Ask about this productRelated genes to: NTRK3 antibody
- Gene:
- NTRK3 NIH gene
- Name:
- neurotrophic receptor tyrosine kinase 3
- Previous symbol:
- -
- Synonyms:
- TRKC
- Chromosome:
- 15q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 1991-07-18
- Date modifiied:
- 2016-10-05
Related products to: NTRK3 antibody
Related articles to: NTRK3 antibody
- NTRK gene fusions are established oncogenic drivers in a diverse spectrum of mesenchymal neoplasms. Although classically described in pediatric entities, NTRK-rearranged sarcomas also occur in adults, where their clinicopathologic features, genomic context, and response to TRK inhibition are less well characterized. - Source: PubMed
Publication date: 2026/08/06
Schwartz MichaelSweeney KieranSmith Steven CAngara KartikReynolds CeliaPappo Alberto SElliott AndrewOberley Matthew JEvans Mark GBahrami Armita - TRK inhibitors (TRKis) have transformed the therapeutic landscape for patients with neurotrophic tyrosine receptor kinase () gene fusion-positive tumors. However, approval of TRKis is based on evidence derived mainly from small, pooled, single-arm clinical trial cohorts. The REALTRK registry aims to describe real-world molecular diagnostic practices, treatment patterns, and clinical outcomes for adult patients with fusion-positive cancers. - Source: PubMed
Publication date: 2026/08/04
Potthoff KarinLange SebastianSeufferlein ThomasHeinrich KathrinClaus RainerBleckmann AnnalenZaiss MatthiasVannier CorinneGrebhardt SinaKoszinowski SophieHillebrand Larissa ERingwald KaiKasenda Benjamin - The BRAF mutation is a common driver variant in differentiated thyroid carcinoma (DTC); however, the clinical significance of its co-mutation patterns in the Chinese population remains unclear. This study aimed to analyze the predictive value of BRAF co-mutations for aggressive clinicopathological features in DTC by detecting a 10-gene panel, providing molecular evidence for refined risk stratification. - Source: PubMed
Publication date: 2026/08/05
Du JingGuo BoZhang YunpengGuo SongyanYang Fan - Inflammatory myofibroblastic tumour (IMT) is a mesenchymal tumour characterised by myofibroblastic cells and the presence of inflammatory cells, such as macrophages, neutrophils, and lymphocytes. IMT can originate from diverse anatomical locations within the body. The macrophage-rich immune microenvironment contributes to cytokine release and inflammation, but IMT is primarily driven by oncogenic alterations. Oncogenic fusions, most commonly involving anaplastic lymphoma kinase (ALK), and other genes, such as ROS1 and NTRK3, are seen in most IMTs. Upregulation of these genes activates downstream signalling pathways such as RAS/MAPK and PI3K/AKT, leading to uncontrolled cell proliferation. Constitutive tyrosine kinase activation disrupts cell-cycle control by suppressing p21/p27, inactivating Rb, and impairing p53-dependent checkpoints, thereby limiting apoptosis. Combining surgery with targeted kinase inhibitors remains the primary therapeutic approach, especially for ALK-positive IMT. On the contrary, ALK-negative IMT harbours distinct oncogenic fusions and is driven by diverse signalling pathways. Thus, it requires therapeutic methods targeting the specific molecular alterations. Resistance to ALK inhibitors can emerge during treatment. This resistance arises through bypass signalling, epigenetic changes, and secondary mutations. This review aims to analyse the interplay between inflammation and genetic fusions in the origin and progression of IMT. The review provides an overview of the therapeutic approaches currently in use, mechanisms of treatment resistance, and potential techniques to improve diagnosis and develop personalised therapeutic strategies. - Source: PubMed
Publication date: 2026/07/21
Maiti SaraReji Archana RoseSenthil SwathiR RakshanaSolairaju RekhaKunjumon RehanaGhosh PayelH P SyamaSadhukhan PritamDutta Arkajyoti - NTRK fusions drive the pathogenesis of a distinctive group of mesenchymal neoplasms with significant impact on classification and targeted therapy. However, unexpected NTRK fusions have been reported in other sarcoma entities, raising uncertainty over their specificity and clinical management. Herein, we investigate the incidence and structural variants of NTRK fusions among a large clinicopathologic and molecular sarcoma cohort. The goal was to distinguish primary driver NTRK fusions from potential passenger events and correlate with sarcoma histotypes. NTRK1-3 fusions were queried across a large spectrum of sarcomas, profiled by targeted DNA and/or RNAseq. Fusions were classified as oncogenic when NTRK was the 3' partner, in-frame, retained kinase domain (KD), and/or RNAseq confirmation; fusions of uncertain significance (FUS) when out-of-frame, lacking full KD, and/or RNAseq negative. We identified 48 cases with NTRK fusions, detected either by pathologist-initiated RNAseq for diagnosis (n = 27) or by clinician-initiated DNAseq for therapeutic target discovery (n = 21). For the latter subset, reflex RNAseq was activated for confirmation. Integrated review confirmed 33 (69%) oncogenic fusions. Remaining were FUS, apart from one indeterminate. In all except three cases, oncogenic fusions occurred in canonical NTRK-driven histotypes. In contrast, NTRK FUS were detected in various pathologic entities, including well-differentiated/dedifferentiated liposarcoma (n = 9, 60%), two osteosarcoma, and single cases of other subtypes. NTRK1 fusions were the most common in both oncogenic and FUS groups (61%, 67%). CDKN2A/B deletions were observed mostly in oncogenic NTRK1 fusions (71%), while MDM2/CDK4 amplifications in the NTRK1 FUS. The FUS group demonstrated lower NTRK mRNA expression, with a mean of -4.60, p < 0.001. Pan-TRK immunohistochemistry was positive in cases with oncogenic NTRK fusions, and negative in FUS cases. Only two-thirds of NTRK fusions detected were functional drivers, mostly from pathologist-driven testing of suggestive histotypes. In contrast, genomic profiling in complex sarcomas often yields passenger FUS, lacking functional impact. - Source: PubMed
Yakoub Mohamed ASukhadia PurvilSaoud CarlaHameed MeeraAntonescu Cristina R