ETV6 antibody - N-terminal region (P100806_P050)
- Known as:
- ETV6 (anti-) - N-terminal region (P100806_P050)
- Catalog number:
- p100806_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- ETV6 antibody - N-terminal region (P100806_P050)
Related genes to: ETV6 antibody - N-terminal region (P100806_P050)
- 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 - N-terminal region (P100806_P050)
Related articles to: ETV6 antibody - N-terminal region (P100806_P050)
- The fusion is a recurrent oncogenic alteration in sporadic pediatric papillary thyroid carcinoma (PTC), frequently associated with multifocal disease and pulmonary metastasis. However, the molecular and cellular consequences of expression in thyroid follicular cells remain poorly defined. Here, we investigated the biological effects of in PCCL3 thyroid cells and compared them with those induced by clinically established pediatric PTC oncogenic drivers, including , , , , and wild-type . -expressing cells exhibited the most robust MAPK/ERK activation, characterized by markedly enhanced ERK and MEK phosphorylation relative to all other oncogenic drivers analyzed. By contrast, STAT3 and AKT signaling remained comparatively modest and did not show consistent oncogene-specific activation patterns. Functionally, expression induced features of thyroid dedifferentiation, including reduced sodium-iodide symporter (NIS) expression and impaired iodide uptake. Concomitantly, -expressing cells exhibited increased frequencies of micronuclei and chromatin bridges, together with disruption of three-dimensional telomere architecture, including reduced telomere signal number and intensity, altered spatial organization, and increased nuclear volume. Three-dimensional structured illumination microscopy (3D-SIM) further demonstrated chromatin remodeling, characterized by increased chromatin condensation accompanied by enlarged interchromatin spaces. Collectively, these findings suggest that is a dominant oncogenic driver of sustained MAPK/ERK signaling coupled to thyroid dedifferentiation, nuclear architectural remodeling, telomere dysfunction, and genomic instability. These coordinated molecular and structural alterations provide a mechanistic basis for the aggressive clinical course observed in -driven pediatric PTC. - Source: PubMed
Publication date: 2026/09/18
Sisdelli LuizaRocha Welbert GomesDias Thomaz Débora MotaHatanaka RoxaneCosta da Silva Renata ElenHenrique GuilhermeSerrano-Nascimento CarolineFabião MatheusRangel-Pozzo AlineMai SabineCerutti Janete Maria - Mammary analog secretory carcinoma (MASC) is a rare malignant tumor of the salivary glands that exhibits significant morphological, immunohistochemical, and molecular similarities with secretory carcinoma of the breast, including the characteristic - gene fusion. The diagnosis of this condition remains challenging due to its histopathologic overlap with other low-grade salivary gland tumors, such as acinic cell carcinoma and mucoepidermoid carcinoma. The following report details two cases of MASC manifesting in the right parotid gland of a 37-year-old male and a 23-year-old female. Both subjects exhibited slow-growing, painless swellings and radiologic findings indicative of benign lesions. The surgical excision procedure was performed on the first patient via extracapsular dissection, while the second patient underwent superficial parotidectomy. Both procedures were carried out under the supervision of intraoperative facial nerve monitoring. A subsequent histopathological and immunohistochemical examination revealed a glandulocystic growth pattern with eosinophilic secretions and strong immunoreactivity for CK7, S100, and mammaglobin. Although molecular testing for the - fusion was not performed, the clinical, morphological, and immunophenotypic findings supported the diagnosis of low-grade secretory carcinoma. The patients exhibited uncomplicated recovery, with transient facial nerve paresis in the second patient resolving within 3 months. The first patient remains disease-free after 40 months of clinical and radiological follow-up, while the second patient has shown no evidence of recurrence after 21 months of follow-up. The cases under consideration serve to emphasize the importance of integrating morphology and immunohistochemistry in routine practice, with molecular confirmation remaining the diagnostic gold standard whenever it is available. It is imperative to be aware of this entity to ensure an accurate diagnosis, optimal surgical management, and appropriate long-term surveillance. Emerging evidence suggests that targeted therapy with NTRK inhibitors may represent a promising option for advanced or recurrent disease. - Source: PubMed
Publication date: 2026/09/26
Ferragina FrancescoBarca IdaTarallo GiuseppeSottile Angelo RIoppolo Maria GraziaCristofaro Maria Giulia - Acinic cell-like carcinoma (AcCC) of the breast is an extremely rare triple-negative breast carcinoma, analogous to acinic cell carcinoma of the salivary gland in morphology and immunohistochemistry. In this study, we report three new cases of breast AcCC, including clinical characteristics, histological morphology, immunophenotype, ultrastructural characteristics, and results of 1 case of next-generation sequencing. Breast AcCCs predominantly comprised small acinar or glandular structures. Tumor cells were positive for cytokeratin, epithelial membrane antigen, lysozyme, α-1-antichymotrypsin, and S-100 protein, while generally being negative for estrogen receptor, progesterone receptor, and human epidermal growth factor receptor 2. Electron microscopy detected zymogen particles in the cytoplasm of cancer cells. Additionally, FISH assay was performed in one case, and the results were negative for the ETV6::NTRK3 fusion gene, potentially differentiating breast AcCC from secretory carcinoma. Next-generation sequencing in one case revealed two missense mutations of PIK3CA gene (c.3140A > G, p.His1047Arg and c.1624G > A, p.Glu542Lys), as well as an in-frame indels mutation (c.1138_1167del, p.Glu380_Ala389del) and a nonsense mutation (c.1138G > T, p.Glu380*) of TBX3 gene. Breast AcCC is confirmed to be generally similar to its salivary gland counterpart and is considered a distinct lesion. Breast AcCC generally presents relatively indolent biological behavior, although tumor progression and extensive metastasis considerably worsen the disease course. In conclusion, we describe the morphological and immunohistochemical features of three cases, along with the molecular profile of one case, of this rare entity. We also summarize the molecular characteristics of breast AcCC cases reported in the literature to date. - Source: PubMed
Publication date: 2026/09/20
Zhao KeZhang KexinQian JianzhongYu XuewenBi JiaxinZhang LuShao Mumin - 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