Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9305
pubmed:dateCreated
2002-2-20
pubmed:abstractText
BCR-ABL, a constitutively activated tyrosine kinase, is the oncogene that causes Philadelphia-chromosome-positive (Ph+) leukaemia. STI571, a competitive inhibitor at the ATP-binding site of BCR-ABL, has been shown to have high activity in this type of leukaemia. However, most patients with advanced disease relapse despite continued treatment with STI571. We aimed to find out whether point mutations in BCR-ABL cause resistance to STI571.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0140-6736
pubmed:author
pubmed:issnType
Print
pubmed:day
9
pubmed:volume
359
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
487-91
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
BCR-ABL gene mutations in relation to clinical resistance of Philadelphia-chromosome-positive leukaemia to STI571: a prospective study.
pubmed:affiliation
Department of Internal Medicine III, Laboratory of Leukemogenesis, Technical University of Munich, Ismaningerstrasse 22, 81675, Munich, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't