Cited by 5,784Endometrial and Cervical Cancer TreatmentsCancer Genomics and DiagnosticsChromatin Remodeling and Cancer

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Integrated genomic characterization of endometrial carcinoma

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The Cancer Genome Atlas Research Network, Levine, Douglas A.·2013·Nature

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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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Figure 1 SCNAs in endometrial carcinomas. a, Tumours were hierarchically clustered into four groups based on SCNAs. The heat map shows SCNAs in each tumour (horizontal axis) plotted by chromosomal location (vertical axis). Chr., chromosome. b, Kaplan–Meier curves of progression-free survival for each copy-number cluster. PowerPoint slideCC BY-NC-SA · PubMed Central

Figure 2 Mutation spectra across endometrial carcinomas. a, Mutation frequencies (vertical axis, top panel) plotted for each tumour (horizontal axis). Nucleotide substitutions are shown in the middle panel, with a high frequency of C-to-A transversions in the samples with POLE exonuclease mutations. CN, copy number. b, Tumours were stratified into the four groups by (1) nucleotide substitution frequencies and patterns, (2) MSI status, and (3) copy-number cluster. SNV, single nucleotide variant. c, POLE-mutant tumours have significantly better progression-free survival, whereas copy-number high tumours have the poorest outcome. d, Recurrently mutated genes are different between the four subgroups. Shown are the mutation frequencies of all genes that were significantly mutated in at least one of the four subgroups (MUSiC, asterisk denotes FDR < 0.05). PowerPoint slideCC BY-NC-SA · PubMed Central

Figure 3 Gene expression across integrated subtypes in endometrial carcinomas. a, Supervised analysis of ∼1,500 genes significantly associated with integrated subtypes. b, Heat map of protein expression clusters, supervised by integrated subtypes. Samples are in columns; genes or proteins are in rows. PowerPoint slideCC BY-NC-SA · PubMed Central

Figure 4 Pathway alterations in endometrial carcinomas. a, The RTK/RAS/β-catenin pathway is altered through several mechanisms that exhibit mutually exclusive patterns. Alteration frequencies are expressed as a percentage of all cases. The right panel shows patterns of occurrence. b, The PI(3)K pathway has mutually exclusive PIK3CA and PIK3R1 alterations that frequently co-occur with PTEN alterations in the MSI and copy-number low subgroups. c, Heat map display of top 1,000 varying pathway features within PARADIGM consensus clusters. Samples were arranged in order of their consensus cluster membership. The genomic subtype for each sample is displayed below the consensus clusters. PowerPoint slideCC BY-NC-SA · PubMed Central

Figure 5 Genomic relationships between endometrial serous-like, ovarian serous, and basal-like breast carcinomas. a, SCNAs for each tumour type. b, Frequency of genomic alterations present in at least 10% of one tumour type. PowerPoint slideCC BY-NC-SA · PubMed Central

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BackgroundMethod

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
Publisher: Springer Science and Business Media LLC
Published: 2013-05-01
Volume: 497
Issue: 7447
Pages: 67-73
ISSN: 0028-0836 (ISSN-L)
1476-4687
DOI: 10.1038/nature12113
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: cc-by-nc-sa
creativecommons.org/licenses/by-nc-sa/3.0/ (tdm)
creativecommons.org/licenses/by-nc-sa/3.0/ (vor)
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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