ETV6 antibody
- Known as:
- ETV6 (anti-)
- Catalog number:
- orb128045
- Product Quantity:
- 200 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
- Mixed-phenotype acute leukemia (MPAL) with BCR::ABL1 fusion is rare, and its clinicopathologic features, genetic landscape, therapeutic response, and patient outcomes remain incompletely defined, as does its relationship to blast-phase chronic myeloid leukemia (CML). In this multicenter study of 44 patients, 86.4% had B/myeloid MPAL, 72.7% showed lymphoid predominance, 40.9% had complex karyotypes (CK), and 68.3% harbored somatic mutations, most commonly RUNX1 mutations (46.3%). RUNX1 mutations frequently co-occurred with AML-associated alterations, whereas DNMT3A, TET2, and BCORL1 mutations were restricted to RUNX1-mutated cases. In contrast, ALL-associated alterations (IKZF1 mutation/deletion and ETV6 mutations) were confined to RUNX1-wild-type patients. TP53 and signaling-pathway mutations (NRAS, KRAS, PTPN11, and FLT3) were not detected. Forty-two patients received induction chemotherapy and/or immunotherapy combined with tyrosine kinase inhibitors: 74.2% of lymphoid-predominant and 63.6% of myeloid-predominant patients receiving ALL- and AML-type therapies, respectively. Ten patients relapsed and 2 had primary refractory disease; some exhibited dynamic shift in predominant lineage immunophenotype, chromosomal alterations, and somatic mutations at relapse or refractory stage. The overall remission rate was 86.8%, with no significant differences across ALL-, AML-, or hybrid-type regimens. After a median follow-up of 24.2 months, the median overall survival (OS) was 52.5 months. CK was associated with inferior OS compared with cases lacking additional chromosomal alterations (p=0.02), whereas RUNX1 mutations were not. No significant differences in genetic profiles, treatment response, or outcomes were observed between patients with and without CML-like features. This study provides a comprehensive genomic and clinical characterization of BCR::ABL1-positive MPAL, supporting improved risk stratification and future therapeutic strategies. - Source: PubMed
Publication date: 2026/05/21
Shen QiudanHuang XiaoyanWang XiaoqiongShuai WenFang HongJabbour ElliasChen WeinaTashakori MehrnooshKhanlari MahsaWu XiaojunShao LinaZhang LingEl Hussein SibaKonoplev SergejKhoury Joseph DTang GuilinWang WeiWang Sa AMedeiros L JeffreyHu Shimin - Three-dimensional genome organization shapes gene regulation during normal B-cell development, and its disruption contributes to the initiation and progression of B-cell acute lymphoblastic leukemia. Through multi-omic studies, Ghebrechristos and colleagues revealed that transcription factors, including ERG in ETV6::RUNX1 leukemia, remodel chromatin interactions to sustain oncogenic gene expression programs, identifying genome architecture as both a driver of leukemogenesis and a potential therapeutic vulnerability. See related article by Ghebrechristos et al., p. XX . - Source: PubMed
Publication date: 2026/05/18
Gruber Tanja A - Secretory breast carcinoma (SBC) is an extremely rare subtype, accounting for ~1% of breast cancers but representing the most common malignant breast tumor in pediatric patients. Although generally indolent, SBC carries a risk of local recurrence even decades after treatment. Its defining molecular hallmark is the ETV6-NTRK3 fusion. - Source: PubMed
Publication date: 2026/05/14
Vlahović ANikolić SDjuričić S MDunđerović DIlić NSarajlija ADenčić Fekete MCvetinović AVasić M - 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