EFM-192A

Cat.No.: CSC-C0358

Species: Homo sapiens (Human)

Source: Pleural Effusion Metastasis

Morphology: epitheloid, adherent growing as monolayer

Culture Properties: monolayer

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Cat.No.

CSC-C0358

Description

Established from the pleural effusion of the left side from a 46-year-old Caucasian woman with metastasizing breast adenocarcinoma in 1985; sister cell lines EFM-192B and C show differences in molecular aspects; erbB-2 gene is amplified and overexpressed

Species

Homo sapiens (Human)

Source

Pleural Effusion Metastasis

Recommended Medium

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

Culture Properties

monolayer

Morphology

epitheloid, adherent growing as monolayer

Karyotype

Human flat-moded near-triploid karyotype with 20% polyploidy - 68(60-70)<3n>XXXX, +X, -1, -4, +9, -12, -17, -17, -18, -22, +6mar, add(1)(p22), add(1)(p?32), add(2)(q35/37), add(3)(q27/29), i(15q), add(17)(p12), dminx1 present at 38%

Disease

Breast Carcinoma

Quality Control

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

Storage and Shipping

Frozen with 70% medium, 20% FBS, 10% DMSO at about 4 x 10^6 cells/ampoule; ship in dry ice; store in liquid nitrogen

Synonyms

EFM192A; EFM192

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.

The EFM-192A cell line is a well-characterized human breast carcinoma model established from the malignant pleural effusion of a patient with metastatic breast cancer. It is classified as a HER2-positive (ERBB2-amplified) breast cancer model, representing a clinically significant subtype that accounts for approximately 15-20% of breast cancers and is associated with aggressive disease. Beyond HER2 amplification, EFM-192A harbors a second key driver mutation: an activating mutation in the PIK3CA gene (H1047R), which is one of the most frequent oncogenic alterations in breast cancer. This co-occurrence of HER2 amplification and PIK3CA mutation makes EFM-192A a genetically representative model of a common and therapeutically challenging tumor profile, reflecting the complex genomic landscape often seen in clinical practice.

HER2-Targeted Agents and Amcenestrant Are Synergistic in HER2+/ER+ Cell Lines

HER2-positive/oestrogen receptor-positive (HER2+/ER+) represents a unique breast cancer subtype. The use of individual HER2- or ER-targeting agents can lead to the acquisition of therapeutic resistance due to compensatory receptor crosstalk. New drug combinations targeting HER2 and ER could improve outcomes for patients with HER2+/ER+ breast cancer. In this study, the pre-clinical rationale is explored for combining amcenestrant (Amc), a selective oestrogen receptor degrader (SERD), with HER2-targeted therapies including trastuzumab, trastuzumab-emtansine (T-DM1) and tyrosine kinase inhibitors (TKIs). The combination of Amc and anti-HER2 therapies was investigated in a panel of four HER2+/ER+ cell lines: BT-474, MDA-MB-361, EFM-192a and a trastuzumab-resistant variant BT-474-T.

Additivity and synergy were observed between Amc and the TKIs neratinib, lapatinib and tucatinib in all cell lines. TKI/Amc combinations reduced p-HER2 and ER levels and resulted in increased apoptosis. In conclusion, the combination of Amc- and HER2-targeted treatments has potential as a therapeutic strategy for the treatment of HER2+/ER+ breast cancer and warrants further clinical investigation to validate safety and efficacy in patients.

Amcenestrant was combined with neratinib tucatinib, lapatinib or T-DM-1 in HER2+/ER+ cell line EFM-192a. — Fig. 1. Loewe synergy tables generated from matrix combination assays examining synergy between HER2-targeted agents and amcenestrant in HER2+/ER+ cell line EFM-192a (Mahdi, Amira F., *et al.*, 2025).

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