克里唑蒂尼
间变性淋巴瘤激酶
医学
碱性抑制剂
癌症研究
肿瘤
病理
基因重排
间充质干细胞
生物
基因
肺癌
遗传学
恶性胸腔积液
作者
James E. Butrynski,David R. D’Adamo,Jason L. Hornick,Paola Dal Cin,Cristina R. Antonescu,Suresh C. Jhanwar,Marc Ladanyi,Marzia Capelletti,Scott J. Rodig,Nikhil H. Ramaiya,Eunice L. Kwak,Jeffrey W. Clark,Keith D. Wilner,James G. Christensen,Pasi A. Jänne,Robert G. Maki,George D. Demetri,Geoffrey I. Shapiro
标识
DOI:10.1056/nejmoa1007056
摘要
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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