ESO-26

Name: ESO-26
Brand: Creative Bioarray

Cat.No.: CSC-C0686

Species: Homo sapiens (Human)

Source: Esophagus

Morphology: ovoid cells growing semiadherently, singly or in clumps

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Cat.No.

CSC-C0686

Description

Established from the primary tumor (pT4N1M1) of a 56-year-old Caucasian man with esophageal adenocarcinoma in 2000; cells are described to carry a p53 mutation (C742T)

Species

Homo sapiens (Human)

Source

Esophagus

Recommended Medium

80-90% RPMI-1640 + 10-20% h.i. FBS

Morphology

ovoid cells growing semiadherently, singly or in clumps

Karyotype

Human hypodiploid karyotype; 39(36-40)<2n>X, -Y, +2, -3, -5, -11, -12, -15, -16, -19, -20, -22, +mar add(X)(p22), del(1)(p32), add(12)(p13), der(13;21)(q10;q10), i(13)(q10), add(17)(p12), add(?18)(q21), add(21)(p11)

Disease

Gastroesophageal Junction Adenocarcinoma

Quality Control

Mycoplasma: negative in microbiological culture, PCR assays
Immunology: cytokeratin +, cytokeratin-7 +, cytokeratin-8 +, cytokeratin-17 -, cytokeratin-18 +, cytokeratin-19 +, desmin -, endothel -, EpCAM +, GFAP -, neurofilament -, vimentin -
Viruses: PCR:

Storage and Shipping

Frozen with 70% medium, 20% FBS, 10% DMSO at about 5 x 10^6 cells/ampoule; ship in dry ice; store in liquid nitrogen

Synonyms

ESO26

Citation Guidance

If you use this products in your scientific publication, it should be cited in the publication as: Creative Bioarray cat no. If your paper has been published, please click here to submit the PubMed ID of your paper to get a coupon.

ESO-26 is a rigorously authenticated human esophageal adenocarcinoma (EAC) cell line established in 2000 from the primary tumor (Stage IV, pT4N1M1) of a 56-year-old Caucasian male patient. As one of only nine EAC lines whose identity has been verified against original patient material through STR profiling, p53 mutation analysis, and xenograft histology, ESO-26 offers exceptional model fidelity.

Molecularly, the line harbors pathogenic TP53 (C742T) and SMAD4 mutations, faithfully recapitulating key driver alterations observed in approximately 69% and 13% of primary EACs, respectively. It displays a hypodiploid karyotype and robust expression of epithelial differentiation markers including cytokeratins 7/8/18/19, EpCAM, and SOX9, alongside demonstrated tumorigenicity and a doubling time of 35–50 hours.

Critically, ESO-26 is supported by publicly available whole-genome sequencing data and integrated into major pharmacogenomic resources including CellMinerCDB, GDSC, and Broad Achilles CRISPR-Cas9 screens. This comprehensive molecular annotation enables precise experimental design, robust genotype-phenotype analysis, and high-throughput therapeutic screening. With authenticated origin, defined oncogenic drivers, and multi-platform omics characterization, ESO-26 stands as a robust, clinically representative platform for advancing mechanistic and translational research in gastroesophageal adenocarcinoma.

Trophoblast Cell Surface Antigen 2 (TROP2) as a Predictive Bio-Marker for the Therapeutic Efficacy of Sacituzumab Govitecan in Adenocarcinoma of the Esophagus

The Trophoblast cell surface antigen 2 (TROP2) is expressed in many carcinomas and may represent a target for treatment. Sacituzumab govitecan (SG) is a TROP2–directed antibody-drug conjugate (ADC). Nearly nothing is known about the biological effectiveness of SG in esophageal adenocarcinoma (EAC).

Established esophageal adenocarcinoma cell lines Eso26, OACM 5.1C and Flo1 were used as a model to demonstrate the relevance of TROP2 expression levels to the effectiveness of treatments with sacituzumab govitecan (SG). Analysis of the TROP2 expression in these cells showed that Eso26 homogenously expresses high levels of TROP2 mRNA and protein, while Flo1 lacks TROP2 expression. OACM 5.1C shows a low-level mRNA expression as well as just a few TROP2-positive tumor cells (Fig. 1A, B). The dilution series of SG showed a ~15-fold decreased response for the TROP2 negative cell line Flo1 compared to TROP2 positive Eso26 (Fig. 1C). SN-38, the active compound of the antibody–drug conjugate SG alone, has little effect equally on both cell lines, demonstrating the protein-dependence of SG. The FLO-1 cell line has a special delayed growth behavior with rapid progression compared to the early onset Eso26 with a similar rapid progression. Together, in vitro experiments show differential efficacy of SG to inhibit EAC cell lines with a positive correlation to TROP2 expression levels.