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Evaluating an Esr1-mutant novel cell population emerging upon ERα-antagonism by single RNA-seq

ABSTRACT: To examine the effects of ERα antagonism (giredestrant) on Esr1-wildtype and Esr1-mutant mammary glands, animals were treated with hormone pellets (E2, P4), then dosed daily with vehicle (MCT) or giredestrant (30 mg/kg, p.o.) for four days. Following dosing, EpCAM+ cells were isolated and used for single cell sequencing. For each condition, cells from 2 animals were pooled for sequencing.

ORGANISM(S): Mus musculus

PROVIDER: GSE205573 | GEO | 2024/10/31

REPOSITORIES: GEO

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Evaluating an Esr1-mutant novel cell population emerging upon ERα-antagonism by bulk ATAC-seq

Project description:To examine the effects of ERα antagonism (giredestrant) on Esr1-wildtype and Esr1-mutant mammary glands, animals were treated with hormone pellets (E2, P4), then dosed daily with vehicle (MCT) or giredestrant (30 mg/kg, p.o.) for four days. Following dosing, individual mammary epithelial cell populations were FACS-isolated and sequenced.

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Project description:Transcriptionally active ESR1 fusions promote endocrine therapy (ET)-resistant growth and metastasis of estrogen receptor-alpha positive (ERα+) breast cancer. Currently, there are no targeted treatment options for tumors harboring active fusions because the ESR1 ligand binding domain (LBD) has been replaced with non-drug binding sequences from the 3’ partner gene. A mass spectrometry (MS)-based Kinase Inhibitor Pulldown Assay (KIPA) demonstrated an increase of multiple receptor tyrosine kinases including RET in T47D cells expressing active ESR1 fusions. Integrated proteogenomics defined tumor subsets that could be responsive to RET and CDK4/6 directed therapy from 22 biologically heterogeneous ERα+ patient-derived xenograft (PDX) tumors. Inhibition of RET by repurposing an FDA-approved drug significantly suppressed ESR1 fusion-driven growth of cell, PDX-derived organoid (PDXO) and PDX models. CDK4/6 inhibitor treatment showed similar tumor reductions to RET inhibition. Here, we reveal therapeutic kinase vulnerabilities in ESR1 fusion-driven tumors, which will lay the framework for future clinical trials.

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