ArticleCommunications biology2025
Genomic hallmarks of endocrine therapy resistance in ER/PR+HER2- breast tumours.
Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Efficacy and safety of pyrotinib in patients with previously treated HER2-positive non-breast solid tumors: a phase 2, open-label basket trial.The oncologist · 2025Trial
- Genomic characterization of ER-positive primary tumors and corresponding relapses identifies potentially targetable alterations.NPJ breast cancer · 2026Article
- Paired genomic profiling of primary tumor and lymph-node metastases identifies candidate prognostic features in penile squamous cell carcinoma.The oncologist · 2026Article
- Unlocking the ferroptotic window: Lipidomic rewiring and metabolic addiction in EMT-driven breast cancer resistance.Cell death discovery · 2026Review
- CDKN1B inactivation impacts ER signaling and drives resistance to endocrine therapy in breast cancer.British journal of cancer · 2026Article
- Endocrine therapy-specific lineage and partial epithelial-mesenchymal reprogramming defines divergent resistant cell-states in ER+ breast cancer.bioRxiv : the preprint server for biology · 2026Article
- Steroidogenic Acute Regulatory Protein in Breast Cancer: Mechanistic Insights into Pathogenesis and Therapeutics.International journal of molecular sciences · 2026Review
- Article
- Clinically actionable alterations in Indian breast cancer patients derived through whole transcriptome sequencing.The Indian journal of medical research · 2026Review
- Concurrent genomic assessment of circulating tumour cells and ctDNA to guide therapy in metastatic breast cancer.BMC cancer · 2025Article
- ctDNA detectability and representativeness in seven body liquids from patients with metastatic breast cancer.Nature communications · 2025Article
- Patient derived xenograft models of hormone receptor positive and HER2 negative breast cancer from Indian patients.Scientific reports · 2025Article
- The hormonal nexus in PIK3CA-mutated meningiomas: implications for targeted therapy and clinical trial design.Journal of neuro-oncology · 2025Review
- Genomic landscape of hormone therapy-resistant HR-positive, HER2-negative breast cancer.Breast cancer research and treatment · 2025Article
- Combination chemotherapy and hormone therapy in patients with hormone receptor positive and HER2 negative metastatic breast cancer.Scientific reports · 2025Article
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Authors and funding
9 authors.
Funding
Abstract
ER/PR+HER2- breast tumours are the most predominant subtype of breast cancer worldwide, including India. Unlike TNBCs, these tumours can be treated with anti-estrogens or aromatase inhibitors. Despite the success of endocrine therapy, a fraction of patients with ER/PR+ breast tumours do not respond to hormone-receptor-specific treatment and encounter disease recurrence contributing to their poor survival. The genomic underpinnings of therapy resistance in ER/PR+HER2- breast tumours are incompletely understood. We have performed whole genome sequencing (WGS) from tumour and normal tissue samples from endocrine-therapy resistant ER/PR+HER2- breast cancer patients who have relapsed on endocrine therapy and have conducted a comparative analysis of WGS data generated from tissues of endocrine therapy sensitive patients who remained free of disease during a minimum 5-year follow-up. Our analysis shows (a) a three-gene (PIK3CA-ESR1-TP53) resistance signature, and (b) impaired DNA double-strand break repair and homologous recombination pathways, were significantly associated with endocrine-therapy resistance and disease recurrence in ER/PR+HER2- tumours. Genome instability, contributing to high burden of copy-number, structural alterations and telomere-shortening identified as major markers of endocrine treatment resistance. Early prediction of endocrine-therapy resistance from the genomic landscape of breast tumours will aid therapeutics. Our finding also opens up the possibility of repurposing PARP inhibitors in treating endocrine therapy-resistant breast cancer patients.
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