CD326 _ EpCAM
- Known as:
- CD326 _ EpCAM
- Catalog number:
- 11-581-C100
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Exbio
- Gene target:
- CD326 _ EpCAM
Related genes to: CD326 _ EpCAM
- Gene:
- EPCAM NIH gene
- Name:
- epithelial cell adhesion molecule
- Previous symbol:
- M4S1, MIC18, TACSTD1
- Synonyms:
- Ly74, TROP1, GA733-2, EGP34, EGP40, EGP-2, KSA, CD326, Ep-CAM, HEA125, KS1/4, MK-1, MH99, MOC31, 323/A3, 17-1A, TACST-1, CO-17A, ESA
- Chromosome:
- 2p21
- Locus Type:
- gene with protein product
- Date approved:
- 1995-10-02
- Date modifiied:
- 2019-04-23
Related products to: CD326 _ EpCAM
Related articles to: CD326 _ EpCAM
- Lynch syndrome (LS) is an autosomal dominant cancer predisposition syndrome caused by germline mutations in DNA mismatch repair genes or, less commonly, EPCAM deletions. LS-associated colorectal carcinomas often present at a young age and may show unusual histomorphological patterns, posing diagnostic challenges. We report a rare case of a 29-year-old female with EPCAM-mutated LS presenting as colonic adenocarcinoma with neuroendocrine-like rosette formation. The tumor initially mimicked mixed adenoneuroendocrine carcinoma (MANEC) due to biphasic histology and the presence of multiple rosettes. However, immunohistochemistry demonstrated negativity for synaptophysin and chromogranin, excluding true neuroendocrine differentiation with diffuse Pan CK and focal CDX2, CK20 positivity along with loss of MSH2 and MSH6. Further molecular analyses confirmed EPCAM exon 5-9 deletion. The tumor was ultimately classified as an MMR-deficient adenocarcinoma with pseudoendocrine morphology. This case broadens the histomorphological spectrum of LS-associated colorectal carcinomas and introduces the concept of a possible pseudoendocrine carcinoma arising in an epithelial malignancy. Recognition of this pattern is crucial to prevent misdiagnosis as MANEC, to guide appropriate management, facilitate familial screening, and highlight that not every rosette signifies neuroendocrine differentiation; some may represent LS in disguise. - Source: PubMed
Publication date: 2026/09/28
Bandyopadhyay ArghyaChakrabarti AsmitaMondal AmbalikaMaji RatnaprabhaBarui Gopinath - Lynch syndrome (LS) is the most common cause of hereditary colorectal and endometrial cancer. LS is caused by germline pathogenic variants (PV) in the mismatch repair genes (MLH1, MSH2, MSH6, PMS2) and EPCAM. Little is known about LS in Iraqi/Chaldean and broader Middle Eastern and North African populations. We describe our institution's experience with a unique MSH2 PV in a cohort of Iraqi/Chaldean patients. Records of patients with LS and Iraqi/Chaldean ancestry seen in a high-volume cancer genetics center between January 2008 and March 2024 were analyzed. A total of 483 LS patients were identified, of whom 60 (12.4%) reported Iraqi/Chaldean ancestry. Of those, 53 individuals (88.3%) from 22 unique families harbored the same PV in MSH2, c.932delA (p.N311Tfs*20) and were analyzed in this study. This variant was detected only in our Iraqi/Chaldean population. Of individuals with this variant, 28 (52.8%) had at least one LS-related cancer diagnosis (17 colorectal, 12 endometrial, 7 renal/urothelial, 6 ovarian, one sebaceous carcinoma), of whom 16 (57.1%) had multiple malignancies. The average age of colorectal cancer onset was 49.6 years. Additionally, 14 families (63.6%) underwent cascade testing, identifying 31 of the MSH2 carriers in this cohort and 25 true negatives. This is the first report of a recurrent MSH2 c.932delA PV in Iraqi/Chaldean patients with LS. These findings suggest a putative LS founder variant in the Iraqi/Chaldean population, and further studies are needed to characterize LS in this population. - Source: PubMed
Publication date: 2026/09/27
Bradley MikaelaRangarajan TaraZakalik Dana - Tuft cells are a rare type of epithelial cell that are essential to regulate innate and adaptive immune responses. Mucosal immunity is also composed primarily of IgA produced by B cells that is secreted onto mucosal surfaces as secretory IgA via the polymeric immunoglobulin receptor (pIgR). The homing of B cells in lymphoid organs is mediated by certain adhesion receptors, such as α4β7 and chemokine receptor 9 (CCR9), that bind to the specific vascular ligands, mucosal vascular addressin cell adhesion molecule 1 (MAdCAM-1) and chemokine ligand 25 (CCL25), respectively. It is unclear whether tuft cells, MAdCAM-1, CCL25, and pIgR are present or expressed in the nasal cavities of pigs. Our study aimed to develop immunohistochemistry (IHC) or immunofluorescence (IF) staining for the detection of tuft cells, MAdCAM-1, CCL25, pIgR, and IgA- or IgG-positive cells in porcine nasal turbinates. The tissues were acquired from the piglets of two different treatment groups in our previous studies that investigated the impact of oral vitamin A supplementation (VA) on the maternal immunity of vitamin A-deficient (VAD) sows and the passive protection of their piglets against rotavirus A (RVA): (1) VAD + VA + RVA and (2) VAD + RVA piglets. Our IHC staining revealed that low numbers of advillin-positive, bottle-shaped cells that morphologically resemble tuft cells were present in the mucosal epithelium and the mucous duct or glands. There were also moderate to large amounts of MAdCAM-1 and CCL25 in the endothelial cells lining the vascular structures present in the lamina propria of nasal turbinates and moderate to large amounts of pIgR in the turbinate mucosal epithelium. Moderate to high numbers of IgA- or IgG-positive cells were present in the lamina propria. There were no differences in IF- or IHC-positive scores or the positive cell numbers of all parameters tested between VAD + VA + RVA and VAD + RVA piglets, suggesting little or no effect of VA on the parameters tested. Our study demonstrated the use of IHC/IF staining methods for the detection of tuft cells, MAdCAM-1, CCL25, pIgR, and IgA- or IgG-positive cells in porcine nasal turbinates, expanding our understanding of the in situ distribution and comparison in the nasal cavity of pigs born to the sows fed vitamin A-deficient diets with or without vitamin A supplementation. - Source: PubMed
Publication date: 2026/09/18
Jung KwonilVlasova Anastasia NSaif Linda J - : Tumor progression is often accompanied by sialylation of cell-surface N-glycan glycoproteins with α2-6-linked sialic acids by the sialyltransferase ST6GAL1. Moreover, a hallmark of human cancers is heterogeneity in ST6GAL1 expression among cancer cells, yet the mechanisms and significance of this variability remain poorly understood. Here, we investigate whether epigenetic changes in ST6GAL1 DNA methylation, which affect intracellular ST6GAL1 and cell-surface α2,6-sialylation of glycoproteins, are associated with the biology of human breast cancer (BCa) cells. : We analyzed CpG island methylation across spatially distinct regions of the human ST6GAL1 promoter (P2 and P3) and the associated loss of ST6GAL1 expression in primary human breast tumors compared with adjacent normal tissue controls. Epigenetic changes in ST6GAL1 DNA methylation and patient progression-free survival (PFS) were evaluated. Small-molecule epigenetic inhibitors (5-aza-dC and MS-275) were used to assess ST6GAL1 transcriptional reactivation and its effects on intracellular ST6GAL1, cell-surface α2,6-sialylation, and cell adhesion to collagen I in cultured BCa cell models. : In estrogen receptor (ER)+ and human epidermal growth factor receptor 2 (HER2)+ primary BCa tissues, ST6GAL1 P3-promoter hypermethylation, but not P2-promoter methylation, significantly correlated with loss of ST6GAL1 expression compared with adjacent normal controls. Higher promoter methylation was significantly associated with improved PFS in ER+ and HER2+ BCa subtypes compared with triple-negative breast cancer (TNBC). ST6GAL1 protein expression and relative transcript levels are higher in adjacent normal controls or human normal breast epithelial cells than in human BCa tissue or cultured cells. In BCa cells, native ST6GAL1 is sensitive to degradation by cycloheximide or MG-132 and even to sialidase treatment. Pharmacological reactivation with 5-aza-dC or MS-275 restored intracellular ST6GAL1 expression and functional cell-surface α2,6-sialylation, thereby enhancing BCa cell adhesion to collagen I. Since ST6GAL1 is also released into the extracellular milieu by cancer cells, and extracellular ST6GAL1 (exoST6) may contribute to cancer cell-surface protein α2,6-sialylation, we also found that 5-aza-dC increased exoST6 levels released in the form of exosome vesicles. : Our results suggest that ST6GAL1 promoter methylation, together with copy-number alterations, drives loss of expression and phenotypic heterogeneity in human BCa, thereby reducing α2,6-sialylation and correlating with improved PFS in the ER+ and HER2+ subtypes. Demethylating agents restore both endogenous ST6GAL1 expression and exosomal exoST6 release in BCa cells, highlighting this targetable epigenetic axis as a promising prognostic biomarker and therapeutic strategy to improve patient survival in progressive diseases. Future studies will focus on evaluating the functional outcomes of targeting cell-native ST6GAL1 versus the exoST6/sialylation pathways and on defining ST6GAL1's role in driving disease progression in vivo. - Source: PubMed
Publication date: 2026/09/16
Maiti AparnaKawashima KeiAn HongjooRedman Lydia J BWu YunAbrams Scott ILau Joseph T YHait Nitai C - Lung cancer recurrence and therapeutic resistance are driven by cancer stem cells (CSCs), yet clinically available CSC-targeted therapies remain lacking. To identify actionable anti-CSC agents, we screened 1018 FDA-approved drugs using a 3D sphere culture system enriching lung CSC-like cells. Trimebutine, a gastrointestinal motility regulator targeting G-protein-coupled receptors (GPCRs), was identified as a potent agent with over 49.5-fold higher selectivity toward lung CSC-like cells (SI > 49.55) compared with standard therapies such as cisplatin (SI = 1.39) and gefitinib (SI = 1.00). In H460-SP spheres, trimebutine markedly impaired sphere-forming capacity, reduced cell viability, and downregulated key CSC surface markers (CD133, CD44) alongside stemness regulators (c-MYC, EpCAM, BMI1, OCT3/4, NANOG, SOX2, SMAD3). Mechanistically, trimebutine suppressed overexpressed calcium and potassium channels (, , , , ), attenuating downstream YAP/TAZ-TEAD signaling within the Hippo pathway to trigger apoptosis. In combination with cisplatin, trimebutine exhibited strong synergistic efficacy (Chou-Talalay combination index, CI = 0.015-0.228) in H460-SP spheres and patient-derived lung tumor organoids, suppressing cell viability, stemness marker suppression, and apoptotic cleavage of caspase-3 and PARP compared to monotherapies. Overall, trimebutine targets lung CSC populations by disrupting GPCR-ion channel-Hippo signaling crosstalk, providing a strong preclinical rationale for trimebutine-cisplatin combination strategies to overcome drug resistance and recurrence in lung cancer. - Source: PubMed
Publication date: 2026/09/15
Seo JiHyeLee HeejinChoi Dong KyuKim Young-KyuWoo SominLee ChangkyuChoi Jeong InJiang GeOh Bae JunLee Dong-SeokMin Sang-Hyun