Linked Life Data

12209587

Source:http://linkedlifedata.com/resource/pubmed/id/12209587

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2002-9-4
pubmed:databankReference
pubmed:abstractText
Non-small cell lung cancers have a high incidence of somatic mutations of the beta-tubulin (class I) gene, suggesting involvement in the acquisition of resistance to taxanes, which exert their effects through binding to beta-tubulin. Since taxanes are often used in the treatment of breast cancer, we carried out a mutational analysis of the class I beta-tubulin (GenBank accession AF070600) gene in breast cancer. We paid special attention to the primer design so as not to amplify the pseudogenes. We identified 1 somatic mutation, codon 306 [Arg (CGC) to Cys (TGC)], and 2 genetic polymorphisms, codon 217 [Leu (CTG) to Leu (CTA)] and (C to T) at 57 bases downstream from exon 4. Our results suggest that acquisition of resistance to taxanes is unlikely to be explained by somatic mutations of the class I beta-tubulin gene in most breast cancers. In addition, the overestimation of the incidence of somatic mutations of the class I beta-tubulin gene due to the pseudogenes is discussed.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0020-7136
pubmed:author
pubmed:copyrightInfo
Copyright 2002 Wiley-Liss, Inc.
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
101
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
46-51
pubmed:dateRevised
2007-7-24
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Mutational analysis of the class I beta-tubulin gene in human breast cancer.
pubmed:affiliation
Department of Surgery and Clinical Oncology, Graduate School of Medicine, Osaka University, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't