ETV6 antibody
- Known as:
- ETV6 (anti-)
- Catalog number:
- orb128045
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- ETV6 antibody
Related genes to: ETV6 antibody
- Gene:
- ETV6 NIH gene
- Name:
- ETS variant 6
- Previous symbol:
- -
- Synonyms:
- TEL
- Chromosome:
- 12p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-28
- Date modifiied:
- 2019-04-23
Related products to: ETV6 antibody
Related articles to: ETV6 antibody
- Acute myocardial infarction (AMI) involves complex immune responses and cellular interaction mechanisms. Although the pathogenesis of AMI is now preliminarily understood, there is still a lack of biomarkers that can accurately and rapidly diagnose its disease characteristics. - Source: PubMed
Publication date: 2026/05/13
Liu ZhenfangSong JiaLi LinglingFan ZiyinXie GenyuanYang Li - gene fusions are oncogenic drivers for a variety of adult and pediatric tumors, making them a target for tumor-agnostic precision medicine. Tropomyosin receptor kinase (TRK) inhibitors are approved by the US Food and Drug Administration for cancers driven by TRK fusions. However, genes can fuse with many different partner genes, leading to diverse TRK fusion proteins, highlighting the importance of identifying the specific fusion partner with optimal pan-cancer diagnostics. This analysis aims to provide an updated descriptive compendium of gene fusions. - Source: PubMed
Publication date: 2026/05/06
Yang Soo-RyumRepetto MatteoRudzinski Erin RLi Marilyn MRoy AngshumoyGutstein LaurenHuang KarenWu JinhuaGlade Bender JuliaBrega NicolettaBuchberg Arthur MBernard-Gauthier VadimHong David SDrilon AlexanderLaetsch Theodore W - Epithelioid fibrous histiocytoma (EFH) is a benign cutaneous neoplasm that is now recognized to be largely driven by rearrangements. Rare cases of EFH and EFH-spectrum tumors with other receptor tyrosine kinase (RTK) fusions including and have been described, demonstrating the molecular heterogeneity of this entity. Herein, we report a 9-year-old female with a 1.5 cm right lateral chest wall lesion showing classic EFH morphology. Histology demonstrated a nodular dermal tumor extending to dermo-epidermal junction above and subcutaneous tissue below. The lesion was characterized by sheets of bland epithelioid/histiocytoid cells with a vaguely whorled architecture, prominent vessels, focal myxoid stroma, and no significant atypia, mitoses, or necrosis. On immunohistochemistry, the lesional cells were highlighted by CD68 and CD163, with patchy CD99 positivity. The lesional cells were negative for AE1/AE3, CD34, SMA, Desmin, S100, SOX10, CD10, ERG, CD1a, Langerin, CD30, and CD31. INI-1 was retained. Targeted solid tumor fusion analysis showed an fusion. This case expands the molecular spectrum of EFH beyond rearrangements and previously described and fusions. - Source: PubMed
Publication date: 2026/05/05
Challa BinduNaous RanaKirschner RichardReshmi Shalini CPrasad Vinay - 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 - 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