TrkC _ NTRK3 Protein
- Known as:
- TrkC _ NTRK3 Protein
- Catalog number:
- 10048-H03H
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Smart Serology
- Gene target:
- TrkC _ NTRK3 Protein
Related genes to: TrkC _ NTRK3 Protein
- 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: TrkC _ NTRK3 Protein
Related articles to: TrkC _ NTRK3 Protein
- Sinonasal adenocarcinomas (SNACs) are the second most common carcinoma category in the sinonasal tract after squamous cell carcinomas and include intestinal type adenocarcinoma, non-intestinal type adenocarcinomas and salivary-type adenocarcinomas. Improved morphologic and molecular characterization have established that most non-ITAC are phenotypically seromucinous with several provisional subtypes (BRAF V600E-mutated sinonasal ductal-like tumors, MAPK/PI3-K altered SNAC, CTNNB1-mutated sinonasal carcinoma, fusion-kinase associated SNAC e.g. ETV6::NTRK3, FGFR-rearranged biphasic SNAC). We report two biphasic/ bicellular ("oncocytic" and "basaloid") SNACs, with multimodal omics characterization, to further underscore the biological complexity of these tumors. One oncocytic case showed HRAS and AKT1 activating mutations; the other basaloid case had a FGFR2::SORB3 fusion. Spatial transcriptomics revealed divergent intra- and inter-tumoral signatures emphasizing the transcriptomic heterogeneity within biphasic components. - Source: PubMed
Publication date: 2026/05/04
Bell DianaWeber Randal SZhang MiaoAfkhami MichelleSeethala Raja R - Inflammatory myofibroblastic tumors (IMT) are mesenchymal neoplasms of intermediate malignant potential, characterized by recurrent gene fusions in potentially targetable receptor tyrosine kinases. Primary thoracic IMTs are rare, and their molecular landscape remains incompletely characterized. A ten-year retrospective (2014-2024) clinicopathological analysis of primary thoracic IMTs was done. Histomorphological evaluation and molecular characterization by a graded approach incorporating immunohistochemistry, fluorescence-in-situ hybridization, multiplex reverse-transcription polymerase chain reaction, and next-generation targeted panel sequencing were performed for the common implicated driver fusions. Thirty IMTs involving the lung (n=17), tracheobronchial tree (n=12), and pleura (n=1) were identified. Median age at diagnosis was 18 years (range: 2 to 51 years), including 14 paediatric and 16 adult patients. Male: female ratio was 2.2:1 and 1.3:1, in adults and children, respectively. Majority (22/30, 73.3%) showed cellular spindle-cell pattern with lymphoplasmacytic inflammation. None showed significant atypia, necrosis, or mitotic activity. Molecular characterisation achieved in 22/30 cases revealed 73.3% (16/22) ALK-IMTs, 23% (5/22) ROS1-IMTs, and a single NTRK3-IMT. No statistically significant differences were seen among molecular subgroups, although ALK-IMTs were diagnosed at a higher median age (24.5 years) as compared to ROS1-IMTs (15 years). On follow-up (median follow up period: 24 months), local recurrence was observed in 23% (3/13) patients, all harbouring ALK-IMTs, one of whom was successfully treated with ALK inhibitor therapy; no disease-related deaths were recorded. Primary thoracic IMT affects children and young adults. Majority are driven by ALK gene rearrangements, followed by ROS1 alterations, underscoring role of molecular profiling in potential therapeutic stratification. - Source: PubMed
Publication date: 2026/05/02
Jacob SherrinNambirajan ArunaGangule Hrishikesh NagbhushanKumar SunilChandrashekhara S HRastogi SameerBarwad AdarshMridha Asit RanjanMadan KaranMalik Prabhat SinghJain Deepali - Neurotrophic tyrosine receptor kinase (NTRK) fusions are crucial in tumorigenesis and in guiding targeted therapy with TRK inhibitors. However, their rarity, fusion heterogeneity, and limitations of conventional pan-TRK immunohistochemistry (IHC) impede accurate clinical detection. This multicenter retrospective study analyzed 374 NGS/FISH-validated samples (195 NTRK - positive and 179 NTRK - negative) collected from 12 Chinese centers to investigate fusion heterogeneity and refine the interpretation of pan-TRK IHC. We developed an amplified protocol by combining the traditional pan-TRK IHC (EPR17341) with the OptiView Amplification kit and established new interpretation criteria. A total of 40 solid tumor types were included, and 23 unique fusion partners were identified. Papillary thyroid cancer was the most common NTRK-positive tumor (49.74 %) and harbored all three NTRK subtypes. Among NTRK-positive samples, NTRK3 (74.87 %) was the most prevalent subtype, followed by NTRK1 (23.59 %). ETS variant transcription factor 6 (ETV6) was the most frequent fusion partner, identified in 122 out of 195 cases. It was uniquely shared across all three NTRK subtypes, with its fusion to NTRK1 being reported for the first time. NTRK1 and NTRK3 exhibited marked fusion partner specificity, with no overlap in their associated partners except for ETV6. The optimized pan-TRK IHC protocol significantly improved staining efficiency by enhancing intensity and clarity. Consequently, the newly established criteria (cytoplasmic intensity ≥1 in ≥50% of tumor cells or any nuclear intensity ≥1) exhibited outstanding detection performance, achieving an overall sensitivity of 94.36% and increasing specificity to 79.89%, compared to 60.22% under the conventional one. Particularly, the detection sensitivity for NTRK3 fusions was significantly enhanced and reached 95.89 %. This study contributes to clarifying NTRK fusion distribution in patients and validates a standardized, sensitive pan-TRK IHC strategy for clinical screening. - Source: PubMed
Publication date: 2026/04/29
Wu ShafeiWang JianYang WentaoHan YuchenZhang ZhihongChen GangMeng BinSun YanLiu YangLi WencaiLi ShengleiWang LifengZhang HongyingGuo LingchuanLiu YuepingLiu XiaodingHong RupingLi KaimiPang JunyiLiang Zhiyong - Salivary gland cancer (SGC) is a rare cancer comprising over 20 subtypes. Although its molecular landscape is increasingly characterised, real-world data on molecular-matched therapies (MMTs) remain limited, and predictive biomarkers are needed. - Source: PubMed
Publication date: 2026/04/30
Weijers J A Mvan Ruitenbeek N Jvan Engen-van Grunsven A C HDriessen C M LDevriese L ASlingerland MHoeben AOosting S FSchreuder W HSewnaik Avan Helvert SSchalken J AVerhaegh G Wvan Herpen C M L - Approximately 85% of all lung cancer cases are classified as non-small cell lung cancer (NSCLC). Given its poor prognosis and resistance to radiotherapy and chemotherapy, there is an urgent need to elucidate its molecular mechanisms to develop novel and more effective therapeutic strategies. In prior research, we identified nobiletin from a compound library and confirmed it as a novel natural BH3 mimetic. Nobiletin synergized with vorinostat to induce autophagy and apoptosis in small-cell lung cancer. In the current study, we further demonstrate that nobiletin, either alone or in combination with vorinostat, exerts inhibitory effects on NSCLC. Specifically, the combination of nobiletin and vorinostat suppressed the proliferation of NSCLC A549 cells. Nobiletin, used alone or with vorinostat, induced apoptosis in A549 cells by mimicking BH3-only proteins, which included down-regulating anti-apoptotic proteins such as B-cell lymphoma-2 (BCL-2) and MCL-1, up-regulating apoptosis-related proteins Cleaved-Caspase-3 and Cleaved-PARP, and increasing BH3-only protein expression. Nobiletin binding to BCL-2 facilitated the dissociation of the Beclin-1/BCL-2 complex, thereby elevating levels of free Beclin-1. Furthermore, the combination of nobiletin and vorinostat enhanced the expression of LC3A/BII and forkhead box O1 (FOXO1), ultimately inducing autophagy in A549 cells. Eukaryotic transcriptome sequencing revealed that the combination treatment primarily inhibits tumor cell proliferation by modulating TRKC protein expression and suppressing phosphorylation of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway. Therefore, our results indicate that nobiletin, a natural BH3 mimetic, synergizes with vorinostat to regulate both apoptosis and autophagy in NSCLC. - Source: PubMed
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