TFF2 monoclonal antibody, clone GE16C
- Known as:
- TFF2 mab (anti-), clonality GE16C
- Catalog number:
- MAB9523
- Product Quantity:
- 1 mL
- Category:
- -
- Supplier:
- Abno
- Gene target:
- TFF2 monoclonal antibody clone GE16C
Related genes to: TFF2 monoclonal antibody, clone GE16C
- Gene:
- TFF2 NIH gene
- Name:
- trefoil factor 2
- Previous symbol:
- SML1
- Synonyms:
- -
- Chromosome:
- 21q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 1991-12-13
- Date modifiied:
- 2015-08-26
Related products to: TFF2 monoclonal antibody, clone GE16C
Related articles to: TFF2 monoclonal antibody, clone GE16C
- The article "Identification of LGR5 and TFF2 as Biomarkers in High-Risk Chronic Atrophic Gastritis: From Multi-Omics Mining to Clinical Validation" [Digestion. 2026; https://doi.org/10.1159/000549887] by Qingqing Zhang, Di Wu, Fengyun Guo, Shengnan Yang, Lijing Bao, Ruiying Zhang and Ping Wang has been retracted by the Publisher and the Editor.Post-publication concerns were raised regarding the integrity of the clinical cohort data reported in the article. The data presented in Table 1 shares the same subgroup size, gender distributions and H. pylori infection rates across all three subgroups to those reported in a previously published article by the same research group [1]. Additionally, the images in Figure 4b and d of this article are published as Figure 2a and b in [1]. The previous publication was not cited in this article.When asked about the similarities between the cohorts, the authors stated that they were two independent cohorts and that the similarities were coincidental. The Editors did not find the authors' explanation sufficient to resolve their concerns, and as a result have lost confidence in the reliability and originality of the reported cohort data.The authors did not respond to our correspondence about the retraction of this article within the timeframe specified. - Source: PubMed
Publication date: 2026/07/31
- Portal vein tumor thrombosis (PVTT) is a critical event that promotes intrahepatic dissemination, induces portal hypertension, and worsens the prognosis of hepatocellular carcinoma (HCC), yet its formation mechanism remains poorly understood. - Source: PubMed
Publication date: 2026/07/18
Shi SenlinLi JianbinZhang MengxianChen ZhuohaoChen JunxiLi LinKong YuhangHuang WuyanHu HongmingLiu ShangjieZhang RongxinHuang WenbinCao Yulun - Eosinophilic gastritis (EoG) is a chronic inflammatory disease characterized by infiltration of eosinophils and mast cells, epithelial remodeling, and fibrosis. Although EoG is increasingly recognized as a distinct type 2 inflammatory disease, the cellular and molecular events that drive disease pathogenesis remain poorly understood. This is due in part to the absence of robust and physiologically relevant experimental models that recapitulate human disease METHODS: Experimental EoG was induced in wild-type and Il13ra1 mice by repeated intragastric oxazolone challenges in skin-sensitized mice. IL-4Rα was neutralized using antibodies. Gastric histopathology was determined by H&E, anti-Ki67, chloroacetate esterase, and anti-MBP staining. Gastric RNA was subjected to RNA sequencing. - Source: PubMed
Publication date: 2026/06/18
Dsilva AnishSharma ShraddhaBarakey ShireenWagner ArielKeisar AliceBar-On TaliItan MichalMunitz Ariel - The pathogenesis of gallbladder adenocarcinoma(GBC) remains inadequately elucidated. While its association with intestinal metaplasia (IM) has been acknowledged, there is a paucity of evidence connecting GBC to the most prevalent metaplastic type-pseudopyloric metaplasia (PPM). Given the morphological similarities between PPM and spasmolytic polypeptide-expressing metaplasia (SPEM), a recognized gastric precancerous condition, we propose that trefoil factor 2 (TFF2)-positive PPM may represent a cellular origin of GBC. Furthermore, we examine the role of the emerging therapeutic target claudin-18 (CLDN18) in this context. Through immunohistochemistry (IHC) analysis of 37 GBC, 30 biliary intraepithelial neoplasia (BilIN), 20 intracholecystic papillary neoplasm (ICPN), 26 IM, and 20 PPM samples, we observed an inverse correlation between CLDN18 expression and vascular invasion, whereas TFF2 expression was positively associated with tumor differentiation. CLDN18 overexpression(a staining intensity ≥ 2 + in ≥ 75% of tumour cells) was identified in 18.9% of GBC cases. This study provides the first evidence that CLDN18 is specifically activated at the precursor stage of gallbladder carcinogenesis, being strictly confined to lesions with an intestinal phenotype (IM, BilIN, ICPN) while remaining entirely negative in normal epithelium and PPM. This "all or none" expression pattern establishes CLDN18 as an ideal biomarker for identifying high risk gallbladder precursor lesions, particularly for recognizing PPM that has undergone malignant prone intestinal differentiation. Furthermore, the subset of GBCs with high CLDN18 expression identifies patients who may benefit from CLDN18 targeted therapies. - Source: PubMed
Publication date: 2026/05/26
Min QinqinJiang XuCheng YaoYu XuewenYang TingtingGu GuiyuanMei KaiyongShao Mumin - Spasmolytic polypeptide-expressing metaplasia (SPEM) arises in the gastric corpus in response to oxyntic atrophy, but its cellular origin and role in gastric cancer remain unclear. - Source: PubMed
Publication date: 2026/04/14
Tu RuhongZheng Hua-LongZheng BiyunZhong QingQian JinYu QianWu FeijingShiokawa ToshiroOchiai YosukeKobayashi HirokiWaterbury Quin TZamechek LeahGao YouxinTakahashi SatoruMizuno SeiyaHuang Chang MingLi PingHayakawa YokuWang Timothy C