Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5607
pubmed:dateCreated
2003-1-31
pubmed:abstractText
Most gastrointestinal stromal tumors (GISTs) have activating mutations in the KIT receptor tyrosine kinase, and most patients with GISTs respond well to Gleevec, which inhibits KIT kinase activity. Here we show that approximately 35% (14 of 40) of GISTs lacking KIT mutations have intragenic activation mutations in the related receptor tyrosine kinase, platelet-derived growth factor receptor alpha (PDGFRA). Tumors expressing KIT or PDGFRA oncoproteins were indistinguishable with respect to activation of downstream signaling intermediates and cytogenetic changes associated with tumor progression. Thus, KIT and PDGFRA mutations appear to be alternative and mutually exclusive oncogenic mechanisms in GISTs.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinases, http://linkedlifedata.com/resource/pubmed/chemical/Protein-Serine-Threonine Kinases, http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-akt, http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-kit, http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Platelet-Derived Growth..., http://linkedlifedata.com/resource/pubmed/chemical/STAT1 Transcription Factor, http://linkedlifedata.com/resource/pubmed/chemical/STAT1 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/STAT3 Transcription Factor, http://linkedlifedata.com/resource/pubmed/chemical/STAT3 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Trans-Activators
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1095-9203
pubmed:author
pubmed:issnType
Electronic
pubmed:day
31
pubmed:volume
299
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
708-10
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:12522257-Animals, pubmed-meshheading:12522257-CHO Cells, pubmed-meshheading:12522257-Chromosome Aberrations, pubmed-meshheading:12522257-Cricetinae, pubmed-meshheading:12522257-DNA-Binding Proteins, pubmed-meshheading:12522257-Enzyme Activation, pubmed-meshheading:12522257-Exons, pubmed-meshheading:12522257-Gastrointestinal Neoplasms, pubmed-meshheading:12522257-Humans, pubmed-meshheading:12522257-Karyotyping, pubmed-meshheading:12522257-Mitogen-Activated Protein Kinases, pubmed-meshheading:12522257-Mutation, pubmed-meshheading:12522257-Oncogenes, pubmed-meshheading:12522257-Phosphorylation, pubmed-meshheading:12522257-Protein-Serine-Threonine Kinases, pubmed-meshheading:12522257-Proto-Oncogene Proteins, pubmed-meshheading:12522257-Proto-Oncogene Proteins c-akt, pubmed-meshheading:12522257-Proto-Oncogene Proteins c-kit, pubmed-meshheading:12522257-Receptor, Platelet-Derived Growth Factor alpha, pubmed-meshheading:12522257-STAT1 Transcription Factor, pubmed-meshheading:12522257-STAT3 Transcription Factor, pubmed-meshheading:12522257-Signal Transduction, pubmed-meshheading:12522257-Trans-Activators
pubmed:year
2003
pubmed:articleTitle
PDGFRA activating mutations in gastrointestinal stromal tumors.
pubmed:affiliation
Department of Medicine, Department of Pathology, Oregon Health & Science University Cancer Institute and Portland VA Medical Center, Portland, OR 97201, USA. heinrich@ohsu.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't