GATA3
- Known as:
- GATA3
- Catalog number:
- NBP1-39915
- Product Quantity:
- 0.05 ml
- Category:
- -
- Supplier:
- ACR
- Gene target:
- GATA3
Ask about this productRelated genes to: GATA3
- 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
Related articles to: GATA3
- Neuroblastoma (NB) is a heterogeneous pediatric malignancy in which many high-risk tumors lack MYCN amplification, necessitating the identification of alternative molecular drivers. Here, integrative transcriptomic analyses of MYCN-nonamplified NB cohorts identified cell division cycle 20 (CDC20) as a candidate associated with high-risk disease and metastasis. CDC20 expression was elevated in aggressive NB across subtypes and correlated with adverse clinical outcomes, with particularly informative prognostic value in MYCN-nonamplified patients. Functional studies established CDC20 as a potent oncogene promoting proliferation, migration, apoptosis resistance, and tumor progression in NB models irrespective of MYCN status. Pharmacological inhibition of CDC20further supported CDC20 as a potential therapeutic vulnerability in NB. Mechanistically, we found that the transcription factor GATA3 directly bound a specific motif within the CDC20 promoter, as validated by ChIP-qPCR and site-directed point mutagenesis, and transcriptionally activates its expression. Reciprocal genetic epistasis experiments further demonstrated that CDC20 depletion attenuated GATA3-driven oncogenic phenotypes, whereas restoration of CDC20 rescued the impaired growth, migration, and survival caused by GATA3 depletion. At the downstream level, CDC20 facilitates NB progression via dual mechanisms: suppressing the pro-apoptotic Bax/Bcl-2 ratio and inducing an epithelial-mesenchymal transition-like phenotype conducive to metastasis. Collectively, our study delineates a previously uncharacterized GATA3-CDC20 regulatory axis that promotes NB progression and identify CDC20 as a potential therapeutic vulnerability across NB subtypes, while highlighting its particular potential for risk stratification in MYCN-nonamplified disease. - Source: PubMed
Publication date: 2026/09/11
Fang XiaonaLan YingxiaLi MengzhenXie WeijiMao LeiHuang JinlinLi QiutingZhang YuSong MengjiaQue YiLu SuyingWang JuanHuang JuntingZhu JiaWang YiSun FeifeiZhang Yizhuo - Ascariasis is a prevalent parasitic infection in both humans and pigs, resulting in significant human morbidity and economic losses in the porcine industry. Experimental infections are often studied by mimicking natural settings, exposing the host to frequent, small doses (trickle infection) or by administering a single (bolus) dose of infective eggs. However, the impact of infection schemes and doses on the host immune response inA. suum infected pigs is still unclear. Using trickle and bolus infections and applying different doses, we found systemic GATA3+CD4+ T cells and eosinophils increased dose-dependently during A. suum body migration, while CD4+ T cells that specifically recognize A. suum antigens showed no association with the infection dose. In contrast, all dose-dependent differences were resolved by 8-9 weeks post infection, when adult worms were present. The results further showed that adult worm burden did not differ detectably across all groups, though a high intragroup variability was observed. Local type 2, germinal center B cell, and Tfh cell responses were dose-dependent in bolus infected animals only. Our data suggest that the initial immune response generated during A. suum larval migration is pivotal in determining the fate of the antiparasite response and adult worm population. Moreover, our results indicate that the host can regulate the worm load independent of the infection dose and scheme. - Source: PubMed
Oser LarissaRoose SaraMidha AnkurSchlosser-Brandenburg JosephineLaubschat AlexandraMusimbi Zaneta DKundik ArkadiHöfler PhilippHelm Christina Svon Samson-Himmelstjerna GeorgGeldhof PeterHartmann SusanneEbner Friederike - Eosinophilic solid and cystic renal cell carcinoma (ESC-RCC) is a recently recognized eosinophilic renal neoplasm characterized by distinctive morphologic, immunophenotypic, and molecular features, including frequent TSC/mTOR pathway alterations. Recently, L1 cell adhesion molecule (L1CAM) has gained increasing recognition as a diagnostically and biologically relevant marker in selected eosinophilic renal neoplasms; however, its expression profile in ESC-RCC has not been systematically investigated. We aimed to evaluate L1CAM expression in a multicenter cohort of ESC-RCCs and correlate the findings with clinicopathologic and immunophenotypic features. A retrospective multicenter cohort of 11 ESC-RCCs was collected. Clinicopathologic and immunophenotypic findings were recorded. Immunohistochemistry for L1CAM was performed on representative whole tissue sections and semi-quantitatively scored based on the percentage of positive tumor cells. The cohort included 9 female and 2 male patients with a median age of 50 years (range, 39-79). L1CAM expression was identified in 7 of 11 tumors (63.6%), including 5 cases with diffuse membranous (3+) staining and 2 cases with intermediate (2+) staining; no tumor showed only focal (1+) expression. All tumors showed the characteristic morphology of ESC-RCC and expressed KRT20, irrespective of L1CAM status. Among tumors evaluated with additional markers, SDHB expression was retained in all 6 tested tumors and GATA3 was negative in all 5 tested tumors. Molecular testing was not performed in this cohort. Follow-up was available for all 11 patients (median, 10 months), with all patients alive without disease at last follow-up. Our findings expand the known immunophenotypic spectrum of ESC-RCC by demonstrating L1CAM expression in a substantial subset of tumors. However, because L1CAM expression is neither sensitive nor specific for ESC-RCC, positive or negative staining does not support or exclude the diagnosis and does not currently justify routine use of L1CAM in the diagnostic evaluation of morphologically suspected ESC-RCC. - Source: PubMed
Publication date: 2026/09/10
Kabul SelvaYaprak Bayrak BusraOzbek BusraOzsagir ElifYıldırım Nazif AlperenOzturk EceJafarzadeh HamedBiltekin BurcuBuyukgok MelekSungu NuranOktay MuratCoban GanimeKosemehmetoglu KemalAcosta Andres MCheng LiangAkgul Mahmut - Wnt signaling drives tumorigenesis in multiple cancers, in part through complex interactions with other oncogenic pathways including the MAPK cascade. In Wnt-addicted cancers, pharmacologic and genetic inhibition of Wnt signaling activates multiple receptor tyrosine kinases (RTKs), increases ERK phosphorylation and induces MAPK target gene expression, but the specific RTKs responsible for this MAPK hyperactivation are not known. Here we performed phosphotyrosine-targeted mass spectrometry, which revealed robust phosphorylation of EPHA2 and EGFR upon Wnt inhibition. Unexpectedly, we find that in xenografts, EPHA2 suppresses EGFR and ERK activation. Most notably, the increased ERK phosphorylation observed in EPHA2 KO tumors is transcriptionally inert, as there is no concomitant increase in MAPK target gene expression until concomitant Wnt inhibition. This suggests a Wnt-activated transcriptional repressor such as GATA3 that gates MAPK signaling in Wnt-high cancers. While Wnt-high KRAS-mutant cancers are resistant to erlotinib alone, adding Wnt inhibitor mitigates this resistance. Additionally, loss of EPHA2 enhances their sensitivity to both erlotinib and Wnt inhibitors. These studies therefore identify therapeutic vulnerabilities in Wnt-high tumors, even within traditionally EGFR inhibitor-resistant, RAS-mutant contexts. . - Source: PubMed
Publication date: 2026/09/08
Wadia Shawn RHu ChangyuanPatnaik SiddhiSridharan ShreyaDaly Roger JVirshup David MMadan Babita - Invasive lobular carcinoma (ILC) of the breast is a common type of breast cancer and is known to have a distinct metastatic pattern, with a predilection for the gastrointestinal tract and peritoneum rather than the lungs and liver. Gastric outlet obstruction (GOO), as the initial manifestation of occult metastatic breast carcinoma, is rare and may closely mimic primary gastrointestinal malignancy. A 67-year-old woman presented with progressive nausea, vomiting, poor oral intake, weight loss, and symptoms consistent with GOO. Computed tomography demonstrated gastric wall thickening, ascites, and peritoneal abnormalities concerning for primary gastric malignancy. Initial endoscopic biopsies of the pyloric channel revealed erosive chemical gastropathy without evidence of malignancy. Given the high clinical suspicion, endoscopic ultrasound-guided fine-needle aspiration (EUS-FNA) was performed, which demonstrated adenocarcinoma. Immunohistochemistry showed positivity for CK7, GATA3, and TRPS1, with negativity for CK20 and CDX2, favoring a breast primary. Subsequent diagnostic laparoscopy with omental, peritoneal, and mesenteric biopsies confirmed metastatic carcinoma with attenuated E-cadherin expression, consistent with invasive lobular breast carcinoma. Despite extensive biopsy-proven peritoneal disease, peritoneal fluid cytology was negative for malignant cells. Biomarker analysis demonstrated estrogen receptor positivity (91%-100%), progesterone receptor positivity, HER2 negativity (1+), and a Ki-67 of 10%-15%. This case highlights several diagnostic challenges in metastatic ILC, including false-negative mucosal biopsies, negative peritoneal cytology despite extensive carcinomatosis, and the need for deeper tissue sampling. Recognition of contemporary immunophenotypic markers, including GATA3 and TRPS1, with attenuated E-cadherin expression, is essential for distinguishing metastatic breast carcinoma from primary gastrointestinal malignancies and for facilitating appropriate systemic therapy. - Source: PubMed
Publication date: 2026/08/08
Pekmezian KristinUbosy SaraNuaimi MustafaParellada JorgeCarlan Steve