Crizotinib in ALK-Rearranged Inflammatory Myofibroblastic Tumor

被引:635
作者
Butrynski, James E. [1 ,2 ]
D'Adamo, David R. [5 ]
Hornick, Jason L. [2 ,3 ]
Dal Cin, Paola [3 ]
Antonescu, Cristina R. [5 ]
Jhanwar, Suresh C. [5 ]
Ladanyi, Marc [5 ]
Capelletti, Marzia [2 ]
Rodig, Scott J. [2 ,3 ]
Ramaiya, Nikhil
Kwak, Eunice L. [2 ,4 ]
Clark, Jeffrey W. [2 ,4 ]
Wilner, Keith D. [6 ]
Christensen, James G. [6 ]
Jaenne, Pasi A. [2 ]
Maki, Robert G. [5 ]
Demetri, George D. [1 ,2 ]
Shapiro, Geoffrey I. [2 ,7 ]
机构
[1] Dana Farber Harvard Canc Ctr, Ludwig Ctr, Boston, MA 02115 USA
[2] Harvard Univ, Sch Med, Boston, MA USA
[3] Brigham & Womens Hosp, Boston, MA 02115 USA
[4] Massachusetts Gen Hosp, Boston, MA 02114 USA
[5] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA
[6] Pfizer Global Res & Dev, La Jolla, CA USA
[7] Dana Farber Canc Inst, Early Drug Dev Ctr, Boston, MA 02115 USA
基金
美国国家卫生研究院;
关键词
ANAPLASTIC LYMPHOMA; KINASE; EXPRESSION; INHIBITOR; IMATINIB; FUSION; 2P23; GENE;
D O I
10.1056/NEJMoa1007056
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
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.
引用
收藏
页码:1727 / 1733
页数:7
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