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Gene fusion involving the insulin-like growth factor 1 receptor in an ALK-negative inflammatory myofibroblastic tumour.

Artikel i vetenskaplig tidskrift
Författare Giuseppe Piarulli
Florian Puls
Bo Wängberg
Henrik Fagman
Magnus Hansson
Jenny Nilsson
Elsa Arbajian
Fredrik Mertens
Publicerad i Histopathology
Volym 74
Nummer/häfte 7
Sidor 1098-1102
ISSN 1365-2559
Publiceringsår 2019
Publicerad vid
Sidor 1098-1102
Språk en
Länkar dx.doi.org/10.1111/his.13839
www.ncbi.nlm.nih.gov/entrez/query.f...
Ämnesord Adult, Duodenal Neoplasms, diagnostic imaging, genetics, pathology, surgery, Fibronectins, genetics, Gene Fusion, Humans, Inflammation, Male, Myofibroblasts, pathology, Myofibroma, diagnostic imaging, genetics, pathology, surgery, Neoplasms, Muscle Tissue, Receptor, IGF Type 1, genetics, Soft Tissue Neoplasms, diagnostic imaging, genetics, pathology, surgery, Tomography, X-Ray Computed
Ämneskategorier Klinisk medicin, Klinisk laboratoriemedicin

Sammanfattning

Inflammatory myofibroblastic tumour (IMT) is a soft tissue tumour primarily affecting children and young adults. Approximately 50% of IMTs have gene fusions involving the receptor tyrosine kinase (RTK)-encoding ALK gene, providing a molecular rationale for treating IMT patients with unresectable tumours with tyrosine kinase inhibitors (TKI). However, a subset of IMT instead displays fusions affecting other RTKencoding genes, so far including NTRK3, PDGFRB and ROS1. Also, IMTs with variant RTK fusions may respond well to TKI treatment, but can be dif?cult to identify as they are negative for ALK staining at immunohistochemistry, the standard method for detection of ALK rearrangements.We used RNA-sequencing to search for alternate fusion events in an ALK-negative IMT.We found a novel fusion gene - FN1-IGF1R. The FN1 gene, encoding ?bronectin, is thought to provide a strong promoter activity for the kinase domain of the RTK insulin-like growth factor 1 receptor, a mechanism similar to previously described RTK fusions in IMT.

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