High grade serous ovarian carcinomas originate in the fallopian tube

High-grade serous ovarian carcinoma (HGSOC) is the most frequent type of ovarian cancer and has a poor outcome. It has been proposed that fallopian tube cancers may be precursors of HGSOC but evolutionary evidence for this hypothesis has been limited. Here, we perform whole-exome sequence and copy n...

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Vydáno v:	Nature communications Ročník 8; číslo 1; s. 1093 - 11
Hlavní autoři:	Labidi-Galy, S. Intidhar, Papp, Eniko, Hallberg, Dorothy, Niknafs, Noushin, Adleff, Vilmos, Noe, Michael, Bhattacharya, Rohit, Novak, Marian, Jones, Siân, Phallen, Jillian, Hruban, Carolyn A., Hirsch, Michelle S., Lin, Douglas I., Schwartz, Lauren, Maire, Cecile L., Tille, Jean-Christophe, Bowden, Michaela, Ayhan, Ayse, Wood, Laura D., Scharpf, Robert B., Kurman, Robert, Wang, Tian-Li, Shih, Ie-Ming, Karchin, Rachel, Drapkin, Ronny, Velculescu, Victor E.
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	London Nature Publishing Group UK 23.10.2017 Nature Publishing Group Nature Portfolio
Témata:	631/67/1517/1709 631/67/69 Aberration Alleles BRCA1 protein BRCA2 protein Breast cancer Cancer Copy number Cystadenocarcinoma, Serous - genetics DNA Copy Number Variations - genetics Etiology Evolution Fallopian tube Fallopian Tube Neoplasms - metabolism Fallopian Tube Neoplasms - pathology Fallopian Tubes - metabolism Fallopian Tubes - pathology Female Genital cancers Gynecological cancer Humanities and Social Sciences Humans Immunohistochemistry Laser Capture Microdissection Lesions Metastases Metastasis multidisciplinary Neoplasms, Cystic, Mucinous, and Serous - metabolism Neoplasms, Cystic, Mucinous, and Serous - pathology Ovarian cancer Ovarian carcinoma Ovarian Neoplasms - genetics p53 Protein Patients PTEN protein Science Science (multidisciplinary) Signatures
ISSN:	2041-1723, 2041-1723
On-line přístup:	Získat plný text
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Abstract	High-grade serous ovarian carcinoma (HGSOC) is the most frequent type of ovarian cancer and has a poor outcome. It has been proposed that fallopian tube cancers may be precursors of HGSOC but evolutionary evidence for this hypothesis has been limited. Here, we perform whole-exome sequence and copy number analyses of laser capture microdissected fallopian tube lesions (p53 signatures, serous tubal intraepithelial carcinomas (STICs), and fallopian tube carcinomas), ovarian cancers, and metastases from nine patients. The majority of tumor-specific alterations in ovarian cancers were present in STICs, including those affecting TP53, BRCA1 , BRCA2 or PTEN . Evolutionary analyses reveal that p53 signatures and STICs are precursors of ovarian carcinoma and identify a window of 7 years between development of a STIC and initiation of ovarian carcinoma, with metastases following rapidly thereafter. Our results provide insights into the etiology of ovarian cancer and have implications for prevention, early detection and therapeutic intervention of this disease. It has previously been proposed that high-grade serous ovarian carcinoma (HGSOC) may originate from the fallopian tube. Here, the authors analyze genetic aberrances in fallopian tube lesions, ovarian cancers, and metastases from HGSOC patients and establish the evolutionary origins of HGSOC in the fallopian tube.
AbstractList	High-grade serous ovarian carcinoma (HGSOC) is the most frequent type of ovarian cancer and has a poor outcome. It has been proposed that fallopian tube cancers may be precursors of HGSOC but evolutionary evidence for this hypothesis has been limited. Here, we perform whole-exome sequence and copy number analyses of laser capture microdissected fallopian tube lesions (p53 signatures, serous tubal intraepithelial carcinomas (STICs), and fallopian tube carcinomas), ovarian cancers, and metastases from nine patients. The majority of tumor-specific alterations in ovarian cancers were present in STICs, including those affecting TP53, BRCA1, BRCA2 or PTEN. Evolutionary analyses reveal that p53 signatures and STICs are precursors of ovarian carcinoma and identify a window of 7 years between development of a STIC and initiation of ovarian carcinoma, with metastases following rapidly thereafter. Our results provide insights into the etiology of ovarian cancer and have implications for prevention, early detection and therapeutic intervention of this disease.High-grade serous ovarian carcinoma (HGSOC) is the most frequent type of ovarian cancer and has a poor outcome. It has been proposed that fallopian tube cancers may be precursors of HGSOC but evolutionary evidence for this hypothesis has been limited. Here, we perform whole-exome sequence and copy number analyses of laser capture microdissected fallopian tube lesions (p53 signatures, serous tubal intraepithelial carcinomas (STICs), and fallopian tube carcinomas), ovarian cancers, and metastases from nine patients. The majority of tumor-specific alterations in ovarian cancers were present in STICs, including those affecting TP53, BRCA1, BRCA2 or PTEN. Evolutionary analyses reveal that p53 signatures and STICs are precursors of ovarian carcinoma and identify a window of 7 years between development of a STIC and initiation of ovarian carcinoma, with metastases following rapidly thereafter. Our results provide insights into the etiology of ovarian cancer and have implications for prevention, early detection and therapeutic intervention of this disease. High-grade serous ovarian carcinoma (HGSOC) is the most frequent type of ovarian cancer and has a poor outcome. It has been proposed that fallopian tube cancers may be precursors of HGSOC but evolutionary evidence for this hypothesis has been limited. Here, we perform whole-exome sequence and copy number analyses of laser capture microdissected fallopian tube lesions (p53 signatures, serous tubal intraepithelial carcinomas (STICs), and fallopian tube carcinomas), ovarian cancers, and metastases from nine patients. The majority of tumor-specific alterations in ovarian cancers were present in STICs, including those affecting TP53, BRCA1 , BRCA2 or PTEN . Evolutionary analyses reveal that p53 signatures and STICs are precursors of ovarian carcinoma and identify a window of 7 years between development of a STIC and initiation of ovarian carcinoma, with metastases following rapidly thereafter. Our results provide insights into the etiology of ovarian cancer and have implications for prevention, early detection and therapeutic intervention of this disease. High-grade serous ovarian carcinoma (HGSOC) is the most frequent type of ovarian cancer and has a poor outcome. It has been proposed that fallopian tube cancers may be precursors of HGSOC but evolutionary evidence for this hypothesis has been limited. Here, we perform whole-exome sequence and copy number analyses of laser capture microdissected fallopian tube lesions (p53 signatures, serous tubal intraepithelial carcinomas (STICs), and fallopian tube carcinomas), ovarian cancers, and metastases from nine patients. The majority of tumor-specific alterations in ovarian cancers were present in STICs, including those affecting TP53, BRCA1, BRCA2 or PTEN. Evolutionary analyses reveal that p53 signatures and STICs are precursors of ovarian carcinoma and identify a window of 7 years between development of a STIC and initiation of ovarian carcinoma, with metastases following rapidly thereafter. Our results provide insights into the etiology of ovarian cancer and have implications for prevention, early detection and therapeutic intervention of this disease. It has previously been proposed that high-grade serous ovarian carcinoma (HGSOC) may originate from the fallopian tube. Here, the authors analyze genetic aberrances in fallopian tube lesions, ovarian cancers, and metastases from HGSOC patients and establish the evolutionary origins of HGSOC in the fallopian tube. High-grade serous ovarian carcinoma (HGSOC) is the most frequent type of ovarian cancer and has a poor outcome. It has been proposed that fallopian tube cancers may be precursors of HGSOC but evolutionary evidence for this hypothesis has been limited. Here, we perform whole-exome sequence and copy number analyses of laser capture microdissected fallopian tube lesions (p53 signatures, serous tubal intraepithelial carcinomas (STICs), and fallopian tube carcinomas), ovarian cancers, and metastases from nine patients. The majority of tumor-specific alterations in ovarian cancers were present in STICs, including those affecting TP53, BRCA1 , BRCA2 or PTEN . Evolutionary analyses reveal that p53 signatures and STICs are precursors of ovarian carcinoma and identify a window of 7 years between development of a STIC and initiation of ovarian carcinoma, with metastases following rapidly thereafter. Our results provide insights into the etiology of ovarian cancer and have implications for prevention, early detection and therapeutic intervention of this disease. It has previously been proposed that high-grade serous ovarian carcinoma (HGSOC) may originate from the fallopian tube. Here, the authors analyze genetic aberrances in fallopian tube lesions, ovarian cancers, and metastases from HGSOC patients and establish the evolutionary origins of HGSOC in the fallopian tube. High-grade serous ovarian carcinoma (HGSOC) is the most frequent type of ovarian cancer and has a poor outcome. It has been proposed that fallopian tube cancers may be precursors of HGSOC but evolutionary evidence for this hypothesis has been limited. Here, we perform whole-exome sequence and copy number analyses of laser capture microdissected fallopian tube lesions (p53 signatures, serous tubal intraepithelial carcinomas (STICs), and fallopian tube carcinomas), ovarian cancers, and metastases from nine patients. The majority of tumor-specific alterations in ovarian cancers were present in STICs, including those affecting TP53, BRCA1, BRCA2 or PTEN. Evolutionary analyses reveal that p53 signatures and STICs are precursors of ovarian carcinoma and identify a window of 7 years between development of a STIC and initiation of ovarian carcinoma, with metastases following rapidly thereafter. Our results provide insights into the etiology of ovarian cancer and have implications for prevention, early detection and therapeutic intervention of this disease. It has previously been proposed that high-grade serous ovarian carcinoma (HGSOC) may originate from the fallopian tube. Here, the authors analyze genetic aberrances in fallopian tube lesions, ovarian cancers, and metastases from HGSOC patients and establish the evolutionary origins of HGSOC in the fallopian tube.
ArticleNumber	1093
Author	Adleff, Vilmos Wang, Tian-Li Labidi-Galy, S. Intidhar Kurman, Robert Shih, Ie-Ming Ayhan, Ayse Papp, Eniko Noe, Michael Jones, Siân Wood, Laura D. Tille, Jean-Christophe Maire, Cecile L. Novak, Marian Bowden, Michaela Drapkin, Ronny Bhattacharya, Rohit Hirsch, Michelle S. Hruban, Carolyn A. Schwartz, Lauren Karchin, Rachel Velculescu, Victor E. Scharpf, Robert B. Niknafs, Noushin Phallen, Jillian Hallberg, Dorothy Lin, Douglas I.
Author_xml	– sequence: 1 givenname: S. Intidhar surname: Labidi-Galy fullname: Labidi-Galy, S. Intidhar organization: Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Department of Oncology, Geneva University Hospitals – sequence: 2 givenname: Eniko surname: Papp fullname: Papp, Eniko organization: Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Personal Genome Diagnostics – sequence: 3 givenname: Dorothy surname: Hallberg fullname: Hallberg, Dorothy organization: Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine – sequence: 4 givenname: Noushin surname: Niknafs fullname: Niknafs, Noushin organization: Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Department of Biomedical Engineering, Institute for Computational Medicine, Johns Hopkins University – sequence: 5 givenname: Vilmos surname: Adleff fullname: Adleff, Vilmos organization: Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine – sequence: 6 givenname: Michael surname: Noe fullname: Noe, Michael organization: Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine – sequence: 7 givenname: Rohit surname: Bhattacharya fullname: Bhattacharya, Rohit organization: Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Department of Computer Science, Institute for Computational Medicine, Johns Hopkins University – sequence: 8 givenname: Marian surname: Novak fullname: Novak, Marian organization: Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Personal Genome Diagnostics – sequence: 9 givenname: Siân surname: Jones fullname: Jones, Siân organization: Personal Genome Diagnostics – sequence: 10 givenname: Jillian surname: Phallen fullname: Phallen, Jillian organization: Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine – sequence: 11 givenname: Carolyn A. surname: Hruban fullname: Hruban, Carolyn A. organization: Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine – sequence: 12 givenname: Michelle S. surname: Hirsch fullname: Hirsch, Michelle S. organization: Department of Pathology, Brigham and Women’s hospital and Harvard Medical School – sequence: 13 givenname: Douglas I. surname: Lin fullname: Lin, Douglas I. organization: Department of Pathology, Brigham and Women’s hospital and Harvard Medical School, Department of Pathology, Beth Israel Deaconess Medical Center – sequence: 14 givenname: Lauren surname: Schwartz fullname: Schwartz, Lauren organization: Department of Pathology, University of Pennsylvania Perelman School of Medicine – sequence: 15 givenname: Cecile L. surname: Maire fullname: Maire, Cecile L. organization: Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School – sequence: 16 givenname: Jean-Christophe surname: Tille fullname: Tille, Jean-Christophe organization: Division of Clinical Pathology, Faculty of Medicine, Geneva University Hospital – sequence: 17 givenname: Michaela surname: Bowden fullname: Bowden, Michaela organization: Department of Pathology, Brigham and Women’s hospital and Harvard Medical School – sequence: 18 givenname: Ayse orcidid: 0000-0003-0136-4271 surname: Ayhan fullname: Ayhan, Ayse organization: Department of Pathology, Seirei Mikatahara Hospital, Department of Tumor Pathology, Hamamatsu University School of Medicine, Department of Molecular Pathology, Hiroshima University School of Medicine, Departments of Gynecology and Obstetrics and Pathology, Johns Hopkins University School of Medicine – sequence: 19 givenname: Laura D. surname: Wood fullname: Wood, Laura D. organization: Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine – sequence: 20 givenname: Robert B. surname: Scharpf fullname: Scharpf, Robert B. organization: Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine – sequence: 21 givenname: Robert surname: Kurman fullname: Kurman, Robert organization: Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Departments of Gynecology and Obstetrics and Pathology, Johns Hopkins University School of Medicine – sequence: 22 givenname: Tian-Li surname: Wang fullname: Wang, Tian-Li organization: Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Departments of Gynecology and Obstetrics and Pathology, Johns Hopkins University School of Medicine – sequence: 23 givenname: Ie-Ming surname: Shih fullname: Shih, Ie-Ming organization: Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Departments of Gynecology and Obstetrics and Pathology, Johns Hopkins University School of Medicine – sequence: 24 givenname: Rachel surname: Karchin fullname: Karchin, Rachel organization: Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Department of Biomedical Engineering, Institute for Computational Medicine, Johns Hopkins University – sequence: 25 givenname: Ronny orcidid: 0000-0002-6912-6977 surname: Drapkin fullname: Drapkin, Ronny email: rdrapkin@pennmedicine.upenn.edu organization: Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Department of Pathology, Brigham and Women’s hospital and Harvard Medical School, Department of Obstetrics and Gynecology, Penn Ovarian Cancer Research Center, University of Pennsylvania Perelman School of Medicine – sequence: 26 givenname: Victor E. orcidid: 0000-0003-1195-438X surname: Velculescu fullname: Velculescu, Victor E. email: velculescu@jhmi.edu organization: Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/29061967$$D View this record in MEDLINE/PubMed
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Snippet	High-grade serous ovarian carcinoma (HGSOC) is the most frequent type of ovarian cancer and has a poor outcome. It has been proposed that fallopian tube... It has previously been proposed that high-grade serous ovarian carcinoma (HGSOC) may originate from the fallopian tube. Here, the authors analyze genetic...
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SubjectTerms	631/67/1517/1709 631/67/69 Aberration Alleles BRCA1 protein BRCA2 protein Breast cancer Cancer Copy number Cystadenocarcinoma, Serous - genetics DNA Copy Number Variations - genetics Etiology Evolution Fallopian tube Fallopian Tube Neoplasms - metabolism Fallopian Tube Neoplasms - pathology Fallopian Tubes - metabolism Fallopian Tubes - pathology Female Genital cancers Gynecological cancer Humanities and Social Sciences Humans Immunohistochemistry Laser Capture Microdissection Lesions Metastases Metastasis multidisciplinary Neoplasms, Cystic, Mucinous, and Serous - metabolism Neoplasms, Cystic, Mucinous, and Serous - pathology Ovarian cancer Ovarian carcinoma Ovarian Neoplasms - genetics p53 Protein Patients PTEN protein Science Science (multidisciplinary) Signatures
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Title	High grade serous ovarian carcinomas originate in the fallopian tube
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