GATA3 Antibody
- Known as:
- GATA3 Antibody
- Catalog number:
- Y212708
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- GATA3 Antibody
Related genes to: GATA3 Antibody
- Gene:
- GATA3 NIH gene
- Name:
- GATA binding protein 3
- Previous symbol:
- -
- Synonyms:
- HDR
- Chromosome:
- 10p14
- Locus Type:
- gene with protein product
- Date approved:
- 1992-11-03
- Date modifiied:
- 2016-10-05
Related products to: GATA3 Antibody
Related articles to: GATA3 Antibody
- Type II innate lymphoid cells (ILC2s) have been implicated in both tumor-promoting and tumor-suppressive functions, but the mechanism(s) underlying this functional heterogeneity is not clear. Here, we tested the hypothesis that signaling through β2-adrenergic receptor (β2-AR) drives the pro-tumor functions of ILC2s within the tumor microenvironment. Using global (β2AR/) and ILC2-specific conditional knockout (IL5β2AR) mouse models, we examined how β2-AR deficiency affects ILC2 function in breast cancer. We studied the impact of β2-AR function on ILC2 phenotype, gene profile, anti-tumor T cell response and breast tumor growth. β2AR inhibition resulted in an enrichment of KLRG1⁺ ILC2s with elevated GATA3 and ST2 expression in breast tumor. Loss of β2-AR signaling in ILC2s reduced their pro-tumorigenic activity and resulted in suppressed tumor growth. Additionally, β2-AR inhibition in ILC2s was associated with increased CD4⁺ T cell infiltration in breast tumors and a greater TNF-α CD8 T cell response. β2-AR deficiency reprograms ILC2s toward a more immunostimulatory phenotype, promoting T cell-mediated anti-tumor immunity. These findings identify activity of the β2-AR as a key regulator of ILC2 plasticity and suggest β2-AR blockade as a promising strategy to enhance cancer immunotherapy. - Source: PubMed
Publication date: 2026/06/20
Choi Jee EunYan QiWang JianminSalgia Nicholas JMuhitch Jason BMacDonald Cameron RRoberts Nathan TJames Caitlin MMcCarthy Philip LMohammadpour HemnDaneshmandi SaeedRepasky Elizabeth A - Tumor recurrence is a major clinical challenge in low-risk non-muscle invasive bladder cancer (NMIBC). Molecular studies have identified two main subtypes with distinct genetic pathways: papillary, low-grade tumors, often with FGFR3 mutations and favorable outcomes, and nonpapillary, high-grade tumors, which are linked to higher rates of progression and muscle invasion. This study evaluates the prognostic value of immunohistochemical (IHC) markers- cluster of differentiation 44 (CD44), cytokeratin 5/6 (CK5/6), cytokeratin 20 (CK20), GATA-binding protein 3 (GATA3), human epidermal growth factor receptor 2 (Cerb-B2), E74-like factor 3 (ELF-3), and tuberous sclerosis complex 1 (TSC-1)-for recurrence in patients with low-risk NMIBC. - Source: PubMed
Publication date: 2026/06/20
Altın EnesDoğan ÇağrıArslan Ayşegül İsalTopkaç Erdem CanYazıcı Cenk MuratÖzcan RıdvanAkgül Hacı MuratŞahin Mehmet Fatih - Urothelial carcinoma arising in a mature cystic teratoma of the ovary is a rare event with only 13 cases reported thus far. In this article, we present the clinicopathologic features of one such case and a review of the literature. The patient was a 76-yr-old African American postmenopausal woman who presented with a painful abdominal mass and weight loss. The left ovarian tumor was 36 cm in greatest dimension and contained several papillary areas, the largest being 10 cm. The patient underwent a total abdominal hysterectomy, bilateral salpingo-oophorectomy, omentectomy and pelvic washings. Microscopically, the papillary excrescences represented an invasive, high-grade papillary urothelial carcinoma, while the cyst in the background was a mature cystic teratoma. Immunohistochemically, the urothelial carcinoma was positive for CK7, CK20, GATA-3, uroplakin II, p40, p63, and ER (20%, weak intensity), while negative for WT1 and PR; p53 expression was aberrant (nuclear overexpression). Next-generation sequencing (NGS) showed a microsatellite-stable tumor with low tumor mutational burden, and molecular alterations typically seen in urothelial carcinomas, including KRAS gain of function, ARID1A loss of function, RB1 loss of function, and two TP53 loss of function mutations. In addition, PDL1 positivity was present, representing a clinically actionable target. The tumor was FIGO stage 1A. No adjuvant therapy was given, and the patient is alive with no evidence of disease after a follow-up of 7 mo. - Source: PubMed
Publication date: 2026/06/22
Repollet Otero Patricia ARamalingam PreethaBevers Michael WMalpica Anais - Fumarate hydratase (FH)-deficient renal cell carcinoma (RCC) can exhibit striking histologic and immunophenotypic heterogeneity. A 36-year-old woman with uterine leiomyomas presented with a 5.1-cm left renal sinus mass and retroperitoneal adenopathy. Biopsy showed juxtaposed lower-grade oncocytic (PAX8 strong, GATA3 weak) and higher-grade pleomorphic (PAX8 negative, GATA3 and CK7 strong) components. DNA sequencing revealed germline pathogenic p.S419P, clonal p.H193D, and subclonal and mutations, establishing FH-deficient RCC associated with hereditary leiomyomatosis and renal cell carcinoma syndrome. Nivolumab + cabozantinib reduced the lesion before nephrectomy, which showed predominantly pleomorphic tumor cells that were PAX8 negative and GATA3/p63 positive, mimicking upper tract urothelial carcinoma. Transcriptome sequencing mapped the tumor midway between renal and bladder cancer. Postoperatively, nivolumab + ipilimumab with radiotherapy achieved disease control. In this hypothesis-generating case report, , , and secondary alterations on an -null background were associated with lineage infidelity, which can create diagnostic challenges that underscores the role for integrated pre‑ and post‑treatment multi‑omics in diagnostically ambiguous renal tumors. - Source: PubMed
Publication date: 2026/06/16
Zhao JianpingAllison Derek BGenovese GiannicolaRock StephanieSpies NoahHensley MichaelKhegai GlebMakeeva AnastasiyaMelikhova DariaBedniagin LevHensley Patrick JMyint Zin WMsaouel Pavlos - A rare subset of somatic tumors shows a striking resemblance to yolk sac tumors (YSTs) of germ cell origin, including somatic carcinomas with YST/enteroblastic differentiation, fetal lung adenocarcinomas (FLACs), and YSTs in older (≥ 40 years) females. These somatic tumors express markers such as SALL4, glypican 3 (GPC 3) and alpha-fetoprotein (αFP). However, it is currently unclear to what extent they express FOXA2, HNF1β, and SOX17, which are pioneer transcription factors and key drivers of YST differentiation and stain the vast majority of chemotherapy-naïve YSTs of germ cell origin. Therefore, a multi-institutional series of seven somatically derived "YST-like" tumors was assembled and evaluated with a comprehensive panel of YST related markers (SALL4, FOXA2, HNF1β, SOX17, αFP, GATA3, and CDX2), to evaluate the potential involvement of FOXA2, HNF1β, and SOX17 in the biology of these tumors. FOXA2 and HNF1β were positive in all (7/7, 100%) YST-like tumors, followed by CDX2 (6/7, 85.7%) and SALL4 (5/7, 71.4%). In contrast, SOX17, GATA3, αFP, and GPC3 were positive in fewer cases, and showed lower percentages and intensities. Four of seven (57.1%) YST-like tumors showed synchronous/accompanying somatic neoplastic components: one clear cell carcinoma of the ovary, two urothelial carcinomas of the bladder, and one invasive non-mucinous (conventional) adenocarcinoma of the lung. HNF1β stained all these components (4/4, 100%), and all of them (4/4, 100%) stained for at least two of the YST markers evaluated (range: 2-4). In conclusion, our results support the use of an immunohistochemical panel to diagnose YST-like tumors, considering not only the most frequently expressed makers (FOXA2 and HNF1β), but also the potential expression (particularly of HNF1β) by the associated somatic neoplastic components lacking an overt YST phenotype. The consistent expression of FOXA2 and HNF1β (but not SOX17) in our cohort underscores the phenotypic overlap between YST-like tumors and YSTs of germ cell origin (type II), including shared expression of multiple pioneer transcription factors which drive the YST phenotype. - Source: PubMed
Publication date: 2026/06/18
Ricci CostantinoDe Leo AntonioGrillini MarcoOrsatti AgneseLobo JoãoFernanda-Pontes FernandaTavares Nuno TiagoVieira JoanaAmbrosi FrancescaGrillini AlessiaFranchini EugeniaVasuri FrancescoNosseir SofiaMollica VeronicaMassari FrancescoAcosta Andres MartinFiorentino MichelangeloLi HuiliBaraban Ezra