Journal
LABORATORY INVESTIGATION
Volume 86, Issue 10, Pages 981-986Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/labinvest.3700466
Keywords
gastrointestinal stromal tumor; small molecule inhibitors; resistance; KIT; non-small-cell lung cancer; EGFR
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A growing number of tumors are characterized by simple genetic changes that activate important biochemical pathways, which are involved in their pathogenesis. These findings have led to the concept of targeted small molecule inhibitor treatment. The prototype for this type of therapy has been treatment of chronic myelogenous leukemia with imatinib mesylate (Gleevec), which targets BCR-ABL kinase. More recently, imatinib has been used to inhibit KIT in gastrointestinal (GI) stromal tumor, a mesenchymal tumor that arises in the GI tract. Furthermore, it has been possible to target EGFR in non-small-cell lung cancer with gefitinib and erlotinib. While initial results have been encouraging, resistance to small molecule kinase inhibitors is a substantial drawback. This paper focuses on what is known about mechanisms of resistance in the treatment of solid tumors by small molecule kinase inhibitors.
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