Crizotinib in<i>ALK</i>-Rearranged Inflammatory Myofibroblastic Tumor

James E. Butrynski(Dana-Farber Cancer Institute), David R. D’Adamo(Memorial Sloan Kettering Cancer Center), Jason L. Hornick(Harvard University), Paola Dal Cin(Brigham and Women's Hospital), Cristina R. Antonescu(Memorial Sloan Kettering Cancer Center), Suresh C. Jhanwar(Memorial Sloan Kettering Cancer Center), Marc Ladanyi(Memorial Sloan Kettering Cancer Center), Marzia Capelletti(Harvard University), Scott J. Rodig(Harvard University), Nikhil H. Ramaiya(Dana-Farber Cancer Institute), Eunice L. Kwak(Massachusetts General Hospital), Jeffrey W. Clark(Massachusetts General Hospital), Keith D. Wilner(Pfizer (United States)), James G. Christensen(Pfizer (United States)), Pasi A. Jänne(Dana-Farber Cancer Institute), Robert G. Maki(Memorial Sloan Kettering Cancer Center), George D. Demetri(Dana-Farber Cancer Institute), Geoffrey I. Shapiro(Dana-Farber Cancer Institute)
New England Journal of Medicine
October 27, 2010
10.1056/nejmoa1007056
Cited by 862

Abstract

Inflammatory myofibroblastic tumor (IMT) is a distinctive mesenchymal neoplasm characterized by a spindle-cell proliferation with an inflammatory infiltrate. Approximately half of IMTs carry rearrangements of the anaplastic lymphoma kinase (ALK) locus on chromosome 2p23, causing aberrant ALK expression. We report a sustained partial response to the ALK inhibitor crizotinib (PF-02341066, Pfizer) in a patient with ALK-translocated IMT, as compared with no observed activity in another patient without the ALK translocation. These results support the dependence of ALK-rearranged tumors on ALK-mediated signaling and suggest a therapeutic strategy for genomically identified patients with the aggressive form of this soft-tissue tumor. (Funded by Pfizer and others; ClinicalTrials.gov number, NCT00585195.).

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