Germline mutations in breast and ovarian cancer pedigrees establish RAD51C as a human cancer susceptibility gene
Alfons Meindl and colleagues report heterozygous germline mutations in RAD51C in families with breast and ovarian cancer. Mutations were found in 1.3% of 480 pedigrees with breast and ovarian cancer, but not in 620 pedigrees with breast cancer only. Germline mutations in a number of genes involved i...
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| Published in | Nature genetics Vol. 42; no. 5; pp. 410 - 414 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
New York
Nature Publishing Group US
01.05.2010
Nature Publishing Group |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Alfons Meindl and colleagues report heterozygous germline mutations in
RAD51C
in families with breast and ovarian cancer. Mutations were found in 1.3% of 480 pedigrees with breast and ovarian cancer, but not in 620 pedigrees with breast cancer only.
Germline mutations in a number of genes involved in the recombinational repair of DNA double-strand breaks are associated with predisposition to breast and ovarian cancer.
RAD51C
is essential for homologous recombination repair, and a biallelic missense mutation can cause a Fanconi anemia–like phenotype. In index cases from 1,100 German families with gynecological malignancies, we identified six monoallelic pathogenic mutations in
RAD51C
that confer an increased risk for breast and ovarian cancer. These include two frameshift-causing insertions, two splice-site mutations and two nonfunctional missense mutations. The mutations were found exclusively within 480 pedigrees with the occurrence of both breast and ovarian tumors (BC/OC; 1.3%) and not in 620 pedigrees with breast cancer only or in 2,912 healthy German controls. These results provide the first unambiguous evidence of highly penetrant mutations associated with human cancer in a
RAD51
paralog and support the 'common disease, rare allele' hypothesis. |
|---|---|
| AbstractList | Germline mutations in a number of genes involved in the recombinational repair of DNA double-strand breaks are associated with predisposition to breast and ovarian cancer. RAD51C is essential for homologous recombination repair, and a biallelic missense mutation can cause a Fanconi anemia-like phenotype. In index cases from 1,100 German families with gynecological malignancies, we identified six monoallelic pathogenic mutations in RAD51C that confer an increased risk for breast and ovarian cancer. These include two frameshift-causing insertions, two splice-site mutations and two nonfunctional missense mutations. The mutations were found exclusively within 480 pedigrees with the occurrence of both breast and ovarian tumors (BC/OC; 1.3%) and not in 620 pedigrees with breast cancer only or in 2,912 healthy German controls. These results provide the first unambiguous evidence of highly penetrant mutations associated with human cancer in a RAD51 paralog and support the 'common disease, rare allele' hypothesis. Alfons Meindl and colleagues report heterozygous germline mutations in RAD51C in families with breast and ovarian cancer. Mutations were found in 1.3% of 480 pedigrees with breast and ovarian cancer, but not in 620 pedigrees with breast cancer only. Germline mutations in a number of genes involved in the recombinational repair of DNA double-strand breaks are associated with predisposition to breast and ovarian cancer. RAD51C is essential for homologous recombination repair, and a biallelic missense mutation can cause a Fanconi anemia–like phenotype. In index cases from 1,100 German families with gynecological malignancies, we identified six monoallelic pathogenic mutations in RAD51C that confer an increased risk for breast and ovarian cancer. These include two frameshift-causing insertions, two splice-site mutations and two nonfunctional missense mutations. The mutations were found exclusively within 480 pedigrees with the occurrence of both breast and ovarian tumors (BC/OC; 1.3%) and not in 620 pedigrees with breast cancer only or in 2,912 healthy German controls. These results provide the first unambiguous evidence of highly penetrant mutations associated with human cancer in a RAD51 paralog and support the 'common disease, rare allele' hypothesis. Germline mutations in a number of genes involved in the recombinational repair of DNA double-strand breaks are associated with predisposition to breast and ovarian cancer. RAD51C is essential for homologous recombination repair, and a biallelic missense mutation can cause a Fanconi anemia-like phenotype. In index cases from 1,100 German families with gynecological malignancies, we identified six monoallelic pathogenic mutations in RAD51C that confer an increased risk for breast and ovarian cancer. These include two frameshift-causing insertions, two splice-site mutations and two nonfunctional missense mutations. The mutations were found exclusively within 480 pedigrees with the occurrence of both breast and ovarian tumors (BC/OC; 1.3%) and not in 620 pedigrees with breast cancer only or in 2,912 healthy German controls. These results provide the first unambiguous evidence of highly penetrant mutations associated with human cancer in a RAD51 paralog and support the 'common disease, rare allele' hypothesis.Germline mutations in a number of genes involved in the recombinational repair of DNA double-strand breaks are associated with predisposition to breast and ovarian cancer. RAD51C is essential for homologous recombination repair, and a biallelic missense mutation can cause a Fanconi anemia-like phenotype. In index cases from 1,100 German families with gynecological malignancies, we identified six monoallelic pathogenic mutations in RAD51C that confer an increased risk for breast and ovarian cancer. These include two frameshift-causing insertions, two splice-site mutations and two nonfunctional missense mutations. The mutations were found exclusively within 480 pedigrees with the occurrence of both breast and ovarian tumors (BC/OC; 1.3%) and not in 620 pedigrees with breast cancer only or in 2,912 healthy German controls. These results provide the first unambiguous evidence of highly penetrant mutations associated with human cancer in a RAD51 paralog and support the 'common disease, rare allele' hypothesis. Germline mutations in a number of genes involved in the recombinational repair of DNA double-strand breaks are associated with predisposition to breast and ovarian cancer. RAD51C is essential for homologous recombination repair, and a biallelic missense mutation can cause a Fanconi anemia-like phenotype. In index cases from 1,100 German families with gynecological malignancies, we identified six monoallelic pathogenic mutations in RAD51C that confer an increased risk for breast and ovarian cancer. These include two frameshift-causing insertions, two splice-site mutations and two nonfunctional missense mutations. The mutations were found exclusively within 480 pedigrees with the occurrence of both breast and ovarian tumors (BC/OC; 1.3%) and not in 620 pedigrees with breast cancer only or in 2,912 healthy German controls. These results provide the first unambiguous evidence of highly penetrant mutations associated with human cancer in a RAD51 paralog and support the 'common disease, rare allele' hypothesis. [PUBLICATION ABSTRACT] |
| Audience | Academic |
| Author | Kast, Karin Niederacher, Dieter Freund, Marcel Erven, Verena Lichtner, Peter Neveling, Kornelia Schaal, Heiner Engel, Christoph Hartmann, Linda Honisch, Ellen Meindl, Alfons Ramser, Juliane Mathew, Christopher G Schindler, Detlev Wiek, Constanze Schmutzler, Rita K Wappenschmidt, Barbara Hanenberg, Helmut Kubisch, Christian Wichmann, Hans E Kiechle, Marion Hellebrand, Heide Müller-Myhsok, Bertram Deißler, Helmut |
| Author_xml | – sequence: 1 givenname: Alfons surname: Meindl fullname: Meindl, Alfons email: alfons.meindl@lrz.tu-muenchen.de organization: Department of Obstetrics and Gynecology, Division of Tumor Genetics, Klinikum rechts der Isar der Technischen Universitaet Muenchen – sequence: 2 givenname: Heide surname: Hellebrand fullname: Hellebrand, Heide organization: Department of Obstetrics and Gynecology, Division of Tumor Genetics, Klinikum rechts der Isar der Technischen Universitaet Muenchen – sequence: 3 givenname: Constanze surname: Wiek fullname: Wiek, Constanze organization: Department of Pediatric Hematology, Oncology and Clinical Immunology, Children's Hospital, Heinrich-Heine-University, Germany – sequence: 4 givenname: Verena surname: Erven fullname: Erven, Verena organization: Department of Pediatric Hematology, Oncology and Clinical Immunology, Children's Hospital, Heinrich-Heine-University, Germany – sequence: 5 givenname: Barbara surname: Wappenschmidt fullname: Wappenschmidt, Barbara organization: Center for Familial Breast and Ovarian Cancer and Center for Integrated Oncology, University Hospital – sequence: 6 givenname: Dieter surname: Niederacher fullname: Niederacher, Dieter organization: Department of Obstetrics and Gynecology, Heinrich-Heine-University – sequence: 7 givenname: Marcel surname: Freund fullname: Freund, Marcel organization: Department of Pediatric Hematology, Oncology and Clinical Immunology, Children's Hospital, Heinrich-Heine-University, Germany – sequence: 8 givenname: Peter surname: Lichtner fullname: Lichtner, Peter organization: Institute of Human Genetics, Helmholtz Zentrum Muenchen – sequence: 9 givenname: Linda surname: Hartmann fullname: Hartmann, Linda organization: Institute of Virology, Heinrich-Heine-University – sequence: 10 givenname: Heiner surname: Schaal fullname: Schaal, Heiner organization: Institute of Virology, Heinrich-Heine-University – sequence: 11 givenname: Juliane surname: Ramser fullname: Ramser, Juliane organization: Department of Obstetrics and Gynecology, Division of Tumor Genetics, Klinikum rechts der Isar der Technischen Universitaet Muenchen – sequence: 12 givenname: Ellen surname: Honisch fullname: Honisch, Ellen organization: Department of Obstetrics and Gynecology, Heinrich-Heine-University – sequence: 13 givenname: Christian surname: Kubisch fullname: Kubisch, Christian organization: Institute of Human Genetics, Center for Molecular Medicine Cologne and Cologne Excellence Cluster on Cellular Stress Response in Aging-Associated Diseases, University of Cologne – sequence: 14 givenname: Hans E surname: Wichmann fullname: Wichmann, Hans E organization: Institute of Epidemiology, Helmholtz Zentrum Muenchen – sequence: 15 givenname: Karin surname: Kast fullname: Kast, Karin organization: Department of Obstetrics and Gynecology, Carl Gustav Carus University – sequence: 16 givenname: Helmut surname: Deißler fullname: Deißler, Helmut organization: Department of Obstetrics and Gynecology, Ulm University – sequence: 17 givenname: Christoph surname: Engel fullname: Engel, Christoph organization: Institute for Medical Informatics, Statistics and Epidemiology, University of Leipzig – sequence: 18 givenname: Bertram surname: Müller-Myhsok fullname: Müller-Myhsok, Bertram organization: Max-Planck-Institute of Psychiatry – sequence: 19 givenname: Kornelia surname: Neveling fullname: Neveling, Kornelia organization: Department of Human Genetics, University of Würzburg – sequence: 20 givenname: Marion surname: Kiechle fullname: Kiechle, Marion organization: Department of Obstetrics and Gynecology, Division of Tumor Genetics, Klinikum rechts der Isar der Technischen Universitaet Muenchen – sequence: 21 givenname: Christopher G surname: Mathew fullname: Mathew, Christopher G organization: Department of Medical and Molecular Genetics, Kings College, Guy's Hospital – sequence: 22 givenname: Detlev surname: Schindler fullname: Schindler, Detlev organization: Department of Human Genetics, University of Würzburg – sequence: 23 givenname: Rita K surname: Schmutzler fullname: Schmutzler, Rita K organization: Center for Familial Breast and Ovarian Cancer and Center for Integrated Oncology, University Hospital – sequence: 24 givenname: Helmut surname: Hanenberg fullname: Hanenberg, Helmut email: helmut.hanenberg@uni-duesseldorf.de organization: Department of Pediatric Hematology, Oncology and Clinical Immunology, Children's Hospital, Heinrich-Heine-University, Germany, Department of Pediatrics, Wells Center for Pediatric Research, Riley Hospital, Indiana University School of Medicine |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=23092426$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/20400964$$D View this record in MEDLINE/PubMed |
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| CODEN | NGENEC |
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| Snippet | Alfons Meindl and colleagues report heterozygous germline mutations in
RAD51C
in families with breast and ovarian cancer. Mutations were found in 1.3% of 480... Germline mutations in a number of genes involved in the recombinational repair of DNA double-strand breaks are associated with predisposition to breast and... |
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| SubjectTerms | 631/208/727/2000 631/208/737 692/699/67/1347 692/699/67/1517/1709 Agriculture Alleles Animal Genetics and Genomics Biological and medical sciences Biomedical and Life Sciences Biomedicine Breast cancer Breast Neoplasms - genetics Cancer Research Case-Control Studies DNA-Binding Proteins - genetics Fanconi Anemia - genetics Female Female genital diseases Fundamental and applied biological sciences. Psychology Gene Function Gene mutations Genes Genetic aspects Genetic Predisposition to Disease Genetic susceptibility Genetics Genetics of eukaryotes. Biological and molecular evolution Germ-Line Mutation Germany Gynecology. Andrology. Obstetrics Health aspects Human Genetics Humans letter Mammary gland diseases Medical sciences Models, Genetic Mutation Ovarian cancer Ovarian Neoplasms - genetics Pedigree Phenotype Proteins Risk factors Tumors |
| Title | Germline mutations in breast and ovarian cancer pedigrees establish RAD51C as a human cancer susceptibility gene |
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