ArticleBreast cancer research : BCR2014
Identification by array comparative genomic hybridization of a new amplicon on chromosome 17q highly recurrent in BRCA1 mutated triple negative breast cancer.
Article in Breast cancer research : BCR, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- Pooled it
- The Ubiquitin-Conjugating Enzyme E2 O (UBE2O) and Its Therapeutic Potential in Human Leukemias and Solid Tumors.Cancers · 2024Review
- Harnessing Epigenetics for Breast Cancer Therapy: The Role of DNA Methylation, Histone Modifications, and MicroRNA.International journal of molecular sciences · 2023Review
- High Level of Ubiquitin Conjugate Enzyme E2O Indicates Poor Prognosis of Patients with Hepatocellular Carcinoma.Current medical science · 2023Article
- The Positive Correlations between the Expression of Histopathological Ubiquitin-Conjugating Enzyme 2O Staining and Prostate Cancer Advancement.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Long Noncoding RNA HCG18 Promotes Malignant Phenotypes of Breast Cancer CellsFrontiers in cell and developmental biology · 2021Article
- Pan-cancer driver copy number alterations identified by joint expression/CNA data analysis.Scientific reports · 2020Article
- UBE2O promotes the proliferation, EMT and stemness properties of breast cancer cells through the UBE2O/AMPKα2/mTORC1-MYC positive feedback loop.Cell death & disease · 2020Article
- Gene Co-expression Is Distance-Dependent in Breast Cancer.Frontiers in oncology · 2020Article
- UBE2O Promotes Progression and Epithelial-Mesenchymal Transition in Head and Neck Squamous Cell Carcinoma.OncoTargets and therapy · 2020Article
- A muscle-specific UBE2O/AMPKα2 axis promotes insulin resistance and metabolic syndrome in obesity.JCI insight · 2019Article
- The association between methylation patterns of DNAH17 and clinicopathological factors in hepatocellular carcinoma.Cancer medicine · 2019Article
- Silencing of casein kinase 1 delta reduces migration and metastasis of triple negative breast cancer cells.Oncotarget · 2018Article
- A survey of microRNA single nucleotide polymorphisms identifies novel breast cancer susceptibility loci in a case-control, population-based study of African-American women.Breast cancer research : BCR · 2018Article
- BRCA promoter methylation in sporadic versus BRCA germline mutation-related breast cancers.Breast cancer research : BCR · 2017Article
- Basal-like breast cancer: molecular profiles, clinical features and survival outcomes.BMC medical genomics · 2017Article
- A UBE2O-AMPKα2 Axis that Promotes Tumor Initiation and Progression Offers Opportunities for Therapy.Cancer cell · 2017Article
- Pattern-based sensing of triple negative breast cancer cells with dual-ligand cofunctionalized gold nanoclusters.Biomaterials · 2017Article
- Differentially expressed miRNAs in triple negative breast cancer between African-American and non-Hispanic white women.Oncotarget · 2016Article
- Current advances in biomarkers for targeted therapy in triple-negative breast cancer.Breast cancer (Dove Medical Press) · 2016Review
Corrections and comments
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Authors and funding
15 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionTriple Negative Breast Cancers (TNBC) represent about 12% to 20% of all breast cancers (BC) and have a worse outcome compared to other BC subtypes. TNBC often show a deficiency in DNA double-strand break repair mechanisms. This is generally related to the inactivation of a repair enzymatic complex involving BRCA1 caused either by genetic mutations, epigenetic modifications or by post-transcriptional regulations. The identification of new molecular biomarkers that would allow the rapid identification of BC presenting a BRCA1 deficiency could be useful to select patients who could benefit from PARP inhibitors, alkylating agents or platinum-based chemotherapy.
methodsGenomic DNA from 131 formalin-fixed paraffin-embedded (FFPE) tumors (luminal A and B, HER2+ and triple negative BC) with known BRCA1 mutation status or unscreened for BRCA1 mutation were analysed by array Comparative Genomic Hybridization (array CGH). One highly significant and recurrent gain in the 17q25.3 genomic region was analysed by fluorescent in situ hybridization (FISH). Expression of the genes of the 17q25.3 amplicon was studied using customized Taqman low density arrays and single Taqman assays (Applied Biosystems).
resultsWe identified by array CGH and confirmed by FISH a gain in the 17q25.3 genomic region in 90% of the BRCA1 mutated tumors. This chromosomal gain was present in only 28.6% of the BRCA1 non-mutated TNBC, 26.7% of the unscreened TNBC, 13.6% of the luminal B, 19.0% of the HER2+ and 0% of the luminal A breast cancers. The 17q25.3 gain was also detected in 50% of the TNBC with BRCA1 promoter methylation. Interestingly, BRCA1 promoter methylation was never detected in BRCA1 mutated BC. Gene expression analyses of the 17q25.3 sub-region showed a significant over-expression of 17 genes in BRCA1 mutated TNBC (n = 15) as compared to the BRCA1 non mutated TNBC (n = 13).
conclusionsIn this study, we have identified by array CGH and confirmed by FISH a recurrent gain in 17q25.3 significantly associated to BRCA1 mutated TNBC. Up-regulated genes in the 17q25.3 amplicon might represent potential therapeutic targets and warrant further investigation.
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