The DOI matches its Crossref record; 52 of the 52 references it cites were found in a registry or an index.
Integrated genomic analyses of ovarian carcinoma
Open accessAbstract
A catalogue of molecular aberrations that cause ovarian cancer is critical for developing and deploying therapies that will improve patients’ lives. The Cancer Genome Atlas project has analysed messenger RNA expression, microRNA expression, promoter methylation and DNA copy number in 489 high-grade serous ovarian adenocarcinomas and the DNA sequences of exons from coding genes in 316 of these tumours. Here we report that high-grade serous ovarian cancer is characterized by TP53 mutations in almost all tumours (96%); low prevalence but statistically recurrent somatic mutations in nine further genes including NF1, BRCA1, BRCA2, RB1 and CDK12; 113 significant focal DNA copy number aberrations; and promoter methylation events involving 168 genes. Analyses delineated four ovarian cancer transcriptional subtypes, three microRNA subtypes, four promoter methylation subtypes and a transcriptional signature associated with survival duration, and shed new light on the impact that tumours with BRCA1/2 (BRCA1 or BRCA2) and CCNE1 aberrations have on survival. Pathway analyses suggested that homologous recombination is defective in about half of the tumours analysed, and that NOTCH and FOXM1 signalling are involved in serous ovarian cancer pathophysiology. The Cancer Genome Atlas (TCGA) project reports here its analysis of messenger RNA and microRNA expression, promoter methylation, DNA copy number and exome sequences in 489 high-grade serous ovarian adenocarcinomas. The analyses help establish new tumour subtypes. Among other insights is the finding that while the gene encoding p53 tumour suppressor is mutated in almost all tumours, nine other loci including NF1, BRCA1, BRCA2, RB1 and CDK12 carry recurrent albeit low-prevalence mutations. Homologous recombination is defective in about half of the tumours studied, and Notch and FOXM1 signalling are involved in the pathophysiology.
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“Notably, the FOXM1 signaling pathway is activated in 84% high-grade serous ovarian cancer [61] and linked to platinum resistance [62, 63].”
From Identification of a novel gene signature predicting response to first-line chemotherapy in BRCA wild-type high-grade serous ovarian cancer patients (2022) · cites this paper as [61]
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“Advances in molecular “omics” strategies have revealed the significant genetic and molecular heterogeneity of OvCa that could influence the prognostic and chemotherapeutic response of patients5–9.”
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“Notably, subsets of colorectal and uterine cancer (COAD, UCEC), which have been previously reported to have no association with polymerase pol h activity, exhibit reduced POLH gene expression 45,46 .”
From DNA polymerase η mutational signatures are found in a variety of different types of cancer (2018) · cites this paper as [46]
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“In high grade serous ovarian cancer, the most common and aggressive form of the disease, >90% of the tumors have inactivated p53 (2).”
From Pharmacologically increasing Mdm2 Inhibits DNA repair and cooperates with genotoxic agents to kill p53-inactivated ovarian cancer cells (2015) · cites this paper as [2]
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1 retracted
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Research works printed but not linked: 2
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Metadata
- Authors
- The Cancer Genome Atlas Research Network
- Venue
- Nature
- Published
- 2011-06-29
- Volume
- 474
- Issue
- 7353
- Pages
- 609-615
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC3163504
- OpenAlex
- W2216554257
- Cited by
- 129
- References
- 50
- Citations by year
- 2026: 51 · 2025: 2 · 2024: 14 · 2023: 8 · 2022: 9 · 2021: 13 · 2020: 10 · 2019: 5 · 2018: 4 · 2017: 1 · 2016: 2 · 2015: 2 · 2014: 2 · 2013: 3 · 2012: 2
- FWCI
- 2.51
- Type
- journal article
- Language
- en
- Update notices
- erratum (2012-08-22)
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Nature (publishedVersion, other-oa)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Carolina Digital Repository (University of North Carolina at Chapel Hill) (submittedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Spiral (Imperial College London) (submittedVersion)
- Padua Research Archive (University of Padova) (submittedVersion, other-oa)
- UNC Libraries
- Funders
- National Institutes of Health
- National Human Genome Research Institute (U54HG003067, U54HG003079, U54HG003273, R01HG005690)
- National Cancer Institute (R01CA094143, R21CA135877, U24CA126554, U24CA143882, R01CA140323, U24CA143843, U24CA143840, U24CA126546, U24CA143858, U24CA126543, U24CA144025, U24CA126563, U24CA143866, U24CA143845, U24CA126544, U24CA143867, U24CA143848, U24CA126551, U24CA143835, U24CA126561, P50CA136393)
- National Institute of Dental and Craniofacial Research (R21DE019713)
- Topics
- Health Sciences › Medicine › Oncology › Ovarian cancer diagnosis and treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › BRCA gene mutations in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Keywords
- TP53 mutation, somatic mutations, BRCA1, BRCA2, neurofibromatosis type 1, RB1, CDK12, DNA copy number aberrations, promoter methylation, microRNA expression, mRNA expression, transcriptomic subtypes, homologous recombination deficiency, Notch signaling, cyclin E1, survival, tumor subtypes
- MeSH terms
- Aged, Carcinoma, Female, Humans, Middle Aged, Mutation, Ovarian Neoplasms, RNA, Messenger, Gene Expression Regulation, Neoplastic, Gene Dosage, DNA Methylation, Gene Expression Profiling, Genomics, MicroRNAs
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