ArticleOncotarget2018
Epigenetic activation of HORMAD1 in basal-like breast cancer: role in Rucaparib sensitivity.
Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 32 citations in OpenAlex.
- Tumour specific HORMAD1 expression perturbs mitotic arrest and drives sensitivity to mitotic kinase inhibitors.Nature communications · 2026Article
- Review
- A novel bioinformatic approach reveals cooperation between Cancer/Testis genes in basal-like breast tumors.Oncogene · 2024Article
- HORMAD1 overexpression predicts response to anthracycline-cyclophosphamide and survival in triple-negative breast cancers.Molecular oncology · 2023Article
- Review
- Article
- Meiotic chromosome organization and its role in recombination and cancer.Current topics in developmental biology · 2023Review
- Functional screening reveals HORMAD1-driven gene dependencies associated with translesion synthesis and replication stress tolerance.Oncogene · 2022Article
- The cancer/testis antigen HORMAD1 mediates epithelial-mesenchymal transition to promote tumor growth and metastasis by activating the Wnt/β-catenin signaling pathway in lung cancer.Cell death discovery · 2022Article
- Gene-environment interaction identification via penalized robust divergence.Biometrical journal. Biometrische Zeitschrift · 2022Article
- Meiotic Genes and DNA Double Strand Break Repair in Cancer.Frontiers in genetics · 2022Review
- HORMAD1 promotes docetaxel resistance in triple negative breast cancer by enhancing DNA damage tolerance.Oncology reports · 2021Article
- Multiomics analysis reveals CT83 is the most specific gene for triple negative breast cancer and its hypomethylation is oncogenic in breast cancer.Scientific reports · 2021Article
- A Novel Neoplastic Fusion Transcript,Clinical cancer research : an official journal of the American Association for Cancer Research · 2021Article
- Aberrantly expressed HORMAD1 disrupts nuclear localization of MCM8-MCM9 complex and compromises DNA mismatch repair in cancer cells.Cell death & disease · 2020Article
- The ectopic expression of meiCT genes promotes meiomitosis and may facilitate carcinogenesis.Cell cycle (Georgetown, Tex.) · 2020Review
- HSF2BP negatively regulates homologous recombination in DNA interstrand crosslink repair.Nucleic acids research · 2020Article
- Meiotic gene activation in somatic and germ cell tumours.Andrology · 2019Review
- The Cancer/Testes (CT) Antigen HORMAD1 promotes Homologous Recombinational DNA Repair and Radioresistance in Lung adenocarcinoma cells.Scientific reports · 2018Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Basal-like breast cancer (BLBC) is an aggressive breast cancer subtype with features similar to the basal cells surrounding the mammary ducts. Treatment of patients with BLBC has been challenging due to the lack of well-defined molecular targets. Due to the clinical and pathological similarities of BLBC with BRCA-deficient breast cancers, the effectiveness of Poly (ADP-ribose) polymerase inhibitors (PARPi) has been tested in early phase clinical trials for patients with advanced BLBC, with limited clinical responses. Recently, it was reported that HORMAD1 overexpression sensitizes BLBC to HR-targeting agents by suppressing homologous recombination. Our independent analysis suggests that HORMAD1 is aberrantly overexpressed in about 80% of BLBC, and its expression in normal tissues is restricted to testis. Our experimental data suggests that HORMAD1 overexpression correlates with focal hypomethylation in BLBC. On the other hand, investigation of the Genomics of Drug Sensitivity in Cancer dataset revealed significantly reduced sensitivity of HORMAD1-overexpressing BLBC cell lines to Rucaparib, a commonly used PARPi. To further assess the role of HORMAD1 in PARPi sensitivity, we generated three HORMAD1-overexpressing xenograft models using the HORMAD1-low BLBC cell lines HCC1954, HCC1806, and BT20; we then subjected these xenograft models to Rucaparib treatment. Ectopic expression of HORMAD1 enhances tumor formations in two of these models, and significantly reduces sensitivity to Rucaparib in the HCC1954 model. Taken together, our data suggest that epigenetic activation of HORMAD1 by hypomethylation in BLBC may endow reduced sensitivity to Rucaparib treatment in some tumor models.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.