ArticleOncogene2010
Integrative molecular profiling of triple negative breast cancers identifies amplicon drivers and potential therapeutic targets.
Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 192 papers, 1 of them a synthesis that pooled it.
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
192 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Prognostic value of FGFR gene amplification in patients with different types of cancer: a systematic review and meta-analysis.PloS one · 2014Pooled it
- Trial
- Phase II, randomized, placebo-controlled study of dovitinib in combination with fulvestrant in postmenopausal patients with HRBreast cancer research : BCR · 2017Trial
- DyVarMap: Integrating Conformational Dynamics and Interpretable Machine Learning for Cancer-Associated Missense Variant Classification in FGFR2.Bioengineering (Basel, Switzerland) · 2026Article
- Metastatic Triple Negative Breast Cancer: Navigating a Rapidly Evolving Therapeutic Landscape.Oncology research · 2026Review
- Review
- RAD51B-EZH2 axis as a potential therapeutic target for TNBC through cell fate conversion.Cell death & disease · 2025Article
- A comprehensive review on targeted therapies for triple negative breast cancer: an evidence-based treatment guideline.Discover oncology · 2025Article
- Overexpression of ORAOV1 and its association with immunotherapy resistance in hepatocellular carcinoma.PeerJ · 2025Article
- LowerBiology · 2024Article
- Advances in the Understanding of the Pathogenesis of Triple-Negative Breast Cancer.Cancer medicine · 2024Review
- Triple-Negative Breast Cancer: Molecular Particularities Still a Challenge.Diagnostics (Basel, Switzerland) · 2024Review
- Identification of a Notch transcriptomic signature for breast cancer.Breast cancer research : BCR · 2024Article
- Fibroblast growth factor receptor signaling in estrogen receptor-positive breast cancer: mechanisms and role in endocrine resistance.Frontiers in oncology · 2024Review
- Early-stage triple negative breast cancer: the therapeutic role of immunotherapy and the prognostic value of pathological complete response.Exploration of targeted anti-tumor therapy · 2024Review
- Obtention of viable cell suspensions from breast cancer tumor biopsies for 3D chromatin conformation and single-cell transcriptome analysis.Frontiers in molecular biosciences · 2024Article
- A review of biological targets and therapeutic approaches in the management of triple-negative breast cancer.Journal of advanced research · 2023Review
- Efficacy of futibatinib, an irreversible fibroblast growth factor receptor inhibitor, in FGFR-altered breast cancer.Scientific reports · 2023Article
- Recent advances in targeted strategies for triple-negative breast cancer.Journal of hematology & oncology · 2023Review
- Next-Generation Sequencing and Triple-Negative Breast Cancer: Insights and Applications.International journal of molecular sciences · 2023Review
132 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
Triple negative breast cancers (TNBCs) have a relatively poor prognosis and cannot be effectively treated with current targeted therapies. We searched for genes that have the potential to be therapeutic targets by identifying genes consistently overexpressed when amplified. Fifty-six TNBCs were subjected to high-resolution microarray-based comparative genomic hybridization (aCGH), of which 24 were subjected to genome-wide gene expression analysis. TNBCs were genetically heterogeneous; no individual focal amplification was present at high frequency, although 78.6% of TNBCs harboured at least one focal amplification. Integration of aCGH and expression data revealed 40 genes significantly overexpressed when amplified, including the known oncogenes and potential therapeutic targets, FGFR2 (10q26.3), BUB3 (10q26.3), RAB20 (13q34), PKN1 (19p13.12) and NOTCH3 (19p13.12). We identified two TNBC cell lines with FGFR2 amplification, which both had constitutive activation of FGFR2. Amplified cell lines were highly sensitive to FGFR inhibitor PD173074, and to RNAi silencing of FGFR2. Treatment with PD173074 induced apoptosis resulting partly from inhibition of PI3K-AKT signalling. Independent validation using publicly available aCGH data sets revealed FGFR2 gene was amplified in 4% (6/165) of TNBC, but not in other subtypes (0/214, P=0.0065). Our analysis demonstrates that TNBCs are heterogeneous tumours with amplifications of FGFR2 in a subgroup of tumours.
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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.