Molecular stratification of endometrioid ovarian carcinoma predicts clinical outcome

Endometrioid ovarian carcinoma (EnOC) demonstrates substantial clinical and molecular heterogeneity. Here, we report whole exome sequencing of 112 EnOC cases following rigorous pathological assessment. We detect a high frequency of mutation in CTNNB1 (43%), PIK3CA (43%), ARID1A (36%), PTEN (29%),  K...

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Published inNature communications Vol. 11; no. 1; p. 4995
Main Authors Hollis, Robert L., Thomson, John P., Stanley, Barbara, Churchman, Michael, Meynert, Alison M., Rye, Tzyvia, Bartos, Clare, Iida, Yasushi, Croy, Ian, Mackean, Melanie, Nussey, Fiona, Okamoto, Aikou, Semple, Colin A., Gourley, Charlie, Herrington, C. Simon
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 05.10.2020
Nature Publishing Group
Nature Portfolio
Subjects
1-Phosphatidylinositol 3-kinase
13
13/51
14
14/63
45
45/23
631/67
631/67/1517
631/67/1517/1709
Adult
Aged
Aged, 80 and over
Biomarkers, Tumor - genetics
Biomarkers, Tumor - metabolism
Carcinoma, Endometrioid - genetics
Carcinoma, Endometrioid - metabolism
Carcinoma, Endometrioid - mortality
Carcinoma, Endometrioid - pathology
Complexity
Diagnosis
DNA Copy Number Variations
Female
Heterogeneity
Humanities and Social Sciences
Humans
MAP kinase
Microsatellite Instability
Middle Aged
Mismatch repair
multidisciplinary
Mutation
Ovarian cancer
Ovarian carcinoma
Ovarian Neoplasms - genetics
Ovarian Neoplasms - metabolism
Ovarian Neoplasms - mortality
Ovarian Neoplasms - pathology
Ovaries
p53 Protein
Prognosis
PTEN protein
Science
Science (multidisciplinary)
Signal Transduction
Taxonomy
Whole Exome Sequencing
Wnt protein
Online AccessGet full text

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Abstract Endometrioid ovarian carcinoma (EnOC) demonstrates substantial clinical and molecular heterogeneity. Here, we report whole exome sequencing of 112 EnOC cases following rigorous pathological assessment. We detect a high frequency of mutation in CTNNB1 (43%), PIK3CA (43%), ARID1A (36%), PTEN (29%),  KRAS  (26%), TP53 (26%) and SOX8 (19%), a recurrently-mutated gene previously unreported in EnOC. POLE and mismatch repair protein-encoding genes were mutated at lower frequency (6%, 18%) with significant co-occurrence. A molecular taxonomy is constructed, identifying clinically distinct EnOC subtypes: cases with TP53 mutation demonstrate greater genomic complexity, are commonly FIGO stage III/IV at diagnosis (48%), are frequently incompletely debulked (44%) and demonstrate inferior survival; conversely, cases with CTNNB1 mutation, which is mutually exclusive with TP53 mutation, demonstrate low genomic complexity and excellent clinical outcome, and are predominantly stage I/II at diagnosis (89%) and completely resected (87%). Moreover, we identify the WNT, MAPK/RAS and PI3K pathways as good candidate targets for molecular therapeutics in EnOC. The molecular classification of endometroid ovarian carcinomas (EnOC) has not been established, preventing the development of stratified therapeutic approaches. Here the authors characterise the molecular landscape of EnOC by whole exome sequencing, identifying clinically distinct disease subtypes.
AbstractList Endometrioid ovarian carcinoma (EnOC) demonstrates substantial clinical and molecular heterogeneity. Here, we report whole exome sequencing of 112 EnOC cases following rigorous pathological assessment. We detect a high frequency of mutation in CTNNB1 (43%), PIK3CA (43%), ARID1A (36%), PTEN (29%),  KRAS  (26%), TP53 (26%) and SOX8 (19%), a recurrently-mutated gene previously unreported in EnOC. POLE and mismatch repair protein-encoding genes were mutated at lower frequency (6%, 18%) with significant co-occurrence. A molecular taxonomy is constructed, identifying clinically distinct EnOC subtypes: cases with TP53 mutation demonstrate greater genomic complexity, are commonly FIGO stage III/IV at diagnosis (48%), are frequently incompletely debulked (44%) and demonstrate inferior survival; conversely, cases with CTNNB1 mutation, which is mutually exclusive with TP53 mutation, demonstrate low genomic complexity and excellent clinical outcome, and are predominantly stage I/II at diagnosis (89%) and completely resected (87%). Moreover, we identify the WNT, MAPK/RAS and PI3K pathways as good candidate targets for molecular therapeutics in EnOC. The molecular classification of endometroid ovarian carcinomas (EnOC) has not been established, preventing the development of stratified therapeutic approaches. Here the authors characterise the molecular landscape of EnOC by whole exome sequencing, identifying clinically distinct disease subtypes.
The molecular classification of endometroid ovarian carcinomas (EnOC) has not been established, preventing the development of stratified therapeutic approaches. Here the authors characterise the molecular landscape of EnOC by whole exome sequencing, identifying clinically distinct disease subtypes.
Endometrioid ovarian carcinoma (EnOC) demonstrates substantial clinical and molecular heterogeneity. Here, we report whole exome sequencing of 112 EnOC cases following rigorous pathological assessment. We detect a high frequency of mutation in CTNNB1 (43%), PIK3CA (43%), ARID1A (36%), PTEN (29%), KRAS (26%), TP53 (26%) and SOX8 (19%), a recurrently-mutated gene previously unreported in EnOC. POLE and mismatch repair protein-encoding genes were mutated at lower frequency (6%, 18%) with significant co-occurrence. A molecular taxonomy is constructed, identifying clinically distinct EnOC subtypes: cases with TP53 mutation demonstrate greater genomic complexity, are commonly FIGO stage III/IV at diagnosis (48%), are frequently incompletely debulked (44%) and demonstrate inferior survival; conversely, cases with CTNNB1 mutation, which is mutually exclusive with TP53 mutation, demonstrate low genomic complexity and excellent clinical outcome, and are predominantly stage I/II at diagnosis (89%) and completely resected (87%). Moreover, we identify the WNT, MAPK/RAS and PI3K pathways as good candidate targets for molecular therapeutics in EnOC.The molecular classification of endometroid ovarian carcinomas (EnOC) has not been established, preventing the development of stratified therapeutic approaches. Here the authors characterise the molecular landscape of EnOC by whole exome sequencing, identifying clinically distinct disease subtypes.
Endometrioid ovarian carcinoma (EnOC) demonstrates substantial clinical and molecular heterogeneity. Here, we report whole exome sequencing of 112 EnOC cases following rigorous pathological assessment. We detect a high frequency of mutation in CTNNB1 (43%), PIK3CA (43%), ARID1A (36%), PTEN (29%), KRAS (26%), TP53 (26%) and SOX8 (19%), a recurrently-mutated gene previously unreported in EnOC. POLE and mismatch repair protein-encoding genes were mutated at lower frequency (6%, 18%) with significant co-occurrence. A molecular taxonomy is constructed, identifying clinically distinct EnOC subtypes: cases with TP53 mutation demonstrate greater genomic complexity, are commonly FIGO stage III/IV at diagnosis (48%), are frequently incompletely debulked (44%) and demonstrate inferior survival; conversely, cases with CTNNB1 mutation, which is mutually exclusive with TP53 mutation, demonstrate low genomic complexity and excellent clinical outcome, and are predominantly stage I/II at diagnosis (89%) and completely resected (87%). Moreover, we identify the WNT, MAPK/RAS and PI3K pathways as good candidate targets for molecular therapeutics in EnOC.
Endometrioid ovarian carcinoma (EnOC) demonstrates substantial clinical and molecular heterogeneity. Here, we report whole exome sequencing of 112 EnOC cases following rigorous pathological assessment. We detect a high frequency of mutation in CTNNB1 (43%), PIK3CA (43%), ARID1A (36%), PTEN (29%),  KRAS  (26%), TP53 (26%) and SOX8 (19%), a recurrently-mutated gene previously unreported in EnOC. POLE and mismatch repair protein-encoding genes were mutated at lower frequency (6%, 18%) with significant co-occurrence. A molecular taxonomy is constructed, identifying clinically distinct EnOC subtypes: cases with TP53 mutation demonstrate greater genomic complexity, are commonly FIGO stage III/IV at diagnosis (48%), are frequently incompletely debulked (44%) and demonstrate inferior survival; conversely, cases with CTNNB1 mutation, which is mutually exclusive with TP53 mutation, demonstrate low genomic complexity and excellent clinical outcome, and are predominantly stage I/II at diagnosis (89%) and completely resected (87%). Moreover, we identify the WNT, MAPK/RAS and PI3K pathways as good candidate targets for molecular therapeutics in EnOC.
ArticleNumber 4995
Author Churchman, Michael
Okamoto, Aikou
Mackean, Melanie
Bartos, Clare
Nussey, Fiona
Hollis, Robert L.
Herrington, C. Simon
Iida, Yasushi
Croy, Ian
Meynert, Alison M.
Rye, Tzyvia
Stanley, Barbara
Semple, Colin A.
Thomson, John P.
Gourley, Charlie
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/33020491$$D View this record in MEDLINE/PubMed
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SSID ssj0000391844
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Snippet Endometrioid ovarian carcinoma (EnOC) demonstrates substantial clinical and molecular heterogeneity. Here, we report whole exome sequencing of 112 EnOC cases...
The molecular classification of endometroid ovarian carcinomas (EnOC) has not been established, preventing the development of stratified therapeutic...
SourceID doaj
pubmedcentral
proquest
crossref
pubmed
springer
SourceType Open Website
Open Access Repository
Aggregation Database
Index Database
Publisher
StartPage 4995
SubjectTerms 1-Phosphatidylinositol 3-kinase
13
13/51
14
14/63
45
45/23
631/67
631/67/1517
631/67/1517/1709
Adult
Aged
Aged, 80 and over
Biomarkers, Tumor - genetics
Biomarkers, Tumor - metabolism
Carcinoma, Endometrioid - genetics
Carcinoma, Endometrioid - metabolism
Carcinoma, Endometrioid - mortality
Carcinoma, Endometrioid - pathology
Complexity
Diagnosis
DNA Copy Number Variations
Female
Heterogeneity
Humanities and Social Sciences
Humans
MAP kinase
Microsatellite Instability
Middle Aged
Mismatch repair
multidisciplinary
Mutation
Ovarian cancer
Ovarian carcinoma
Ovarian Neoplasms - genetics
Ovarian Neoplasms - metabolism
Ovarian Neoplasms - mortality
Ovarian Neoplasms - pathology
Ovaries
p53 Protein
Prognosis
PTEN protein
Science
Science (multidisciplinary)
Signal Transduction
Taxonomy
Whole Exome Sequencing
Wnt protein
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Title Molecular stratification of endometrioid ovarian carcinoma predicts clinical outcome
URI https://link.springer.com/article/10.1038/s41467-020-18819-5
https://www.ncbi.nlm.nih.gov/pubmed/33020491
https://www.proquest.com/docview/2449453399
https://search.proquest.com/docview/2448843579
https://pubmed.ncbi.nlm.nih.gov/PMC7536188
https://doaj.org/article/232b42338ac04ca39f011da44d0890a8
Volume 11
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