Heinrich, Michael C.;
Corless, Christopher L.;
Duensing, Anette;
McGreevey, Laura;
Chen, Chang-Jie;
Joseph, Nora;
Singer, Samuel;
Griffith, Diana J.;
Haley, Andrea;
Town, Ajia;
Demetri, George D.;
Fletcher, Christopher D. M.;
Fletcher, Jonathan A.
PDGFRA Activating Mutations in Gastrointestinal Stromal Tumors
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Medientyp:
E-Artikel
Titel:
PDGFRA Activating Mutations in Gastrointestinal Stromal Tumors
Beteiligte:
Heinrich, Michael C.;
Corless, Christopher L.;
Duensing, Anette;
McGreevey, Laura;
Chen, Chang-Jie;
Joseph, Nora;
Singer, Samuel;
Griffith, Diana J.;
Haley, Andrea;
Town, Ajia;
Demetri, George D.;
Fletcher, Christopher D. M.;
Fletcher, Jonathan A.
Erschienen:
American Association for the Advancement of Science (AAAS), 2003
Beschreibung:
<jats:p>
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 ∼35% (14 of 40) of GISTs lacking
<jats:italic>KIT</jats:italic>
mutations have intragenic activation mutations in the related receptor tyrosine kinase, platelet-derived growth factor receptor α (
<jats:italic>PDGFRA</jats:italic>
). Tumors expressing KIT or PDGFRA oncoproteins were indistinguishable with respect to activation of downstream signaling intermediates and cytogenetic changes associated with tumor progression. Thus,
<jats:italic>KIT</jats:italic>
and
<jats:italic>PDGFRA</jats:italic>
mutations appear to be alternative and mutually exclusive oncogenic mechanisms in GISTs.
</jats:p>