ArticleScientific reports2024
NTRK2 expression in gastrointestinal stromal tumors with a special emphasis on the clinicopathological and prognostic impacts.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 7 citations in OpenAlex.
- A Systematic Review with a Demonstrative Case of KIT and DOG-1 Expressing Gastrointestinal Stromal Tumors Harboring ETV6-NTRK3 Fusions.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Pooled it
- Comparison of nomograms and predictive tools in gastrointestinal stromal tumor.Journal of gastrointestinal oncology · 2026Article
- Nitric oxide inhibition ameliorates cortical proteomic changes in the Cntnap2Molecular autism · 2026Article
- Potential Involvement of Myostatin in Smooth Muscle Differentiation in Pleomorphic Leiomyosarcoma.International journal of molecular sciences · 2025Article
- A case of quadruple wild-type gastrointestinal stromal tumor with CDC42BPB::NTRK3 fusion and abundant lymphoid infiltration.Diagnostic pathology · 2025Article
- Differential diagnosis of gastrointestinal stromal tumors versus leiomyomas by special stains.BMC gastroenterology · 2024Article
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Authors and funding
21 authors at 4 institutions in 2 countries.
Funding
Abstract
Gastrointestinal stromal tumors (GISTs) are typically characterized by activating mutations of the KIT proto-oncogene receptor tyrosine kinase (KIT) or platelet-derived growth factor receptor alpha (PDGFRA). Recently, the neurotrophic tyrosine receptor kinase (NTRK) fusion was reported in a small subset of wild-type GIST. We examined trk IHC and NTRK gene expressions in GIST. Pan-trk immunohistochemistry (IHC) was positive in 25 (all 16 duodenal and 9 out of 16 small intestinal GISTs) of 139 cases, and all pan-trk positive cases showed diffuse and strong expression of c-kit. Interestingly, all of these cases showed only trkB but not trkA/trkC expression. Cap analysis of gene expression (CAGE) analysis identified increased number of genes whose promoters were activated in pan-trk/trkB positive GISTs. Imbalanced expression of NTRK2, which suggests the presence of NTRK2 fusion, was not observed in any of trkB positive GISTs, despite higher mRNA expression. TrkB expression was found in duodenal GISTs and more than half of small intestinal GISTs, and this subset of cases showed poor prognosis. However, there was not clear difference in clinical outcomes according to the trkB expression status in small intestinal GISTs. These findings may provide a possible hypothesis for trkB overexpression contributing to the tumorigenesis and aggressive clinical outcome in GISTs of duodenal origin.
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