed:pagination | 515-21 | lld:pubmed |
pubmed-article:9641496 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
pubmed-article:9641496 | pubmed:meshHeading | pubmed-meshheading:9641496-... | lld:pubmed |
pubmed-article:9641496 | pubmed:meshHeading | pubmed-meshheading:9641496-... | lld:pubmed |
pubmed-article:9641496 | pubmed:meshHeading | pubmed-meshheading:9641496-... | lld:pubmed |
pubmed-article:9641496 | pubmed:meshHeading | pubmed-meshheading:9641496-... | lld:pubmed |
pubmed-article:9641496 | pubmed:meshHeading | pubmed-meshheading:9641496-... | lld:pubmed |
pubmed-article:9641496 | pubmed:meshHeading | pubmed-meshheading:9641496-... | lld:pubmed |
pubmed-article:9641496 | pubmed:meshHeading | pubmed-meshheading:9641496-... | lld:pubmed |
pubmed-article:9641496 | pubmed:meshHeading | pubmed-meshheading:9641496-... | lld:pubmed |
pubmed-article:9641496 | pubmed:meshHeading | pubmed-meshheading:9641496-... | lld:pubmed |
pubmed-article:9641496 | pubmed:meshHeading | pubmed-meshheading:9641496-... | lld:pubmed |
pubmed-article:9641496 | pubmed:meshHeading | pubmed-meshheading:9641496-... | lld:pubmed |
pubmed-article:9641496 | pubmed:year | 1998 | lld:pubmed |
pubmed-article:9641496 | pubmed:articleTitle | K-ras mutation in focal proliferative lesions of human pancreas. | lld:pubmed |
pubmed-article:9641496 | pubmed:affiliation | Department of Pathology, Dartmouth Medical School, Lebanon, New Hampshire 03756, USA. | lld:pubmed |
pubmed-article:9641496 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:9641496 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:9641496 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:9641496 | lld:pubmed |
http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:9641496 | lld:pubmed |
http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:9641496 | lld:pubmed |
http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:9641496 | lld:pubmed |
http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:9641496 | lld:pubmed |
http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:9641496 | lld:pubmed |
http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:9641496 | lld:pubmed |