Somatic loss of function mutations in neurofibromin 1 and MYC associated factor X genes identified by exome-wide sequencing in a wild-type GIST case

  • Approximately 10–15 % of gastrointestinal stromal tumors (GISTs) lack gain of function mutations in the KIT and platelet-derived growth factor receptor alpha (PDGFRA) genes. An alternate mechanism of oncogenesis through loss of function of the succinate-dehydrogenase (SDH) enzyme complex has been identified for a subset of these “wild type” GISTs.

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Metadaten
Author:Martin G. Belinsky, Lori Rink, Kathy Q. Cai, Stephen J. Capuzzi, Yen Hoang, Jeremy Chien, Andrew K. Godwin, Margaret von Mehren
URN:urn:nbn:de:kobv:526-opus4-6292
DOI:https://doi.org/10.1186/s12885-015-1872-y
ISSN:1471-2407
Parent Title (English):BMC Cancer
Document Type:Article
Language:English
Year of Publication:2015
Publishing Institution:Technische Hochschule Wildau
Release Date:2016/07/05
Tag:KIT; MAX; NF1; PDGFRA; gastrointestinal stromal tumor (GIST); succinate dehydrogenase (SDH); wild type
Volume:15
Issue:887
Source:Belinsky et al. Somatic loss of function mutations in neurofibromin 1 and MYC associated factor X genes identified by exome-wide sequencing in a wild-type GIST case. BMC Cancer (2015) 15:887
Faculties an central facilities:Fachbereich Ingenieur- und Naturwissenschaften
Dewey Decimal Classification:6 Technik, Medizin, angewandte Wissenschaften / 61 Medizin und Gesundheit / 616 Krankheiten
Licence (German):Creative Commons - CC BY - Namensnennung 4.0 International
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