ArticleClinical cancer research : an official journal of the American Association for Cancer Research2009
Integrated genome-wide DNA copy number and expression analysis identifies distinct mechanisms of primary chemoresistance in ovarian carcinomas.
Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 175 papers, 2 of them syntheses that pooled it.
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The trial behind it
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Who cites it
175 citing papers in PubMed, 2 syntheses or guidelines pooled it, 301 citations in OpenAlex.
- Morphological and molecular characterization of epithelial ovarian cancer: SEOM-SEAP consensus guidelines for biomarker integration in clinical practice.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Guideline
- DNA-Based Liquid Biopsy for Evaluating Surgical and Postsurgical Outcomes in Gynecologic Malignancies: A Systematic Review.Journal of clinical laboratory analysis · 2026Pooled it
- Trial
- Epirubicin, Cisplatin, and Capecitabine for Primary Platinum-Resistant or Platinum-Refractory Epithelial Ovarian Cancer: Results of a Retrospective, Single-Institution Study.International journal of gynecological cancer : official journal of the International Gynecological Cancer Society · 2015Trial
- Prognostically relevant gene signatures of high-grade serous ovarian carcinoma.The Journal of clinical investigation · 2013Trial
- Review
- Cyclin E1 overexpression identifies a therapeutically relevant poor prognostic patient subgroup in high-grade serous ovarian cancer.NPJ precision oncology · 2026Article
- Evaluation of quantitative polymerase chain reaction for detecting BRCA1 or BRCA2 copy number loss in high-grade serous ovarian cancer.Scientific reports · 2026Article
- CTPS1 is an unexplored vulnerability in breast and ovarian cancer.Theranostics · 2026Article
- Multiomic analysis of CCNE1 amplification associated molecular and immune features in gynecological cancers.Discover oncology · 2025Article
- Genomic complexity and evolution of high-grade serous ovarian cancer treated with platinum-based chemotherapy: advancing precision oncology beyond BRCA1/BRCA2.Journal of ovarian research · 2025Article
- p16 expression confers sensitivity to CDK2 inhibitors in cyclin E1-driven ovarian cancers.Science signaling · 2025Article
- Homologous Recombination Proficiency in High-Grade Serous Epithelial Ovarian Cancer Tumors: The Dark Side of the Moon.Current issues in molecular biology · 2025Review
- Targeting CDK2 for cancer therapy.Cell reports · 2025Review
- High PRMT5 levels, maintained by KEAP1 inhibition, drive chemoresistance in high-grade serous ovarian cancer.The Journal of clinical investigation · 2025Article
- Cyclin E1/CDK2 activation defines a key vulnerability to WEE1 kinase inhibition in gynecological cancers.NPJ precision oncology · 2025Article
- Targeting synthetic lethality: an effective therapeutic approach in ovarian and endometrial cancers.Therapeutic advances in medical oncology · 2025Review
- ECGA: A web server to explore and analyze extrachromosomal gene in cancer.Computational and structural biotechnology journal · 2024Article
- Targeting CDK2 to combat drug resistance in cancer therapy.Future oncology (London, England) · 2024Review
- LSD1 Demethylates and Destabilizes Autophagy Protein LC3B in Ovarian Cancer.Biomolecules · 2024Article
115 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
26 authors at 6 institutions in 4 countries.
Funding
Abstract
purposeA significant number of women with serous ovarian cancer are intrinsically refractory to platinum-based treatment. We analyzed somatic DNA copy number variation and gene expression data to identify key mechanisms associated with primary resistance in advanced-stage serous cancers. EXPERIMENTAL
designGenome-wide copy number variation was measured in 118 ovarian tumors using high-resolution oligonucleotide microarrays. A well-defined subset of 85 advanced-stage serous tumors was then used to relate copy number variation to primary resistance to treatment. The discovery-based approach was complemented by quantitative-PCR copy number analysis of 12 candidate genes as independent validation of previously reported associations with clinical outcome. Likely copy number variation targets and tumor molecular subtypes were further characterized by gene expression profiling.
resultsAmplification of 19q12, containing cyclin E (CCNE1), and 20q11.22-q13.12, mapping immediately adjacent to the steroid receptor coactivator NCOA3, was significantly associated with poor response to primary treatment. Other genes previously associated with copy number variation and clinical outcome in ovarian cancer were not associated with primary treatment resistance. Chemoresistant tumors with high CCNE1 copy number and protein expression were associated with increased cellular proliferation but so too was a subset of treatment-responsive patients, suggesting a cell-cycle independent role for CCNE1 in modulating chemoresponse. Patients with a poor clinical outcome without CCNE1 amplification overexpressed genes involved in extracellular matrix deposition.
conclusionsWe have identified two distinct mechanisms of primary treatment failure in serous ovarian cancer, involving CCNE1 amplification and enhanced extracellular matrix deposition. CCNE1 copy number is validated as a dominant marker of patient outcome in ovarian cancer.
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What OpenQuestion holds
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.