Fusion of the ALK gene to the clathrin heavy chain gene, CLTC, in inflammatory myofibroblastic tumor

被引：238

作者：

Bridge, JA

Kanamori, M

Ma, ZG

Pickering, D

Hill, DA

Lydiatt, W

Lui, MY

Colleoni, GWB

Antonescu, CR

Ladanyi, M

Morris, SW

机构：

[1] Univ Nebraska, Med Ctr, Dept Pathol, Omaha, NE 68198 USA

[2] Univ Nebraska, Med Ctr, Dept Pediat, Omaha, NE 68198 USA

[3] Univ Nebraska, Med Ctr, Dept Orthopaed Surg, Omaha, NE 68198 USA

[4] Univ Nebraska, Med Ctr, Dept Otolaryngol, Ctr Human Mol Genet, Omaha, NE 68198 USA

[5] St Jude Childrens Res Hosp, Dept Pathol, Memphis, TN 38105 USA

[6] St Jude Childrens Res Hosp, Dept Hematol Oncol, Memphis, TN 38105 USA

[7] Univ Tennessee, Coll Med, Dept Pediat, Memphis, TN 38163 USA

[8] Mem Sloan Kettering Canc Ctr, Dept Pathol, New York, NY 10021 USA

来源：

AMERICAN JOURNAL OF PATHOLOGY | 2001年 / 159卷 / 02期

关键词：

D O I：

10.1016/S0002-9440(10)61711-7

中图分类号：

R36 [病理学];

学科分类号：

100104 ;

摘要：

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)].

引用

页码：411 / 415

页数：5

共 22 条

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