Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2007-4-17
pubmed:abstractText
In recent years, immunohistochemical staining for KIT (CD117) has become integral to the diagnosis of gastrointestinal stromal tumors (GISTs), nearly 90% of which harbor activating mutations in the KIT receptor tyrosine kinase gene. Approximately 80% of patients with metastatic GIST show at least some clinical response to the targeted small molecule KIT inhibitor imatinib. The response to imatinib is closely correlated with the presence and type of KIT mutation. GISTs with the most common KIT exon 11 mutations have the highest response rate by far, whereas GISTs lacking mutations in KIT or the alternative receptor tyrosine kinase PDGFRA show much lower rates of response to imatinib. Less than 5% of GISTs are KIT-immunonegative; and many of these tumors have activating mutations of PDGFRA, some of which are also inhibited by imatinib. Most patients who initially respond to imatinib become resistant and eventually progress, which coincides with the selection of imatinib-resistant secondary KIT mutations in the kinase domain. Sunitinib has recently been approved for patients with GIST, principally those who fail imatinib therapy; and additional small molecule inhibitors are in the pipeline. It is becoming evident that alternative approaches to direct KIT inhibition will be required for long-term survival of patients with advanced GISTs. This review examines the role of KIT in the diagnosis and management of patients with GIST.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0046-8177
pubmed:author
pubmed:issnType
Print
pubmed:volume
38
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
679-87
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
The role of KIT in the management of patients with gastrointestinal stromal tumors.
pubmed:affiliation
Department of Pathology, Brigham and Women's Hospital Boston, MA 02115, USA.
pubmed:publicationType
Journal Article, Review