# EpCAM

Source: https://onco.cc/targets/epcam/  
OnCo record `epcam` (Target). Data CC BY-NC 4.0, attribute "Data from OnCo (onco.cc)"; commercial use needs a licence.

## TL;DR

An adhesion protein on almost all carcinoma cells and the capture molecule for circulating tumour cell tests; the target of the first bispecific antibody ever approved (catumaxomab, 2009).

## Summary

EpCAM (CD326) is expressed on most carcinomas (colorectal, gastric, pancreatic, breast, ovarian, lung) and on circulating tumour cells (CellSearch). Catumaxomab (EpCAM×CD3 trifunctional) was approved in the EU in 2009 for malignant ascites, withdrawn commercially in 2017 and re-approved in 2025; edrecolomab (adjuvant colon) failed in the 1990s; oportuzumab monatox (intravesical, BCG-unresponsive NMIBC) received an FDA CRL in 2021. Solitomab (BiTE) was too toxic because of normal epithelial expression. EpCAM CAR-T and ADCs are being tested in gastric and colorectal cancer, and germline EPCAM deletions cause Lynch syndrome via MSH2 silencing.

## Fields

- Kind: Target
- Last checked: 2026-09-08
- Tags: gap-fill
- Symbol: EPCAM
- Class: surface-antigen
- Biology: Type I transmembrane glycoprotein mediating Ca-independent homotypic cell adhesion; regulated intramembrane proteolysis releases EpICD, which co-activates Wnt/β-catenin target genes (c-MYC, cyclin D1).
- Where found: Colorectal, gastric, pancreatic and biliary adenocarcinoma (>90%); Breast, ovarian, endometrial and prostate cancer (high); Circulating tumour cells (capture antigen); Normal epithelia (basolateral, lower level)

## Notes

- Ovarian and urothelial rates are not well characterised by a single figure: the largest series (Spizzo 2011, doi:10.1136/jcp.2011.090274) reports adenocarcinomas as mostly positive but urothelial and squamous carcinomas as frequently EpCAM-negative and recommends IHC before any EpCAM-directed therapy.
- Colorectal cancer: deletions of the 3' exons of EPCAM cause Lynch syndrome without any mutation in a mismatch repair gene, by transcriptional read-through that methylates and silences the adjacent MSH2 promoter in EpCAM-expressing tissue (Ligtenberg 2009). EPCAM copy-number analysis is therefore part of a complete Lynch syndrome panel.

## Sources

- Wikipedia: https://en.wikipedia.org/wiki/Epithelial_cell_adhesion_molecule
- EMA: Korjuny (catumaxomab): https://www.ema.europa.eu/en/medicines/human/EPAR/korjuny

## Connected records

- cancers: [Bladder & urothelial cancer](https://onco.cc/cancers/urothelial/), [Colorectal cancer](https://onco.cc/cancers/colorectal/), [Gastric & gastro-oesophageal junction cancer](https://onco.cc/cancers/gastric/), [Ovarian cancer](https://onco.cc/cancers/ovarian/), [Pancreatic ductal adenocarcinoma](https://onco.cc/cancers/pancreatic/)
- technologies: [Bispecific antibodies](https://onco.cc/technologies/bispecific-antibody/), [CAR-T cell therapy](https://onco.cc/technologies/car-t/), [Liquid biopsy (ctDNA)](https://onco.cc/technologies/liquid-biopsy/)
- drugs: [Catumaxomab](https://onco.cc/drugs/catumaxomab/), [M701](https://onco.cc/drugs/m701/)
- pathways: [Intravasation & circulating tumour cells](https://onco.cc/pathways/intravasation-ctc-survival/), [Mismatch repair & microsatellite instability](https://onco.cc/pathways/mismatch-repair-msi/)
- terms: [Lynch syndrome](https://onco.cc/terms/lynch-syndrome/)
- key papers: [Heritable somatic methylation and inactivation of MSH2 in families with Lynch syndrome due to deletion of the 3' exons of TACSTD1](https://onco.cc/key-papers/paper-ligtenberg-epcam-deletion-msh2-silencing-nat-genet-2009/)

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