Genetic susceptibility to radiation-induced breast cancer after Hodgkin lymphoma
Female Hodgkin lymphoma (HL) patients treated with chest radiotherapy (RT) have a very high risk of breast cancer. The contribution of genetic factors to this risk is unclear. We therefore examined 211 155 germline single-nucleotide polymorphisms (SNPs) for gene-radiation interaction on breast cance...
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| Published in | Blood Vol. 133; no. 10; pp. 1130 - 1139 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
07.03.2019
American Society of Hematology |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0006-4971 1528-0020 1528-0020 |
| DOI | 10.1182/blood-2018-07-862607 |
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| Abstract | Female Hodgkin lymphoma (HL) patients treated with chest radiotherapy (RT) have a very high risk of breast cancer. The contribution of genetic factors to this risk is unclear. We therefore examined 211 155 germline single-nucleotide polymorphisms (SNPs) for gene-radiation interaction on breast cancer risk in a case-only analysis including 327 breast cancer patients after chest RT for HL and 4671 first primary breast cancer patients. Nine SNPs showed statistically significant interaction with RT on breast cancer risk (false discovery rate, <20%), of which 1 SNP in the PVT1 oncogene attained the Bonferroni threshold for statistical significance. A polygenic risk score (PRS) composed of these SNPs (RT-interaction-PRS) and a previously published breast cancer PRS (BC-PRS) derived in the general population were evaluated in a case-control analysis comprising the 327 chest-irradiated HL patients with breast cancer and 491 chest-irradiated HL patients without breast cancer. Patients in the highest tertile of the RT-interaction-PRS had a 1.6-fold higher breast cancer risk than those in the lowest tertile. Remarkably, we observed a fourfold increased RT-induced breast cancer risk in the highest compared with the lowest decile of the BC-PRS. On a continuous scale, breast cancer risk increased 1.4-fold per standard deviation of the BC-PRS, similar to the effect size found in the general population. This study demonstrates that genetic factors influence breast cancer risk after chest RT for HL. Given the high absolute breast cancer risk in radiation-exposed women, these results can have important implications for the management of current HL survivors and future patients.
•The risk of RT-induced breast cancer after HL is strongly associated with a PRS for breast cancer in the general population.•A PRS, based on 9 SNPs interacting with RT in the occurrence of breast cancer after HL, also increased RT-induced breast cancer risk.
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| AbstractList | Female Hodgkin lymphoma (HL) patients treated with chest radiotherapy (RT) have a very high risk of breast cancer. The contribution of genetic factors to this risk is unclear. We therefore examined 211 155 germline single-nucleotide polymorphisms (SNPs) for gene-radiation interaction on breast cancer risk in a case-only analysis including 327 breast cancer patients after chest RT for HL and 4671 first primary breast cancer patients. Nine SNPs showed statistically significant interaction with RT on breast cancer risk (false discovery rate, <20%), of which 1 SNP in the PVT1 oncogene attained the Bonferroni threshold for statistical significance. A polygenic risk score (PRS) composed of these SNPs (RT-interaction-PRS) and a previously published breast cancer PRS (BC-PRS) derived in the general population were evaluated in a case-control analysis comprising the 327 chest-irradiated HL patients with breast cancer and 491 chest-irradiated HL patients without breast cancer. Patients in the highest tertile of the RT-interaction-PRS had a 1.6-fold higher breast cancer risk than those in the lowest tertile. Remarkably, we observed a fourfold increased RT-induced breast cancer risk in the highest compared with the lowest decile of the BC-PRS. On a continuous scale, breast cancer risk increased 1.4-fold per standard deviation of the BC-PRS, similar to the effect size found in the general population. This study demonstrates that genetic factors influence breast cancer risk after chest RT for HL. Given the high absolute breast cancer risk in radiation-exposed women, these results can have important implications for the management of current HL survivors and future patients.
•The risk of RT-induced breast cancer after HL is strongly associated with a PRS for breast cancer in the general population.•A PRS, based on 9 SNPs interacting with RT in the occurrence of breast cancer after HL, also increased RT-induced breast cancer risk.
[Display omitted] Female Hodgkin lymphoma (HL) patients treated with chest radiotherapy (RT) have a very high risk of breast cancer. The contribution of genetic factors to this risk is unclear. We therefore examined 211 155 germline single-nucleotide polymorphisms (SNPs) for gene-radiation interaction on breast cancer risk in a case-only analysis including 327 breast cancer patients after chest RT for HL and 4671 first primary breast cancer patients. Nine SNPs showed statistically significant interaction with RT on breast cancer risk (false discovery rate, <20%), of which 1 SNP in the oncogene attained the Bonferroni threshold for statistical significance. A polygenic risk score (PRS) composed of these SNPs (RT-interaction-PRS) and a previously published breast cancer PRS (BC-PRS) derived in the general population were evaluated in a case-control analysis comprising the 327 chest-irradiated HL patients with breast cancer and 491 chest-irradiated HL patients without breast cancer. Patients in the highest tertile of the RT-interaction-PRS had a 1.6-fold higher breast cancer risk than those in the lowest tertile. Remarkably, we observed a fourfold increased RT-induced breast cancer risk in the highest compared with the lowest decile of the BC-PRS. On a continuous scale, breast cancer risk increased 1.4-fold per standard deviation of the BC-PRS, similar to the effect size found in the general population. This study demonstrates that genetic factors influence breast cancer risk after chest RT for HL. Given the high absolute breast cancer risk in radiation-exposed women, these results can have important implications for the management of current HL survivors and future patients. There is a Blood Commentary on this article in this issue. The risk of RT-induced breast cancer after HL is strongly associated with a PRS for breast cancer in the general population. A PRS, based on 9 SNPs interacting with RT in the occurrence of breast cancer after HL, also increased RT-induced breast cancer risk. Female Hodgkin lymphoma (HL) patients treated with chest radiotherapy (RT) have a very high risk of breast cancer. The contribution of genetic factors to this risk is unclear. We therefore examined 211 155 germline single-nucleotide polymorphisms (SNPs) for gene-radiation interaction on breast cancer risk in a case-only analysis including 327 breast cancer patients after chest RT for HL and 4671 first primary breast cancer patients. Nine SNPs showed statistically significant interaction with RT on breast cancer risk (false discovery rate, <20%), of which 1 SNP in the PVT1 oncogene attained the Bonferroni threshold for statistical significance. A polygenic risk score (PRS) composed of these SNPs (RT-interaction-PRS) and a previously published breast cancer PRS (BC-PRS) derived in the general population were evaluated in a case-control analysis comprising the 327 chest-irradiated HL patients with breast cancer and 491 chest-irradiated HL patients without breast cancer. Patients in the highest tertile of the RT-interaction-PRS had a 1.6-fold higher breast cancer risk than those in the lowest tertile. Remarkably, we observed a fourfold increased RT-induced breast cancer risk in the highest compared with the lowest decile of the BC-PRS. On a continuous scale, breast cancer risk increased 1.4-fold per standard deviation of the BC-PRS, similar to the effect size found in the general population. This study demonstrates that genetic factors influence breast cancer risk after chest RT for HL. Given the high absolute breast cancer risk in radiation-exposed women, these results can have important implications for the management of current HL survivors and future patients. Female Hodgkin lymphoma (HL) patients treated with chest radiotherapy (RT) have a very high risk of breast cancer. The contribution of genetic factors to this risk is unclear. We therefore examined 211 155 germline single-nucleotide polymorphisms (SNPs) for gene-radiation interaction on breast cancer risk in a case-only analysis including 327 breast cancer patients after chest RT for HL and 4671 first primary breast cancer patients. Nine SNPs showed statistically significant interaction with RT on breast cancer risk (false discovery rate, <20%), of which 1 SNP in the PVT1 oncogene attained the Bonferroni threshold for statistical significance. A polygenic risk score (PRS) composed of these SNPs (RT-interaction-PRS) and a previously published breast cancer PRS (BC-PRS) derived in the general population were evaluated in a case-control analysis comprising the 327 chest-irradiated HL patients with breast cancer and 491 chest-irradiated HL patients without breast cancer. Patients in the highest tertile of the RT-interaction-PRS had a 1.6-fold higher breast cancer risk than those in the lowest tertile. Remarkably, we observed a fourfold increased RT-induced breast cancer risk in the highest compared with the lowest decile of the BC-PRS. On a continuous scale, breast cancer risk increased 1.4-fold per standard deviation of the BC-PRS, similar to the effect size found in the general population. This study demonstrates that genetic factors influence breast cancer risk after chest RT for HL. Given the high absolute breast cancer risk in radiation-exposed women, these results can have important implications for the management of current HL survivors and future patients.Female Hodgkin lymphoma (HL) patients treated with chest radiotherapy (RT) have a very high risk of breast cancer. The contribution of genetic factors to this risk is unclear. We therefore examined 211 155 germline single-nucleotide polymorphisms (SNPs) for gene-radiation interaction on breast cancer risk in a case-only analysis including 327 breast cancer patients after chest RT for HL and 4671 first primary breast cancer patients. Nine SNPs showed statistically significant interaction with RT on breast cancer risk (false discovery rate, <20%), of which 1 SNP in the PVT1 oncogene attained the Bonferroni threshold for statistical significance. A polygenic risk score (PRS) composed of these SNPs (RT-interaction-PRS) and a previously published breast cancer PRS (BC-PRS) derived in the general population were evaluated in a case-control analysis comprising the 327 chest-irradiated HL patients with breast cancer and 491 chest-irradiated HL patients without breast cancer. Patients in the highest tertile of the RT-interaction-PRS had a 1.6-fold higher breast cancer risk than those in the lowest tertile. Remarkably, we observed a fourfold increased RT-induced breast cancer risk in the highest compared with the lowest decile of the BC-PRS. On a continuous scale, breast cancer risk increased 1.4-fold per standard deviation of the BC-PRS, similar to the effect size found in the general population. This study demonstrates that genetic factors influence breast cancer risk after chest RT for HL. Given the high absolute breast cancer risk in radiation-exposed women, these results can have important implications for the management of current HL survivors and future patients. Female Hodgkin lymphoma (HL) patients treated with chest radiotherapy (RT) have a very high risk of breast cancer. The contribution of genetic factors to this risk is unclear. We therefore examined 211 155 germline single-nucleotide polymorphisms (SNPs) for gene-radiation interaction on breast cancer risk in a case-only analysis including 327 breast cancer patients after chest RT for HL and 4671 first primary breast cancer patients. Nine SNPs showed statistically significant interaction with RT on breast cancer risk (false discovery rate, <20%), of which 1 SNP in the PVT1 oncogene attained the Bonferroni threshold for statistical significance. A polygenic risk score (PRS) composed of these SNPs (RT-interaction-PRS) and a previously published breast cancer PRS (BC-PRS) derived in the general population were evaluated in a case-control analysis comprising the 327 chest-irradiated HL patients with breast cancer and 491 chest-irradiated HL patients without breast cancer. Patients in the highest tertile of the RT-interaction-PRS had a 1.6-fold higher breast cancer risk than those in the lowest tertile. Remarkably, we observed a fourfold increased RT-induced breast cancer risk in the highest compared with the lowest decile of the BC-PRS. On a continuous scale, breast cancer risk increased 1.4-fold per standard deviation of the BC-PRS, similar to the effect size found in the general population. This study demonstrates that genetic factors influence breast cancer risk after chest RT for HL. Given the high absolute breast cancer risk in radiation-exposed women, these results can have important implications for the management of current HL survivors and future patients. |
| Author | Robison, Leslie L. van der Baan, Frederieke H. Dennis, Joe Swerdlow, Anthony J. Hauptmann, Michael Peto, Julian Janus, Cécile P.M. van Eggermond, Anna M. Anton-Culver, Hoda Cooke, Rosie Broeks, Annegien Aleman, Berthe M.P. Russell, Nicola S. Hooning, Maartje J. Haiman, Christopher A. Sawyer, Elinor J. Strong, Louise C. de Haan, Hugoline G. Easton, Douglas F. Bhatia, Smita Devilee, Peter Orr, Nick Opstal-van Winden, Annemieke W.J. Cox, Angela Couch, Fergus J. van Leeuwen, Flora E. Pharoah, Paul Krol, Augustinus D.G. Schmidt, Marjanka K. De Bruin, Marie L. |
| Author_xml | – sequence: 1 givenname: Annemieke W.J. surname: Opstal-van Winden fullname: Opstal-van Winden, Annemieke W.J. organization: Department of Epidemiology and Biostatistics, The Netherlands Cancer Institute, Amsterdam, The Netherlands – sequence: 2 givenname: Hugoline G. orcidid: 0000-0003-1126-4776 surname: de Haan fullname: de Haan, Hugoline G. organization: Department of Epidemiology and Biostatistics, The Netherlands Cancer Institute, Amsterdam, The Netherlands – sequence: 3 givenname: Michael surname: Hauptmann fullname: Hauptmann, Michael organization: Department of Epidemiology and Biostatistics, The Netherlands Cancer Institute, Amsterdam, The Netherlands – sequence: 4 givenname: Marjanka K. orcidid: 0000-0002-2228-429X surname: Schmidt fullname: Schmidt, Marjanka K. organization: Department of Epidemiology and Biostatistics, The Netherlands Cancer Institute, Amsterdam, The Netherlands – sequence: 5 givenname: Annegien surname: Broeks fullname: Broeks, Annegien organization: Division of Molecular Pathology, Core Facility Molecular Pathology and Biobanking, The Netherlands Cancer Institute, Amsterdam, The Netherlands – sequence: 6 givenname: Nicola S. surname: Russell fullname: Russell, Nicola S. organization: Department of Radiation Oncology, The Netherlands Cancer Institute, Amsterdam, The Netherlands – sequence: 7 givenname: Cécile P.M. surname: Janus fullname: Janus, Cécile P.M. organization: Department of Radiation Oncology, Erasmus MC Cancer Institute, Rotterdam, The Netherlands – sequence: 8 givenname: Augustinus D.G. surname: Krol fullname: Krol, Augustinus D.G. organization: Department of Radiation Oncology, Leiden University Medical Center, Leiden, The Netherlands – sequence: 9 givenname: Frederieke H. surname: van der Baan fullname: van der Baan, Frederieke H. organization: Department of Epidemiology and Biostatistics, The Netherlands Cancer Institute, Amsterdam, The Netherlands – sequence: 10 givenname: Marie L. orcidid: 0000-0001-9197-7068 surname: De Bruin fullname: De Bruin, Marie L. organization: Department of Epidemiology and Biostatistics, The Netherlands Cancer Institute, Amsterdam, The Netherlands – sequence: 11 givenname: Anna M. surname: van Eggermond fullname: van Eggermond, Anna M. organization: Department of Epidemiology and Biostatistics, The Netherlands Cancer Institute, Amsterdam, The Netherlands – sequence: 12 givenname: Joe orcidid: 0000-0003-4591-1214 surname: Dennis fullname: Dennis, Joe organization: Center for Cancer Genetic Epidemiology, Department of Public Health and Primary Care, University of Cambridge, Cambridge, United Kingdom – sequence: 13 givenname: Hoda surname: Anton-Culver fullname: Anton-Culver, Hoda organization: Department of Epidemiology, University of California Irvine, Irvine, CA – sequence: 14 givenname: Christopher A. surname: Haiman fullname: Haiman, Christopher A. organization: Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA – sequence: 15 givenname: Elinor J. surname: Sawyer fullname: Sawyer, Elinor J. organization: Innovation Hub, Guy's Cancer Centre, King's College London, London, United Kingdom – sequence: 16 givenname: Angela surname: Cox fullname: Cox, Angela organization: Sheffield Cancer Research, Department of Oncology, University of Sheffield, Sheffield, United Kingdom – sequence: 17 givenname: Peter surname: Devilee fullname: Devilee, Peter organization: Department of Pathology, Leiden University Medical Center, Leiden, The Netherlands – sequence: 18 givenname: Maartje J. surname: Hooning fullname: Hooning, Maartje J. organization: Department of Medical Oncology, Family Cancer Clinic, Erasmus MC Cancer Institute, Rotterdam, The Netherlands – sequence: 19 givenname: Julian surname: Peto fullname: Peto, Julian organization: Department of Non-Communicable Disease Epidemiology, London School of Hygiene and Tropical Medicine, London, United Kingdom – sequence: 20 givenname: Fergus J. surname: Couch fullname: Couch, Fergus J. organization: Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN – sequence: 21 givenname: Paul orcidid: 0000-0001-8494-732X surname: Pharoah fullname: Pharoah, Paul organization: Centre for Cancer Genetic Epidemiology, Department of Oncology, University of Cambridge, Cambridge, United Kingdom – sequence: 22 givenname: Nick surname: Orr fullname: Orr, Nick organization: The Breast Cancer Now Toby Robins Research Centre, The Institute of Cancer Research, London, United Kingdom – sequence: 23 givenname: Douglas F. surname: Easton fullname: Easton, Douglas F. organization: Center for Cancer Genetic Epidemiology, Department of Public Health and Primary Care, University of Cambridge, Cambridge, United Kingdom – sequence: 24 givenname: Berthe M.P. surname: Aleman fullname: Aleman, Berthe M.P. organization: Department of Radiation Oncology, The Netherlands Cancer Institute, Amsterdam, The Netherlands – sequence: 25 givenname: Louise C. surname: Strong fullname: Strong, Louise C. organization: MD Anderson Cancer Center, Houston, TX – sequence: 26 givenname: Smita surname: Bhatia fullname: Bhatia, Smita organization: Institute for Cancer Outcomes and Survivorship, University of Alabama at Birmingham, Birmingham, AL – sequence: 27 givenname: Rosie surname: Cooke fullname: Cooke, Rosie organization: Division of Genetics and Epidemiology, The Institute of Cancer Research, London, United Kingdom – sequence: 28 givenname: Leslie L. surname: Robison fullname: Robison, Leslie L. organization: Department of Epidemiology and Cancer Control, St. Jude Children's Research Hospital, Memphis, TN – sequence: 29 givenname: Anthony J. surname: Swerdlow fullname: Swerdlow, Anthony J. organization: Division of Genetics and Epidemiology, The Institute of Cancer Research, London, United Kingdom – sequence: 30 givenname: Flora E. surname: van Leeuwen fullname: van Leeuwen, Flora E. email: f.v.leeuwen@nki.nl organization: Department of Epidemiology and Biostatistics, The Netherlands Cancer Institute, Amsterdam, The Netherlands |
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| Snippet | Female Hodgkin lymphoma (HL) patients treated with chest radiotherapy (RT) have a very high risk of breast cancer. The contribution of genetic factors to this... There is a Blood Commentary on this article in this issue. The risk of RT-induced breast cancer after HL is strongly associated with a PRS for breast cancer in... |
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| SubjectTerms | Adult Aged Aged, 80 and over Breast Neoplasms - etiology Breast Neoplasms - genetics Cancer Survivors Case-Control Studies Female Genetic Predisposition to Disease Genotype Hodgkin Disease - complications Hodgkin Disease - genetics Hodgkin Disease - radiotherapy Humans Lymphoid Neoplasia Middle Aged Neoplasms, Radiation-Induced - genetics Neoplasms, Second Primary - genetics Odds Ratio Polymorphism, Single Nucleotide Quality Control Radiotherapy Dosage Regression Analysis Risk Young Adult |
| Title | Genetic susceptibility to radiation-induced breast cancer after Hodgkin lymphoma |
| URI | https://dx.doi.org/10.1182/blood-2018-07-862607 https://www.ncbi.nlm.nih.gov/pubmed/30573632 https://www.proquest.com/docview/2159983835 https://pubmed.ncbi.nlm.nih.gov/PMC6405334 |
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