ArticlePloS one2016
Analysis of Paired Primary-Metastatic Hormone-Receptor Positive Breast Tumors (HRPBC) Uncovers Potential Novel Drivers of Hormonal Resistance.
Article in PloS one, 2016. 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.
- Topological Data Analysis Reveals a Subgroup of Luminal B Breast Cancer.IEEE open journal of engineering in medicine and biology · 2025Article
- An essential gene signature of breast cancer metastasis reveals targetable pathways.Breast cancer research : BCR · 2024Article
- Eph receptors and ephrins in cancer progression.Nature reviews. Cancer · 2024Review
- The role of EphA7 in different tumors.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022Review
- Prolonged estrogen deprivation triggers a broad immunosuppressive phenotype in breast cancer cells.Molecular oncology · 2022Article
- MicroRNA-146b-5p/EPHA7 axis regulates cell invasion, metastasis, proliferation, and temozolomide-induced chemoresistance via regulation of IRAK4/TRAF6/NF-κB signaling pathway in aggressive pituitary adenoma.Histology and histopathology · 2022Article
- FGFR1 amplification or overexpression and hormonal resistance in luminal breast cancer: rationale for a triple blockade of ER, CDK4/6, and FGFR1.Breast cancer research : BCR · 2021Article
- Acquired mutations and transcriptional remodeling in long-term estrogen-deprived locoregional breast cancer recurrences.Breast cancer research : BCR · 2021Article
- Clinical and mutational profiles of adult medulloblastoma groups.Acta neuropathologica communications · 2020Article
- Although c‑MYC contributes to tamoxifen resistance, it improves cisplatin sensitivity in ER‑positive breast cancer.International journal of oncology · 2020Article
- Histone methyltransferases regulate the transcriptional expression of ERα and the proliferation of tamoxifen-resistant breast cancer cells.Breast cancer research and treatment · 2020Article
- Cross-activating c-Met/β1 integrin complex drives metastasis and invasive resistance in cancer.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Comparative clinical utility of tumor genomic testing and cell-free DNA in metastatic breast cancer.Breast cancer research and treatment · 2017Article
- A strategy to apply quantitative epistasis analysis on developmental traits.BMC genetics · 2017Article
- New Strategies in Metastatic Hormone Receptor-Positive Breast Cancer: Searching for Biomarkers to Tailor Endocrine and Other Targeted Therapies.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017Article
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We sought to identify genetic variants associated with disease relapse and failure to hormonal treatment in hormone-receptor positive breast cancer (HRPBC). We analyzed a series of HRPBC with distant relapse, by sequencing pairs (n = 11) of tumors (primary and metastases) at >800X. Comparative genomic hybridization was performed as well. Top hits, based on the frequency of alteration and severity of the changes, were tested in the TCGA series. Genes determining the most parsimonious prognostic signature were studied for their functional role in vitro, by performing cell growth assays in hormonal-deprivation conditions, a setting that mimics treatment with aromatase inhibitors. Severe alterations were recurrently found in 18 genes in the pairs. However, only MYC, DNAH5, CSFR1, EPHA7, ARID1B, and KMT2C preserved an independent prognosis impact and/or showed a significantly different incidence of alterations between relapsed and non-relapsed cases in the TCGA series. The signature composed of MYC, KMT2C, and EPHA7 best discriminated the clinical course, (overall survival 90,7 vs. 144,5 months; p = 0.0001). Having an alteration in any of the genes of the signature implied a hazard ratio of death of 3.25 (p<0.0001), and early relapse during the adjuvant hormonal treatment. The presence of the D348N mutation in KMT2C and/or the T666I mutation in the kinase domain of EPHA7 conferred hormonal resistance in vitro. Novel inactivating mutations in KMT2C and EPHA7, which confer hormonal resistance, are linked to adverse clinical course in HRPBC.
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