Human Ep-CAM Monoclonal Antibody
- Known as:
- Human Ep-CAM Monoclonal Antibody
- Catalog number:
- x1779m
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Exalpha
- Gene target:
- Human Ep-CAM Monoclonal Antibody
Ask about this productRelated genes to: Human Ep-CAM Monoclonal Antibody
- 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: Human Ep-CAM Monoclonal Antibody
Related articles to: Human Ep-CAM Monoclonal Antibody
- Accurate detection of lymph node (LN) metastases is critical for prognosis and surgical decision-making in head and neck squamous cell carcinoma (HNSCC) and other epithelial cancers. Standard histopathology examines only a small fraction of LN tissue, limiting sensitivity for micrometastases and isolated tumour cells. Scalable approaches are needed to improve staging accuracy and reduce overtreatment. We adapted the FDA-approved CELLSEARCH System, originally developed for circulating tumour cell detection, for use on dissociated 50 μm formalin-fixed paraffin-embedded (FFPE) LN sections. Tumour cells were enriched via EpCAM-based immunomagnetic capture, stained with cytokeratin (CK)/DAPI and quantified using the ACCEPT (Automated CTC Classification, Enumeration and Phenotyping Technology) image analysis tool. Specificity and reproducibility were tested in 50 metastasis-positive and 50 metastasis-free LNs from patients with HNSCC. Enriched cells underwent single-cell and pooled whole-genome amplification (WGA), quality-controlled by a genomic integrity index and profiled for copy number alterations (CNA) by low-pass whole-genome sequencing. Tumour cells were detected in 100% of LN metastases (range: 37-12,479), with counts strongly correlating with histological tumour area (p < 0.0001). Rare background events in control LNs were excluded by manual CELLSEARCH review. Based on their frequency, a threshold of > 12 cells was defined to classify samples as positive, yielding an assay specificity and sensitivity of 100%. Reproducibility across adjacent sections was high. Despite FFPE preservation, WGA succeeded in 27% of single cells and > 75% of pooled fractions. CNA profiling yielded 50 high-quality tumour genomes, revealing typical HNSCC alterations and marked inter-/intra-patient heterogeneity. This adapted CELLSEARCH workflow enables sensitive detection and genomic profiling of tumour cells from FFPE LN tissue. Demonstrated in HNSCC as a proof of concept, the approach is broadly applicable to epithelial cancers where LN staging is prognostically decisive. © 2026 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland. - Source: PubMed
Publication date: 2026/09/21
Bergmann TristanHölbling MarianneSudarsanam MonicaDriemel ChristianeDaniels Maximilian ESwierz JoannaJaschinski SandraSeidl MaximilianKübler Norbert RKnoefel Wolfram TNeves Rui PlSproll Karl CStoecklein Nikolas H - Epithelial Cell Adhesion Molecule positive (EpCAM) extracellular vesicles (EVs) can promote cancer progression and metastasis. Thus, it is necessary to develop targeted strategies to disable EpCAM EVs. - Source: PubMed
Publication date: 2026/08/05
Su NingZhang WenjiaTang JiayuLiu WeiZhao JiandongGao MingxiaZhang Xiangmin - EpCAM is overexpressed in solid tumors and is a promising pan-tumor imaging target, yet clinically applicable PET tracers are limited. We developed and evaluated a novel EpCAM-targeted tracer, Ga-DOTA-EP-1. The peptide sequence EP-1 (YEVHTYYLD) was previously identified as an EpCAM-binding ligand via high-throughput bi-functional microarray screening. Based on this scaffold, we performed chemical modification by conjugating a DOTA chelator via an Acp linker to enable Ga radiolabeling for PET imaging. After labeling, stability, lipophilicity, protein binding, and specificity were evaluated in EpCAM-positive and -negative cell lines. In vivo PET imaging, biodistribution, immunohistochemistry, and toxicity were performed in tumor-bearing mice, followed by a preliminary clinical study. Ga-DOTA-EP-1 exhibited high radiochemical purity and excellent stability. Cellular uptake was significantly higher in EpCAM-positive cells (P < 0.05), with high binding affinity confirmed by blocking and IC assays. PET imaging showed markedly higher uptake in EpCAM-positive xenografts, significantly reduced by blocking. Preliminary clinical imaging demonstrated favorable safety and clear visualization of hepatic metastases. These findings suggest that Ga-DOTA-EP-1 has the potential to serve as an EpCAM-targeted PET tracer with favorable specificity and a promising safety profile for further clinical evaluation. - Source: PubMed
Publication date: 2026/09/18
Tang ShijieLiu YanggangHui ShiboLiu MiaoZhang YangAi YihengChen YueLi XiangQiu Lin - Lymph node (LN) metastasis is a major determinant of prognosis in gastric cancer, yet the immune microenvironment of metastatic versus non-metastatic nodes remains incompletely defined. Spatial resolution of tumor-immune interactions may clarify mechanisms of immune escape associated with nodal progression. We performed compartment-resolved spatial transcriptomic profiling to characterize immune gene expression in gastric cancer LNs. Forty-seven formalin-fixed paraffin-embedded LNs from 13 patients with T2-T4, M0 gastric adenocarcinoma (N1-2: n = 7; N3: n = 6) were analyzed using the NanoString GeoMx Digital Spatial Profiler and an 84-gene immune pathways panel. Twenty-nine non-metastatic and 18 metastatic LNs were profiled. Regions of interest were segmented into tumor and immune compartments, yielding 65 spatially defined compartments. Differential expression was assessed across three comparisons: metastatic versus non-metastatic LNs; metastatic LNs from N1-2 versus N3 patients; and non-metastatic LNs from N1-2 versus N3 patients. Within the immune compartments, non-metastatic LNs showed higher expression of T-cell activation and checkpoint genes (CD3E, CD27, PDCD1, CTLA4), consistent with preserved immune surveillance. Metastatic LNs were enriched for WNT signaling and adhesion-related genes (CTNNB1, ITGAV) and epithelial markers (EPCAM), indicating tumor-driven immune remodeling. N3 metastatic LNs demonstrated increased ICOSLG, IL6, and IFNGR1 expression, suggesting chronic inflammatory activation and immune dysfunction. Notably, non-metastatic LNs from N3 patients upregulated antigen-presentation genes (CD74, HLA-DRB), consistent with early immune conditioning. No significant differences emerged in tumor compartments or pseudo-bulk analyses. Spatial transcriptomic profiling reveals nodal burden-associated immune remodeling, and identifies candidate biomarkers and therapeutic targets for precision immunotherapy in gastric cancer. - Source: PubMed
Publication date: 2026/09/17
Suwatthanarak ThanawatNampoolsuksan ChawisaTanjak PariyadaThanormjit KullanistAcharayothin OnchiraChaiboonchoe AmphunSuwatthanarak TharathornPithukpakorn ManopChalermwai Wipapat VickiSwangsri JirawatMethasate AsadaChinswangwatanakul VitoonParakonthun Thammawat - Birt-Hogg-Dubé (BHD) syndrome is a hereditary cancer predisposition syndrome caused by pathogenic variants in the folliculin (FLCN) gene and is associated with an increased risk of multifocal renal tumors. FLCN-mutated tumors (FMTs) often exhibit morphological heterogeneity with mixed morphological features resembling renal oncocytoma (RO) and chromophobe renal cell carcinoma (chRCC), yet the molecular basis underlying the heterogeneous morphologic features and the morphologic-genomic correlations remain poorly defined. In our prior work, we identified mutually exclusive expressions of L1 cell adhesion molecule (L1CAM) and forkhead box I1 tboxI1 (FOXI1) labeling the two morphologically distinct cellular populations in BHD-associated FMTs, leading to the hypothesis that these two tumor compartments may have distinct molecular features and may reflect different nephron epithelial differentiation states. In this follow-up study, we tested this hypothesis using L1CAM and FOXI1 as morphology-guided markers for spatial transcriptomic profiling of the distinct tumor compartments in FMTs with the NanoString GeoMX Digital Spatial Profiler (DSP). Six FMTs from three patients with BHD and three normal kidney tissues were analyzed. L1CAM+ and FOXI1+ area of interest (AOI) were collected from tumor areas with various tumor compositions, including L1CAM+ dominant, FOXI1+ dominant, and mixed tumor areas. Spatial transcriptomic analysis identified distinct gene expression signatures in L1CAM+ and FOXI1+ FMT compartments independent of the local tumor compositions. FOXI1+ tumor cells showed robust enrichment for intercalated cells (IC)-associated gene signatures. In contrast, L1CAM+ tumor cells exhibited a heterogeneous transcriptional profile, with partial overlap across a spectrum of renal tubular epithelial cell types rather than a definitive principal cell-like identity. Despite this compartment-specific differences, both compartments share expression of a panel of tumor signature genes, including glycoprotein nmb (GPNMB) gene, and a core of cancer related biological functions and signaling pathways. Together, these findings refined the prior dichotomous model of BHD-associated renal tumors and support a model in which L1CAM+ and FOXI1+ tumor compartments represent divergent evolutionary or differentiation states with a common FLCN-mutant neoplastic transcriptional program. This spatial transcriptomic profiling provides molecular evidence for the morphological heterogeneity of FMTs and insights on the tumor biology of BHD-associated FMTs. - Source: PubMed
Publication date: 2026/09/17
Wang Xiao-MingZhang YupingMannan RahulZhou JiayiWang SusannaChinnaiyan Arul MDhanasekaran Saravana MMehra Rohit