ETV6 antibody
- Known as:
- ETV6 (anti-)
- Catalog number:
- orb48366
- 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
- The conversion of transcriptionally silent GGAA microsatellites (GGAAµSats) into functional enhancers by FET::ETS oncogenic fusions is a hallmark of Ewing sarcoma. However, emerging evidence implicates non-fused, full-length oncogenic ETS transcription factors in activating these repeats in other malignancies. Evaluating the in vivo transcriptional requirements of various human ETS factors in Drosophila, we found that human ETV4 associates with and robustly activates GGAAµSats in a tissue-specific manner. This activation is strongly inhibited by the human ETS repressor ETV6. Taking advantage of low genetic redundancy in Drosophila, we identified Cabeza (Caz), the single fly FET ortholog, as a necessary cofactor for ETV4-mediated transcription at GGAAµSats. Conversely, EWS::FLI1-mediated transcriptional activation of GGAAµSats is entirely independent of endogenous Caz, highlighting the distinct mechanics of covalent tethering versus non-covalent physical complexes. Collectively, our findings provide in vivo evidence that non-fused ETS factors cooperate with endogenous FET proteins to drive transcription from silent GGAA repeats, mechanistically validating this regulatory transformation known to operate as an oncogenic mechanism beyond Ewing sarcoma. - Source: PubMed
Publication date: 2026/09/22
Molnar CristinaReina JoseMora JaumeGonzalez Cayetano - ZNF384-rearranged (ZNF384-r) B-cell acute lymphoblastic leukemia (B-ALL) is a rare subtype in which the prognostic significance of persistent molecular measurable residual disease (MRD), particularly isolated ZNF384 transcript positivity with negative multiparameter flow cytometric (MFC) MRD, before allogeneic hematopoietic stem cell transplantation (allo-HSCT) remains unclear. We retrospectively analyzed 60 patients with ZNF384-r B-ALL who underwent allo-HSCT in complete remission (CR) between April 2020 and December 2024. Pre-transplant MRD was assessed by MFC and RT-qPCR targeting ZNF384 fusion transcripts. The most common fusion partners were EP300::ZNF384 (43.3%) and TCF3::ZNF384 (31.7%); 58.3% of patients harbored kinase/RAS pathway mutations. Diagnostic immunophenotyping confirmed the characteristic ZNF384-r phenotype, with more frequent uniform CD33 expression in EP300::ZNF384 and other fusion subgroups than in TCF3::ZNF384 (P<0.05). After a median follow-up of 28.2 months, the 3-year overall survival (OS), leukemia-free survival (LFS), cumulative incidence of relapse (CIR), and non-relapse mortality (NRM) were 81.9%, 78.7%, 10.0%, and 11.3%, respectively. Molecular MRD remained detectable in 12 patients (20.0%), including 9 (15.0%) with discordant MFC-negative/molecular-positive (MFC-/Mol+) MRD. All nine discordant cases were alive at last follow-up, with 3-year OS and LFS of 100% and 80.0%, respectively. Molecular MRD positivity was not associated with inferior OS (83.3% vs 81.8%; P = 0.806), LFS (66.7% vs 80.5%; P = 0.516), or CIR (25.0% vs 7.3%; P = 0.255). Similarly, recurrent genomic alterations, including kinase/RAS pathway, IKZF1, ETV6, and KMT2A/D abnormalities, were not significantly associated with post-transplant survival (all P>0.05). Among patients who achieved CR and proceeded to allo-HSCT, favorable outcomes were observed across molecular MRD and genomic subgroups. In particular, isolated pre-transplant ZNF384 transcript positivity with MFC-MRD negativity was not significantly associated with inferior post-transplant outcomes, although these findings are exploratory and require validation in larger, preferably multicenter cohorts. - Source: PubMed
Publication date: 2026/09/19
Zhang Xue-ShuangZhao Yan-LiZhang Jian-PingXiong MinCao Xing-YuLiu De-YanSun Rui-JuanWei Zhi-JieZhou Jia-RuiLong JingLu Yue - NTRK (neurotrophic receptor tyrosine kinase)-rearranged spindle cell tumours are rare sarcomas predominantly occurring in the extremities and trunk, with only rare gastrointestinal tract cases reported to date. A man in his late 30s presented with abdominal pain. Given the CT evidence of a large transmural tumour requiring radical resection irrespective of histological subtype, the multidisciplinary team proceeded directly to surgery without preoperative colonoscopy. Diagnosis was established through histopathology, immunohistochemistry (IHC) and next-generation sequencing (NGS). Right hemicolectomy revealed an 8 cm transmural spindle cell neoplasm with necrosis, vascular invasion and perineural infiltration. IHC showed diffuse strong CD31 positivity but negativity for CD117, DOG-1, S100 and smooth muscle markers. NGS identified an ETS Translocation Variant 6-Neurotrophic Tyrosine Receptor Kinase 3 gene ( fusion. Applying the American Joint Committee on Cancer (AJCC) 8th edition criteria for soft tissue sarcoma by analogy, the tumour was staged pT2N0M0 (stage IIIA, high grade). Adjuvant chemotherapy was discussed after multidisciplinary review of the complete (R0) resection but was declined by the patient for financial reasons; close surveillance was adopted. The patient remained recurrence-free at the 8-month follow-up. This case adds to the limited number of reported gastrointestinal NTRK-rearranged sarcomas and expands the anatomic and molecular spectrum of these tumours. CD31 expression was an unexpected observational finding in this case and requires independent validation before it can be considered a characteristic immunohistochemical feature. Molecular confirmation is essential for accurate diagnosis and for identifying patients who may be eligible for tropomyosin receptor kinase (TRK) inhibitor therapy. - Source: PubMed
Publication date: 2026/09/17
Zheng Yuan-YinMao Ying-YuLin Mao-HuaLiu Xiao-Bin - Germline pathogenic variants in are recognized as causes of inherited thrombocytopenia and leukemia predisposition. We report a family harboring a germline variant, c.1072A>T (p.I358F), which has not been previously associated with this phenotype. Three family members exhibited chronic thrombocytopenia, and two had a history of acute lymphoblastic leukemia. The germline variant was located within the ETS DNA-binding domain, where leukemia-associated germline variants have been reported to cluster. This report underscores the need for careful family history assessment and long-term follow-up to identify hereditary leukemia predisposition syndromes and ensure appropriate genetic evaluation. - Source: PubMed
Publication date: 2026/09/15
Waragai TomokoNakano YoshikoMochizuki KazuhiroKikuta AtsushiAkaihata MitsukoTakahashi NobuhisaKudo ShingoSasaki YuiKato MotohiroSano Hideki - This study aimed to expand the morphologic and molecular spectrum of NTRK-rearranged uterine tumors by reporting 3 cases of NTRK3-fusion cervical sarcoma and conducting a literature review, thereby strengthening the understanding of their clinicopathologic features, differential diagnosis and treatments. We collected 3 cases of NTRK3-fusion cervical sarcoma and reviewed their clinical presentation, histomorphology, immunohistochemistry, fluorescence in situ hybridization (FISH) and next-generation sequencing (NGS) findings. Previously reported cases were identified from the English-language literature in PubMed, and the differential diagnosis of uterine spindle cell tumors was discussed. The tumors in all 3 cases were composed of uniform spindle cells with mild to moderate atypia and focal lymphocytic infiltration. Mitotic activity varied from 10 to 30 per 10 high-power fields. Immunohistochemically, all cases showed CD34 and pan-TRK positivity, and 2 cases showed patchy to diffuse S-100 staining. NGS identified NTRK3 fusions in all cases (SPECC1L::NTRK3, ETV6::NTRK3, KHDRBS1::NTRK3). All 3 patients experienced recurrence, and 2 remained stable after receiving TRK inhibitor therapy. Integration of our cases with 68 previously reported cases revealed that NTRK3-fusion uterine tumors tend to be larger, with higher mitotic counts, a higher proportion of cases with International Federation of Gynecology and Obstetrics (FIGO) stage above IB, higher recurrence rates, and increased disease-specific mortality. NTRK3-fusion cervical sarcomas represent a rare but clinically significant subset of NTRK-rearranged tumors characterized by their potential for recurrence and metastasis. The molecular identification of NTRK-rearranged neoplasms is highly significant, as patients may benefit from TRK inhibitor therapy. - Source: PubMed
Publication date: 2026/09/16
Xiong WanHu JunboWang ZhiganYu FangChen Qiongrong