Development of c-Kit-expressing Small-Cell Lung Cancer in a Chronic Myeloid Leukemia Patient During Imatinib Treatment
 

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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. Read more at http://jncicancerspectrum.oxfordjournals.org >>
 

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