J. Natl. Cancer Inst. 2004, 96, 1723-24.
Carlo Gambacorti-Passerini, Rocco
Piazza, Lucia Tornaghi,
Silvana Pilotti, Enrico Pogliani
Affiliations of authors: University of Milano Bicocca/National Cancer
Institute, Milan, Italy, and McGill University, Montreal, Canada (CG);
University of Milano Bicocca, Milan, Italy (RP); National Cancer Institute
Milano and San Gerardo Hospital, Monza (LT); National Cancer Institute,
Milan (SP); University of Milano Bicocca and San Gerardo Hospital, Monza,
Italy (EP)
Correspondence to: Carlo Gambacorti-Passerini, MD, University of Milano
Bicocca C/O National Cancer Institute, Via Venezian 1, 20133 Milano, Italy
(e-mail:
carlo.gambacorti@Istitutotumori.mi.it)
Imatinib inhibits the activities of three oncogenic tyrosine kinases—Abl,
c-Kit, and platelet-derived growth factor receptor (PDGFR)—with similar
affinity. Imatinib exerts important clinical activities in cancers in which
any of these three tyrosine kinases play a causal role in the transformation
process (e.g., Abl and chronic myeloid leukemia [CML]) (1–3). In particular,
imatinib has marked clinical activity in patients affected by
gastrointestinal stromal tumors (GIST), a type of cancer frequently caused
by activating mutations of c-KIT; in this setting, the presence of c-KIT
mutations are an important predictor of the clinical response to imatinib.
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