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(American Journal of Pathology. 2001;159:411-415.)
© 2001 American Society for Investigative Pathology

Short Communications

Fusion of the ALK Gene to the Clathrin Heavy Chain Gene, CLTC, in Inflammatory Myofibroblastic Tumor

Julia A. Bridge*{dagger}{ddagger}, Masahiko Kanamori*, Zhigui Ma§, Diane Pickering{dagger}, D. Ashley Hill§, William Lydiatt, Man Yee Lui||, Gisele W. B. Colleoni||, Cristina R. Antonescu||, Marc Ladanyi|| and Stephan W. Morris§**{dagger}{dagger}

From the Departments of Pathology,*
Pediatrics,{dagger}
Orthopaedic Surgery,{ddagger}
and Otolaryngology,
Center for Human Molecular Genetics, University of Nebraska Medical Center, Omaha, Nebraska; the Departments of Pathology§
and Hematology-Oncology,**
St. Jude Children’s Research Hospital, Memphis, Tennessee; the Department of Pediatrics,{dagger}{dagger}
University of Tennessee, College of Medicine, Memphis, Tennessee; and the Department of Pathology,||
Memorial Sloan-Kettering Cancer Center, New York, New York

Inflammatory myofibroblastic tumor (IMT) is a rare, but distinctive mesenchymal neoplasm composed of fascicles of bland myofibroblasts admixed with a prominent inflammatory component. Genetic studies of IMTs have demonstrated chromosomal abnormalities of 2p23 and rearrangement of the anaplastic lymphoma kinase (ALK) gene locus. In a subset of IMTs, the ALK C-terminal kinase domain is fused with a tropomyosin N-terminal coiled-coil domain. In the current study, fusion of ALK with the clathrin heavy chain (CTLC) gene localized to 17q23 was detected in two cases of IMT. One of these cases exhibited a 2;17 translocation in addition to other karyotypic anomalies [46,XX,t(2;17)(p23;q23),add(16)(q24)].




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