ArticleBreast cancer research and treatment2024
Liver tropism of ER mutant breast cancer is characterized by unique molecular changes and immune infiltration.
Article in Breast cancer research and treatment, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- The role of the SLC25A15 transporter in the formation of liver metastasis in ESR1-mutated breast cancer.Oncogene · 2026Article
- Characterization of ESR1 alterations in patients with breast and gynecologic cancers.Breast cancer research : BCR · 2026Article
- Regulation of metastatic organotropism.Trends in cancer · 2025Review
- Co-targeting of metabolism using dietary and pharmacologic approaches reduces breast cancer metastatic burden.NPJ breast cancer · 2025Article
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5 authors at 3 institutions in 2 countries.
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Abstract
purposeHotspot estrogen receptor alpha (ER/ESR1) mutations are recognized as the driver for both endocrine resistance and metastasis in advanced ER-positive (ER+) breast cancer, but their contributions to metastatic organ tropism remain insufficiently understood. In this study, we aim to comprehensively profile the organotropic metastatic pattern for ESR1 mutant breast cancer.
methodsThe organ-specific metastatic pattern of ESR1 mutant breast cancer was delineated using multi-omics data from multiple publicly available cohorts of ER+ metastatic breast cancer patients. Gene mutation/copy number variation (CNV) and differential gene expression analyses were performed to identify the genomic and transcriptomic alterations uniquely associated with ESR1 mutant liver metastasis. Upstream regulator, downstream pathway, and immune infiltration analysis were conducted for subsequent mechanistic investigations.
resultsESR1 mutation-driven liver tropism was revealed by significant differences, encompassing a higher prevalence of liver metastasis in patients with ESR1 mutant breast cancer and an enrichment of mutations in liver metastatic samples. The significant enrichment of AGO2 copy number amplifications (CNAs) and multiple gene expression changes were revealed uniquely in ESR1 mutant liver metastasis. We also unveiled alterations in downstream signaling pathways and immune infiltration, particularly an enrichment of neutrophils, suggesting potential therapeutic vulnerabilities.
conclusionOur data provide a comprehensive characterization of the behaviors and mechanisms of ESR1 mutant liver metastasis, paving the way for the development of personalized therapy to target liver metastasis for patients with ESR1 mutant breast cancer.
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