The contribution of deleterious germline mutations in BRCA1, BRCA2 and the mismatch repair genes to ovarian cancer in the population

The aim of this study was to estimate the contribution of deleterious mutations in BRCA1, BRCA2, MLH1, MSH2, MSH6 and PMS2 to invasive epithelial ovarian cancer (EOC) in the population. The coding sequence and splice site boundaries of all six genes were amplified in germline DNA from 2240 invasive...

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Published in:	Human molecular genetics Vol. 23; no. 17; p. 4703
Main Authors:	Song, Honglin, Cicek, Mine S, Dicks, Ed, Harrington, Patricia, Ramus, Susan J, Cunningham, Julie M, Fridley, Brooke L, Tyrer, Jonathan P, Alsop, Jennifer, Jimenez-Linan, Mercedes, Gayther, Simon A, Goode, Ellen L, Pharoah, Paul D P
Format:	Journal Article
Language:	English
Published:	England 01.09.2014
Subjects:	Adult Age of Onset Aged BRCA1 Protein - genetics BRCA2 Protein - genetics DNA Mismatch Repair - genetics Female Genetic Predisposition to Disease Germ-Line Mutation - genetics Humans Middle Aged Mutation, Missense - genetics Ovarian Neoplasms - genetics Ovarian Neoplasms - pathology Risk Factors Young Adult
ISSN:	1460-2083, 1460-2083
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Abstract	The aim of this study was to estimate the contribution of deleterious mutations in BRCA1, BRCA2, MLH1, MSH2, MSH6 and PMS2 to invasive epithelial ovarian cancer (EOC) in the population. The coding sequence and splice site boundaries of all six genes were amplified in germline DNA from 2240 invasive EOC cases and 1535 controls. Barcoded fragment libraries were sequenced using the Illumina GAII or HiSeq and sequence data for each subject de-multiplexed prior to interpretation. GATK and Annovar were used for variant detection and annotation. After quality control 2222 cases (99.2%) and 1528 controls (99.5%) were included in the final analysis. We identified 193 EOC cases (8.7%) carrying a deleterious mutation in at least one gene compared with 10 controls (0.65%). Mutations were most frequent in BRCA1 and BRCA2, with 84 EOC cases (3.8%) carrying a BRCA1 mutation and 94 EOC cases (4.2%) carrying a BRCA2 mutation. The combined BRCA1 and BRCA2 mutation prevalence was 11% in high-grade serous disease. Seventeen EOC cases carried a mutation in a mismatch repair gene, including 10 MSH6 mutation carriers (0.45%) and 4 MSH2 mutation carriers (0.18%). At least 1 in 10 women with high-grade serous EOC has a BRCA1 or BRCA2 mutation. The development of next generation sequencing technologies enables rapid mutation screening for multiple susceptibility genes at once, suggesting that routine clinical testing of all incidence cases should be considered.
AbstractList	The aim of this study was to estimate the contribution of deleterious mutations in BRCA1, BRCA2, MLH1, MSH2, MSH6 and PMS2 to invasive epithelial ovarian cancer (EOC) in the population. The coding sequence and splice site boundaries of all six genes were amplified in germline DNA from 2240 invasive EOC cases and 1535 controls. Barcoded fragment libraries were sequenced using the Illumina GAII or HiSeq and sequence data for each subject de-multiplexed prior to interpretation. GATK and Annovar were used for variant detection and annotation. After quality control 2222 cases (99.2%) and 1528 controls (99.5%) were included in the final analysis. We identified 193 EOC cases (8.7%) carrying a deleterious mutation in at least one gene compared with 10 controls (0.65%). Mutations were most frequent in BRCA1 and BRCA2, with 84 EOC cases (3.8%) carrying a BRCA1 mutation and 94 EOC cases (4.2%) carrying a BRCA2 mutation. The combined BRCA1 and BRCA2 mutation prevalence was 11% in high-grade serous disease. Seventeen EOC cases carried a mutation in a mismatch repair gene, including 10 MSH6 mutation carriers (0.45%) and 4 MSH2 mutation carriers (0.18%). At least 1 in 10 women with high-grade serous EOC has a BRCA1 or BRCA2 mutation. The development of next generation sequencing technologies enables rapid mutation screening for multiple susceptibility genes at once, suggesting that routine clinical testing of all incidence cases should be considered. The aim of this study was to estimate the contribution of deleterious mutations in BRCA1, BRCA2, MLH1, MSH2, MSH6 and PMS2 to invasive epithelial ovarian cancer (EOC) in the population. The coding sequence and splice site boundaries of all six genes were amplified in germline DNA from 2240 invasive EOC cases and 1535 controls. Barcoded fragment libraries were sequenced using the Illumina GAII or HiSeq and sequence data for each subject de-multiplexed prior to interpretation. GATK and Annovar were used for variant detection and annotation. After quality control 2222 cases (99.2%) and 1528 controls (99.5%) were included in the final analysis. We identified 193 EOC cases (8.7%) carrying a deleterious mutation in at least one gene compared with 10 controls (0.65%). Mutations were most frequent in BRCA1 and BRCA2, with 84 EOC cases (3.8%) carrying a BRCA1 mutation and 94 EOC cases (4.2%) carrying a BRCA2 mutation. The combined BRCA1 and BRCA2 mutation prevalence was 11% in high-grade serous disease. Seventeen EOC cases carried a mutation in a mismatch repair gene, including 10 MSH6 mutation carriers (0.45%) and 4 MSH2 mutation carriers (0.18%). At least 1 in 10 women with high-grade serous EOC has a BRCA1 or BRCA2 mutation. The development of next generation sequencing technologies enables rapid mutation screening for multiple susceptibility genes at once, suggesting that routine clinical testing of all incidence cases should be considered.The aim of this study was to estimate the contribution of deleterious mutations in BRCA1, BRCA2, MLH1, MSH2, MSH6 and PMS2 to invasive epithelial ovarian cancer (EOC) in the population. The coding sequence and splice site boundaries of all six genes were amplified in germline DNA from 2240 invasive EOC cases and 1535 controls. Barcoded fragment libraries were sequenced using the Illumina GAII or HiSeq and sequence data for each subject de-multiplexed prior to interpretation. GATK and Annovar were used for variant detection and annotation. After quality control 2222 cases (99.2%) and 1528 controls (99.5%) were included in the final analysis. We identified 193 EOC cases (8.7%) carrying a deleterious mutation in at least one gene compared with 10 controls (0.65%). Mutations were most frequent in BRCA1 and BRCA2, with 84 EOC cases (3.8%) carrying a BRCA1 mutation and 94 EOC cases (4.2%) carrying a BRCA2 mutation. The combined BRCA1 and BRCA2 mutation prevalence was 11% in high-grade serous disease. Seventeen EOC cases carried a mutation in a mismatch repair gene, including 10 MSH6 mutation carriers (0.45%) and 4 MSH2 mutation carriers (0.18%). At least 1 in 10 women with high-grade serous EOC has a BRCA1 or BRCA2 mutation. The development of next generation sequencing technologies enables rapid mutation screening for multiple susceptibility genes at once, suggesting that routine clinical testing of all incidence cases should be considered.
Author	Alsop, Jennifer Dicks, Ed Pharoah, Paul D P Song, Honglin Tyrer, Jonathan P Jimenez-Linan, Mercedes Gayther, Simon A Goode, Ellen L Fridley, Brooke L Cicek, Mine S Ramus, Susan J Cunningham, Julie M Harrington, Patricia
Author_xml	– sequence: 1 givenname: Honglin surname: Song fullname: Song, Honglin email: hs310@medschl.cam.ac.uk organization: CR-UK Department of Oncology, University of Cambridge, Strangeways Research Laboratory, Cambridge, UK, hs310@medschl.cam.ac.uk – sequence: 2 givenname: Mine S surname: Cicek fullname: Cicek, Mine S organization: Department of Health Sciences Research, Mayo Clinic, Rochester, MN, USA – sequence: 3 givenname: Ed surname: Dicks fullname: Dicks, Ed organization: CR-UK Department of Oncology, University of Cambridge, Strangeways Research Laboratory, Cambridge, UK – sequence: 4 givenname: Patricia surname: Harrington fullname: Harrington, Patricia organization: CR-UK Department of Oncology, University of Cambridge, Strangeways Research Laboratory, Cambridge, UK – sequence: 5 givenname: Susan J surname: Ramus fullname: Ramus, Susan J organization: Department of Preventive Medicine, Keck School of Medicine, USC/Norris Comprehensive Cancer Center, University of Southern California, CA, USA – sequence: 6 givenname: Julie M surname: Cunningham fullname: Cunningham, Julie M organization: Department of Health Sciences Research, Mayo Clinic, Rochester, MN, USA – sequence: 7 givenname: Brooke L surname: Fridley fullname: Fridley, Brooke L organization: Department of Biostatistics, University of Kansas Medical Center, Kansas, USA and – sequence: 8 givenname: Jonathan P surname: Tyrer fullname: Tyrer, Jonathan P organization: CR-UK Department of Oncology, University of Cambridge, Strangeways Research Laboratory, Cambridge, UK – sequence: 9 givenname: Jennifer surname: Alsop fullname: Alsop, Jennifer organization: CR-UK Department of Oncology, University of Cambridge, Strangeways Research Laboratory, Cambridge, UK – sequence: 10 givenname: Mercedes surname: Jimenez-Linan fullname: Jimenez-Linan, Mercedes organization: Department of Histopathology, Addenbrooke's Hospital, Cambridge, UK – sequence: 11 givenname: Simon A surname: Gayther fullname: Gayther, Simon A organization: Department of Preventive Medicine, Keck School of Medicine, USC/Norris Comprehensive Cancer Center, University of Southern California, CA, USA – sequence: 12 givenname: Ellen L surname: Goode fullname: Goode, Ellen L organization: Department of Health Sciences Research, Mayo Clinic, Rochester, MN, USA – sequence: 13 givenname: Paul D P surname: Pharoah fullname: Pharoah, Paul D P organization: CR-UK Department of Oncology, University of Cambridge, Strangeways Research Laboratory, Cambridge, UK
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SubjectTerms	Adult Age of Onset Aged BRCA1 Protein - genetics BRCA2 Protein - genetics DNA Mismatch Repair - genetics Female Genetic Predisposition to Disease Germ-Line Mutation - genetics Humans Middle Aged Mutation, Missense - genetics Ovarian Neoplasms - genetics Ovarian Neoplasms - pathology Risk Factors Young Adult
Title	The contribution of deleterious germline mutations in BRCA1, BRCA2 and the mismatch repair genes to ovarian cancer in the population
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