TY - JOUR
T1 - Imatinib resistance in gastrointestinal stromal tumors
AU - Chen, Lei L.
AU - Sabripour, Mahyar
AU - Andtbacka, Robert H.I.
AU - Patel, Shreyaskumar R.
AU - Feig, Barry W.
AU - Macapinlac, Homer A.
AU - Choi, Haesun
AU - Wu, Elsie F.
AU - Frazier, Marsha L.
AU - Benjamin, Robert S.
N1 - Funding Information:
We thank W.K. Hong for divisional support, L.A. Gratten for manuscript preparation, and T.A. Simmons for clinical data preparation. M.S. was supported in part by cancer prevention fellowships funded by National Cancer Institute grant R25 CA57730 (principal investigator R.M. Chamberlain). Other support includes an Institutional Research Grant from the University of Texas M.D. Anderson Cancer Center, National Cancer Institute grants CA16672 (supporting the DNA sequencing core facility, nucleic acid core facility, and tissue procurement and banking facility), U01-CA70172-01, N0-CM-17003, and the Goodwin Foundation.
PY - 2005/7
Y1 - 2005/7
N2 - Conventional chemotherapeutic drugs are ineffective in treatment of gastrointestinal stromal tumors (GISTs). Imatinib (STI571, Gleevec, Glivec; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, ABL, BCR-ABL, PDGFRA, and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs. Unfortunately, imatinib resistance has emerged. The reported mechanism of imatinib resistance in GISTs involves missense mutation in the kinase domain of KIT, including Thr670IIe, Tyr823Asp, and Val654Ala. The established mechanisms and potential mechanisms of imatinib resistance in GISTs, the imaging studies indicative of early development of imatinib resistance, and the management of imatinib-resistant GISTs are discussed.
AB - Conventional chemotherapeutic drugs are ineffective in treatment of gastrointestinal stromal tumors (GISTs). Imatinib (STI571, Gleevec, Glivec; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, ABL, BCR-ABL, PDGFRA, and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs. Unfortunately, imatinib resistance has emerged. The reported mechanism of imatinib resistance in GISTs involves missense mutation in the kinase domain of KIT, including Thr670IIe, Tyr823Asp, and Val654Ala. The established mechanisms and potential mechanisms of imatinib resistance in GISTs, the imaging studies indicative of early development of imatinib resistance, and the management of imatinib-resistant GISTs are discussed.
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U2 - 10.1007/s11912-005-0053-6
DO - 10.1007/s11912-005-0053-6
M3 - Review article
C2 - 15946589
AN - SCOPUS:23444437980
SN - 1523-3790
VL - 7
SP - 293
EP - 299
JO - Current oncology reports
JF - Current oncology reports
IS - 4
ER -