The mutational landscape of normal human endometrial epithelium

All normal somatic cells are thought to acquire mutations, but understanding of the rates, patterns, causes and consequences of somatic mutations in normal cells is limited. The uterine endometrium adopts multiple physiological states over a lifetime and is lined by a gland-forming epithelium 1 , 2...

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Vydáno v:	Nature (London) Ročník 580; číslo 7805; s. 640 - 646
Hlavní autoři:	Moore, Luiza, Leongamornlert, Daniel, Coorens, Tim H. H., Sanders, Mathijs A., Ellis, Peter, Dentro, Stefan C., Dawson, Kevin J., Butler, Tim, Rahbari, Raheleh, Mitchell, Thomas J., Maura, Francesco, Nangalia, Jyoti, Tarpey, Patrick S., Brunner, Simon F., Lee-Six, Henry, Hooks, Yvette, Moody, Sarah, Mahbubani, Krishnaa T., Jimenez-Linan, Mercedes, Brosens, Jan J., Iacobuzio-Donahue, Christine A., Martincorena, Inigo, Saeb-Parsy, Kourosh, Campbell, Peter J., Stratton, Michael R.
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	London Nature Publishing Group UK 30.04.2020 Nature Publishing Group
Témata:	14 14/63 45 45/23 631/208/737 631/67/69 692/308/2056 Acquisitions & mergers Adult Age Age of Onset Aged Aged, 80 and over Aging - genetics Analysis Biopsy Cancer Carcinogenesis - genetics Clone Cells - cytology Cloning Confidence intervals Deoxyribonucleic acid DNA DNA Mutational Analysis DNA sequencing Endometrial cancer Endometrial Neoplasms - genetics Endometrium Endometrium - cytology Endometrium - metabolism Endometrium - pathology Epithelial cells Epithelial Cells - cytology Epithelial Cells - metabolism Epithelial Cells - pathology Epithelium Epithelium - metabolism Epithelium - pathology Female Gene sequencing Genetic aspects Genomes Glands Health Humanities and Social Sciences Humans Middle Aged multidisciplinary Mutation Mutation (Biology) Nucleotide sequencing Parity - genetics Physiological aspects Physiology Science Science (multidisciplinary) Signatures Somatic cells Statistical analysis Stem cells Time Factors Uterine cancer Uterus Whole genome sequencing Womens health Young Adult United Kingdom
ISSN:	0028-0836, 1476-4687, 1476-4687
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Abstract	All normal somatic cells are thought to acquire mutations, but understanding of the rates, patterns, causes and consequences of somatic mutations in normal cells is limited. The uterine endometrium adopts multiple physiological states over a lifetime and is lined by a gland-forming epithelium 1 , 2 . Here, using whole-genome sequencing, we show that normal human endometrial glands are clonal cell populations with total mutation burdens that increase at about 29 base substitutions per year and that are many-fold lower than those of endometrial cancers. Normal endometrial glands frequently carry ‘driver’ mutations in cancer genes, the burden of which increases with age and decreases with parity. Cell clones with drivers often originate during the first decades of life and subsequently progressively colonize the epithelial lining of the endometrium. Our results show that mutational landscapes differ markedly between normal tissues—perhaps shaped by differences in their structure and physiology—and indicate that the procession of neoplastic change that leads to endometrial cancer is initiated early in life. Whole-genome sequencing of normal human endometrial glands shows that most are clonal cell populations and frequently carry cancer driver mutations that occur early in life, and that parity has a protective effect.
AbstractList	All normal somatic cells are thought to acquire mutations, but understanding of the rates, patterns, causes and consequences of somatic mutations in normal cells is limited. The uterine endometrium adopts multiple physiological states over a lifetime and is lined by a gland-forming epithelium.sup.1,2. Here, using whole-genome sequencing, we show that normal human endometrial glands are clonal cell populations with total mutation burdens that increase at about 29 base substitutions per year and that are many-fold lower than those of endometrial cancers. Normal endometrial glands frequently carry 'driver' mutations in cancer genes, the burden of which increases with age and decreases with parity. Cell clones with drivers often originate during the first decades of life and subsequently progressively colonize the epithelial lining of the endometrium. Our results show that mutational landscapes differ markedly between normal tissues--perhaps shaped by differences in their structure and physiology--and indicate that the procession of neoplastic change that leads to endometrial cancer is initiated early in life. All normal somatic cells are thought to acquire mutations, but understanding of the rates, patterns, causes and consequences of somatic mutations in normal cells is limited. The uterine endometrium adopts multiple physiological states over a lifetime and is lined by a gland-forming epithelium1,2. Here, using whole-genome sequencing, we show that normal human endometrial glands are clonal cell populations with total mutation burdens that increase at about 29 base substitutions per year and that are many-fold lower than those of endometrial cancers. Normal endometrial glands frequently carry 'driver' mutations in cancer genes, the burden of which increases with age and decreases with parity. Cell clones with drivers often originate during the first decades of life and subsequently progressively colonize the epithelial lining of the endometrium. Our results show that mutational landscapes differ markedly between normal tissues-perhaps shaped by differences in their structure and physiology-and indicate that the procession of neoplastic change that leads to endometrial cancer is initiated early in life. All normal somatic cells are thought to acquire mutations, but understanding of the rates, patterns, causes and consequences of somatic mutations in normal cells is limited. The uterine endometrium adopts multiple physiological states over a lifetime and is lined by a gland-forming epithelium 1 , 2 . Here, using whole-genome sequencing, we show that normal human endometrial glands are clonal cell populations with total mutation burdens that increase at about 29 base substitutions per year and that are many-fold lower than those of endometrial cancers. Normal endometrial glands frequently carry ‘driver’ mutations in cancer genes, the burden of which increases with age and decreases with parity. Cell clones with drivers often originate during the first decades of life and subsequently progressively colonize the epithelial lining of the endometrium. Our results show that mutational landscapes differ markedly between normal tissues—perhaps shaped by differences in their structure and physiology—and indicate that the procession of neoplastic change that leads to endometrial cancer is initiated early in life. Whole-genome sequencing of normal human endometrial glands shows that most are clonal cell populations and frequently carry cancer driver mutations that occur early in life, and that parity has a protective effect. All normal somatic cells are thought to acquire mutations, but understanding of the rates, patterns, causes and consequences of somatic mutations in normal cells is limited. The uterine endometrium adopts multiple physiological states over a lifetime and is lined by a gland-forming epithelium1,2. Here, using whole-genome sequencing, we show that normal human endometrial glands are clonal cell populations with total mutation burdens that increase at about 29 base substitutions per year and that are many-fold lower than those of endometrial cancers. Normal endometrial glands frequently carry 'driver' mutations in cancer genes, the burden of which increases with age and decreases with parity. Cell clones with drivers often originate during the first decades of life and subsequently progressively colonize the epithelial lining of the endometrium. Our results show that mutational landscapes differ markedly between normal tissues-perhaps shaped by differences in their structure and physiology-and indicate that the procession of neoplastic change that leads to endometrial cancer is initiated early in life.All normal somatic cells are thought to acquire mutations, but understanding of the rates, patterns, causes and consequences of somatic mutations in normal cells is limited. The uterine endometrium adopts multiple physiological states over a lifetime and is lined by a gland-forming epithelium1,2. Here, using whole-genome sequencing, we show that normal human endometrial glands are clonal cell populations with total mutation burdens that increase at about 29 base substitutions per year and that are many-fold lower than those of endometrial cancers. Normal endometrial glands frequently carry 'driver' mutations in cancer genes, the burden of which increases with age and decreases with parity. Cell clones with drivers often originate during the first decades of life and subsequently progressively colonize the epithelial lining of the endometrium. Our results show that mutational landscapes differ markedly between normal tissues-perhaps shaped by differences in their structure and physiology-and indicate that the procession of neoplastic change that leads to endometrial cancer is initiated early in life. All normal somatic cells are thought to acquire mutations, but understanding of the rates, patterns, causes and consequences of somatic mutations in normal cells is limited. The uterine endometrium adopts multiple physiological states over a lifetime and is lined by a gland-forming epithelium . Here, using whole-genome sequencing, we show that normal human endometrial glands are clonal cell populations with total mutation burdens that increase at about 29 base substitutions per year and that are many-fold lower than those of endometrial cancers. Normal endometrial glands frequently carry 'driver' mutations in cancer genes, the burden of which increases with age and decreases with parity. Cell clones with drivers often originate during the first decades of life and subsequently progressively colonize the epithelial lining of the endometrium. Our results show that mutational landscapes differ markedly between normal tissues-perhaps shaped by differences in their structure and physiology-and indicate that the procession of neoplastic change that leads to endometrial cancer is initiated early in life. All normal somatic cells are thought to acquire mutations, but understanding of the rates, patterns, causes and consequences of somatic mutations in normal cells is limited. The uterine endometrium adopts multiple physiological states over a lifetime and is lined by a gland-forming epithelium.sup.1,2. Here, using whole-genome sequencing, we show that normal human endometrial glands are clonal cell populations with total mutation burdens that increase at about 29 base substitutions per year and that are many-fold lower than those of endometrial cancers. Normal endometrial glands frequently carry 'driver' mutations in cancer genes, the burden of which increases with age and decreases with parity. Cell clones with drivers often originate during the first decades of life and subsequently progressively colonize the epithelial lining of the endometrium. Our results show that mutational landscapes differ markedly between normal tissues--perhaps shaped by differences in their structure and physiology--and indicate that the procession of neoplastic change that leads to endometrial cancer is initiated early in life. Whole-genome sequencing of normal human endometrial glands shows that most are clonal cell populations and frequently carry cancer driver mutations that occur early in life, and that parity has a protective effect.
Audience	Academic
Author	Sanders, Mathijs A. Iacobuzio-Donahue, Christine A. Butler, Tim Dentro, Stefan C. Tarpey, Patrick S. Coorens, Tim H. H. Lee-Six, Henry Mitchell, Thomas J. Martincorena, Inigo Nangalia, Jyoti Moore, Luiza Leongamornlert, Daniel Brunner, Simon F. Hooks, Yvette Mahbubani, Krishnaa T. Saeb-Parsy, Kourosh Jimenez-Linan, Mercedes Campbell, Peter J. Moody, Sarah Brosens, Jan J. Maura, Francesco Ellis, Peter Dawson, Kevin J. Rahbari, Raheleh Stratton, Michael R.
Author_xml	– sequence: 1 givenname: Luiza orcidid: 0000-0001-5315-516X surname: Moore fullname: Moore, Luiza organization: Cancer, Ageing and Somatic Mutation (CASM), Wellcome Sanger Institute, Department of Pathology, Cambridge University Hospitals NHS Foundation Trust – sequence: 2 givenname: Daniel surname: Leongamornlert fullname: Leongamornlert, Daniel organization: Cancer, Ageing and Somatic Mutation (CASM), Wellcome Sanger Institute – sequence: 3 givenname: Tim H. H. surname: Coorens fullname: Coorens, Tim H. H. organization: Cancer, Ageing and Somatic Mutation (CASM), Wellcome Sanger Institute – sequence: 4 givenname: Mathijs A. surname: Sanders fullname: Sanders, Mathijs A. organization: Cancer, Ageing and Somatic Mutation (CASM), Wellcome Sanger Institute, Department of Hematology, Erasmus University Medical Center – sequence: 5 givenname: Peter surname: Ellis fullname: Ellis, Peter organization: Cancer, Ageing and Somatic Mutation (CASM), Wellcome Sanger Institute, Inivata Ltd – sequence: 6 givenname: Stefan C. surname: Dentro fullname: Dentro, Stefan C. organization: Cancer, Ageing and Somatic Mutation (CASM), Wellcome Sanger Institute, European Molecular Biology Laboratory, European Bioinformatics Institute (EMBL-EBI) – sequence: 7 givenname: Kevin J. surname: Dawson fullname: Dawson, Kevin J. organization: Cancer, Ageing and Somatic Mutation (CASM), Wellcome Sanger Institute – sequence: 8 givenname: Tim orcidid: 0000-0001-5803-1035 surname: Butler fullname: Butler, Tim organization: Cancer, Ageing and Somatic Mutation (CASM), Wellcome Sanger Institute – sequence: 9 givenname: Raheleh orcidid: 0000-0002-1839-7785 surname: Rahbari fullname: Rahbari, Raheleh organization: Cancer, Ageing and Somatic Mutation (CASM), Wellcome Sanger Institute – sequence: 10 givenname: Thomas J. orcidid: 0000-0003-0761-9503 surname: Mitchell fullname: Mitchell, Thomas J. organization: Cancer, Ageing and Somatic Mutation (CASM), Wellcome Sanger Institute – sequence: 11 givenname: Francesco surname: Maura fullname: Maura, Francesco organization: Cancer, Ageing and Somatic Mutation (CASM), Wellcome Sanger Institute, Myeloma Service, Department of Medicine, Memorial Sloan Kettering Cancer Center – sequence: 12 givenname: Jyoti surname: Nangalia fullname: Nangalia, Jyoti organization: Cancer, Ageing and Somatic Mutation (CASM), Wellcome Sanger Institute – sequence: 13 givenname: Patrick S. surname: Tarpey fullname: Tarpey, Patrick S. organization: Cancer, Ageing and Somatic Mutation (CASM), Wellcome Sanger Institute – sequence: 14 givenname: Simon F. surname: Brunner fullname: Brunner, Simon F. organization: Cancer, Ageing and Somatic Mutation (CASM), Wellcome Sanger Institute – sequence: 15 givenname: Henry orcidid: 0000-0003-4831-8088 surname: Lee-Six fullname: Lee-Six, Henry organization: Cancer, Ageing and Somatic Mutation (CASM), Wellcome Sanger Institute – sequence: 16 givenname: Yvette surname: Hooks fullname: Hooks, Yvette organization: Cancer, Ageing and Somatic Mutation (CASM), Wellcome Sanger Institute – sequence: 17 givenname: Sarah surname: Moody fullname: Moody, Sarah organization: Cancer, Ageing and Somatic Mutation (CASM), Wellcome Sanger Institute – sequence: 18 givenname: Krishnaa T. orcidid: 0000-0002-1327-2334 surname: Mahbubani fullname: Mahbubani, Krishnaa T. organization: Department of Surgery, University of Cambridge, Cambridge NIHR Biomedical Research Centre, Department of Haematology, University of Cambridge – sequence: 19 givenname: Mercedes surname: Jimenez-Linan fullname: Jimenez-Linan, Mercedes organization: Department of Pathology, Cambridge University Hospitals NHS Foundation Trust – sequence: 20 givenname: Jan J. orcidid: 0000-0003-0116-9329 surname: Brosens fullname: Brosens, Jan J. organization: Tommy’s National Miscarriage Research Centre, Warwick Medical School, University of Warwick – sequence: 21 givenname: Christine A. orcidid: 0000-0002-4672-3023 surname: Iacobuzio-Donahue fullname: Iacobuzio-Donahue, Christine A. organization: Department of Pathology, Memorial Sloan Kettering Cancer Center, Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center – sequence: 22 givenname: Inigo surname: Martincorena fullname: Martincorena, Inigo organization: Cancer, Ageing and Somatic Mutation (CASM), Wellcome Sanger Institute – sequence: 23 givenname: Kourosh orcidid: 0000-0002-0633-3696 surname: Saeb-Parsy fullname: Saeb-Parsy, Kourosh organization: Department of Surgery, University of Cambridge, Cambridge NIHR Biomedical Research Centre – sequence: 24 givenname: Peter J. orcidid: 0000-0002-3921-0510 surname: Campbell fullname: Campbell, Peter J. organization: Cancer, Ageing and Somatic Mutation (CASM), Wellcome Sanger Institute – sequence: 25 givenname: Michael R. orcidid: 0000-0001-6035-153X surname: Stratton fullname: Stratton, Michael R. email: mrs@sanger.ac.uk organization: Cancer, Ageing and Somatic Mutation (CASM), Wellcome Sanger Institute
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/32350471$$D View this record in MEDLINE/PubMed
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Snippet	All normal somatic cells are thought to acquire mutations, but understanding of the rates, patterns, causes and consequences of somatic mutations in normal...
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Title	The mutational landscape of normal human endometrial epithelium
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