GATA3 Luciferase Reporter Vector
- Known as:
- GATA3 Luciferase Reporter Vector
- Catalog number:
- LR0031
- Product Quantity:
- 10 ug
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- GATA3 Luciferase Reporter Vector
Related genes to: GATA3 Luciferase Reporter Vector
- 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 Luciferase Reporter Vector
Related articles to: GATA3 Luciferase Reporter Vector
- Breast cancer with gastric metastasis is extremely rare. Non-persistence with adjuvant endocrine therapy is associated with increased recurrence/metastasis risk in hormone receptor-positive (HR+) breast cancer. A 33-year-old female was initially diagnosed with left breast cancer in July 2011, undergoing modified radical mastectomy, adjuvant chemotherapy, radiotherapy, and endocrine therapy (discontinued voluntarily after 1 year). In February 2025, she presented with low back pain and epigastric discomfort; examinations confirmed gastric and multiple bone metastases (ER+,PR+,HER2-). She received first-line endocrine therapy (letrozole+ribociclib+goserelin) combined with denosumab. Re-examination in September 2025 showed normal CEA, significantly decreased CA153, and no disease progression per RECIST 1.1. This case suggests that early endocrine therapy discontinuation may potentially contribute to late recurrence/metastasis. Breast cancer gastric metastasis diagnosis relies on medical history, gastroscopy, and immunohistochemistry (GATA3+, CK7+, CK20-). The combination regimen yielded favorable efficacy, providing clinical reference for similar rare cases. - Source: PubMed
Publication date: 2026/04/14
Lu MinjunHu GuinvShen Qinyan - Cancer therapeutics frequently fail in clinical trials because of poor therapeutic index (efficacy-to-toxicity ratio). We systematically identified targets likely to have a good therapeutic index, revealing insulin receptor substrate 4 (IRS4) as a dependency in -expressing cancers. Pan-cancer analysis of pediatric-enriched cancers revealed expression consistent with dependency in 68% of choroid plexus, 37% of malignant rhabdoid, 31% of NUT midline, and 5% of osteosarcomas, while in adult cancers, it was expressed in 8% of uterine leiomyosarcomas and 1 to 2% of lung squamous, stomach, and breast carcinomas. expression in adult tumors was associated with enhancer hijacking rearrangements, including recurrent and in breast cancer, while rhabdoid and NUT midline cancers expressed epigenetically. IRS4 fueled cancer dependency through PI3K-Akt activation, and domain analysis revealed the PH and PTB domains, which have a predicted drug pocket, to be dispensable, suggesting degradation-based modalities. These data reveal IRS4 as a target in IRS4-expressing cancers and suggest inhibitory approaches. - Source: PubMed
Publication date: 2026/04/29
Banu KhadijaKhan Mohammad AslamLi SihanReynolds-Gagliano MorganWang XiaofeiMobley Robert JBarnett Kelly RWielgosz Matthew MBauler MatthewWincek ChristopherKodali KiranWang WeiPagala VishwajeethHigh Anthony APutnam DanielKotecha Rishi SCheung Laurence CMa XiaotuThrom Robert EPruett-Miller Shondra MSavic DanielBrady Samuel W - Papillary renal neoplasm with reverse polarity (PRNRP) is a recently recognized renal tumor characterized by papillary architecture lined by a single layer of low-grade eosinophilic cells with apically located nuclei. In the latest WHO classification, they are not recognized as a distinct entity but rather as a morphological pattern of papillary renal cell carcinoma. To date, limited studies have compared PRNRP with eosinophilic/oncocytic papillary renal cell carcinoma (E/OPRCC), which they are not infrequently confused with, although a few previous comparisons with classic papillary renal cell carcinoma have already identified several distinguishing features. A comparative analysis of 15 of PRNRPs and 16 of E/OPRCC cases was conducted, evaluating their histopathological, immunophenotypic, interphase cytogenetic, and molecular profiles. PRNRPs demonstrated distinctive morphological features, including consistent apical nuclear positioning, absence of foamy macrophages in the papillary cores (p = 0.0001), and a lower nucleolar grade compared to E/OPRCCs (p = < 0.0001). Immunohistochemically, PRNRPs exhibited strong and uniform GATA3 expression and were negative for vimentin, CD10, and CD13, in contrast to E/OPRCCs. Cytogenetically, PRNRPs lacked trisomies of chromosomes 7 and 17, which were present in ~ 40% of E/OPRCCs (p = 0.0262). Notably, all PRNRP cases harbored KRAS mutations, absent in E/OPRCCs (p < 0.0001). Our findings support the classification of PRNRP as a distinct renal tumor entity, separated from both classic papillary renal cell carcinoma and its eosinophilic/oncocytic morphological variant. - Source: PubMed
Publication date: 2026/04/29
Marletta StefanoFiorini DeniseCaliò AnnaMarcolini LisaStefanizzi LaviniaGiacometti CinziaPedron SerenaVicentini CaterinaMartignoni Guido - The chromatin organizer SATB1 is indispensable for thymic regulatory T cell (Treg cell) development and T helper cell induction. Several gene loci have been described to be SATB1-controlled, including the transcription factor GATA3 and the cytokine loci IL-4 and IL-17. However, the global effects of SATB1 on fully differentiated human CD4 conventional T cells (Tconv cells) and Treg cells, and thus SATB1's potential as a target for T cell engineering, are poorly understood. We describe SATB1-regulated gene signatures as largely subset-specific, with broader effects on Treg cells. Despite of the distinct gene-regulatory patterns, we observe overarching dysregulated cytokine and JAK-STAT signaling after ablation. Functionally, KO reduces human Treg cell suppressive capacities but boosts tumor clearance via CD4 CAR T cells in a preclinical, humanized mouse model. Together, Treg destabilization and simultaneous increased activation of CD4 CAR T cells by SATB1 modulation may be an interesting strategy to boost the efficiency of CAR T cell therapies. - Source: PubMed
Publication date: 2026/02/16
Kolb SaskiaDiekmann LeonieLochert Elizabeth DWarmuth LindaRitter JuliaWeber MichaelHoffmann MarkusList MarkusKotlarz DanielSerr IsabelleDaniel CarolinBusch Dirk HSchmidl ChristianSchumann Kathrin - The features of patients with multiple urothelial tumors remain to be elucidated. We intend to differentiate primary upper tract urothelial carcinoma with synchronous urothelial bladder cancer (UTUC + sUBC) and UTUC with metachronous UBC (UTUC + mUBC) cases to determine whether these temporal patterns reflect biologically distinct processes. A subgroup analysis of a retrospective cohort of UTUC ( = 114) was performed comparing UTUC + sUBC ( = 14) with UTUC + mUBC ( = 29). IHC expression of cytokeratin 5/6 (CK5/6), CK20, GATA3, and p53 was evaluated to assess relevant subtypes. Genetic characterization comprised , , , and status. Kaplan-Meier analyses estimated the progression-free survival (PFS) and overall survival (OS) of both UTUC subgroups, and the log-rank test was used to assess differences between subgroups. Our study reveals no significant differences in phenotype or genomic profile between synchronous and metachronous UTUC-UBC cases ( > 0.05). Nevertheless, patients with synchronous UBC revealed significantly worse outcomes in PFS (2y-PFS 23.1% vs. 52.1%, = 0.029) and OS (2y-OS 40.4% vs. 84.4%, = 0.016) than those with metachronous disease. These discrepancies could arise from as yet-uncharacterized molecular features or microenvironmental influences. - Source: PubMed
Publication date: 2026/03/26
Meireles SaraDias CarolinaMarques AnaSilva JoãoCosta LuísLopes José ManuelSoares Paula