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Integrated genomic characterization of endometrial carcinoma
Open accessAbstract
SummaryWe performed an integrated genomic, transcriptomic, and proteomic characterization of 373 endometrial carcinomas using array- and sequencing-based technologies. Uterine serous tumors and ~25% of high-grade endometrioid tumors have extensive copy number alterations, few DNA methylation changes, low ER/PR levels, and frequent TP53 mutations. Most endometrioid tumors have few copy number alterations or TP53 mutations but frequent mutations in PTEN, CTNNB1, PIK3CA, ARID1A, KRAS and novel mutations in the SWI/SNF gene ARID5B. A subset of endometrioid tumors we identified had a dramatically increased transversion mutation frequency, and newly identified hotspot mutations in POLE. Our results classified endometrial cancers into four categories: POLE ultramutated, microsatellite instability hypermutated, copy number low, and copy number high. Uterine serous carcinomas share genomic features with ovarian serous and basal-like breast carcinomas. We demonstrated that the genomic features of endometrial carcinomas permit a reclassification that may impact post-surgical adjuvant treatment for women with aggressive tumors.
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“AR is up-regulated in 9.8% of endometrial adenocarcinoma grade 3 samples [63, 90].”
From Role of aldo-keto reductase family 1 (AKR1) enzymes in human steroid metabolism (2014) · cites this paper as [90]
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Metadata
- Authors
- The Cancer Genome Atlas Research Network, & Levine, D. A.
- Affiliations
- Memorial Sloan Kettering Cancer Center (US)
- Corresponding author
- Levine, Douglas A.
- ORCID
- Levine, Douglas A.
- Venue
- Nature
- Published
- 2013-05-01
- Volume
- 497
- Issue
- 7447
- Pages
- 67-73
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC3704730
- OpenAlex
- W2041440766
- Cited by
- 5,784
- References
- 40
- Citations by year
- 2026: 467 · 2025: 580 · 2024: 559 · 2023: 595 · 2022: 591 · 2021: 572 · 2020: 455 · 2019: 384 · 2018: 320 · 2017: 328 · 2016: 313 · 2015: 285 · 2014: 231 · 2013: 96
- FWCI
- 345.78
- Type
- journal article
- Language
- en
- Update notices
- erratum (2013-06-12)
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Nature (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- National Institutes of Health
- National Human Genome Research Institute (U54HG003067, U54HG003079, U54HG003273)
- National Cancer Institute (P50CA098258, U24CA143882, R01CA180006, U24CA143843, U24CA143840, U24CA143858, U24CA144025, U24CA143866, U24CA143883, U24CA143845, U24CA143867, U24CA143848, U24CA143799, U24CA143835, P30CA008748, P30CA016672, P30CA016056, P30CA016086)
- Topics
- Health Sciences › Medicine › Obstetrics and Gynecology › Endometrial and Cervical Cancer Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Keywords
- endometrial cancer, uterine serous carcinoma, endometrioid carcinoma, copy number alterations, TP53 mutation, POLE mutation, microsatellite instability, ARID5B, SWI/SNF chromatin remodeling, CTNNB1, PIK3CA, KRAS, PTEN, DNA methylation, oestrogen receptor, progesterone receptor, adjuvant therapy, genomic profiling
- MeSH terms
- Poly-ADP-Ribose Binding Proteins, Breast Neoplasms, Chromosome Aberrations, DNA Mutational Analysis, DNA Polymerase II, DNA-Binding Proteins, Female, Humans, Ovarian Neoplasms, Transcription Factors, Signal Transduction, Genome, Human, Gene Expression Regulation, Neoplastic, Endometrial Neoplasms, Genomics, DNA Copy Number Variations, Exome
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