Epigenetic age and long-term cancer risk following a stroke
Background: The association between increased cancer risk following a cerebrovascular event (CVE) has been previously reported. We hypothesize that biological age (B-age) acceleration is involved in this association. Our study aims to examine B-age as a novel contributing factor to cancer developmen...
| Autores: | , , , , , , , , , , , |
|---|---|
| Tipo de recurso: | artículo |
| Estado: | Versión publicada |
| Fecha de publicación: | 2024 |
| País: | España |
| Institución: | Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya) |
| Repositorio: | Recercat. Dipósit de la Recerca de Catalunya |
| OAI Identifier: | oai:recercat.cat:10230/71920 |
| Acceso en línea: | http://hdl.handle.net/10230/71920 http://dx.doi.org/10.1186/s13073-024-01408-2 |
| Access Level: | acceso abierto |
| Palabra clave: | Aging Cancer DNA methylation Epigenetic clock Stroke |
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Epigenetic age and long-term cancer risk following a stroke |
| title |
Epigenetic age and long-term cancer risk following a stroke |
| spellingShingle |
Epigenetic age and long-term cancer risk following a stroke Suárez-Pérez, Antoni Aging Cancer DNA methylation Epigenetic clock Stroke |
| title_short |
Epigenetic age and long-term cancer risk following a stroke |
| title_full |
Epigenetic age and long-term cancer risk following a stroke |
| title_fullStr |
Epigenetic age and long-term cancer risk following a stroke |
| title_full_unstemmed |
Epigenetic age and long-term cancer risk following a stroke |
| title_sort |
Epigenetic age and long-term cancer risk following a stroke |
| dc.creator.none.fl_str_mv |
Suárez-Pérez, Antoni Macias-Gómez, Adrià Fernández-Pérez, Isabel Vallverdú-Prats, Marta Cuadrado-Godia, Elisa Giralt-Steinhauer, Eva Campanale, Maia Guisado-Alonso, Daniel Rodríguez-Campello, Ana Jiménez-Balado, Joan Jiménez Conde, Jordi Ois Santiago, Angel Javier |
| author |
Suárez-Pérez, Antoni |
| author_facet |
Suárez-Pérez, Antoni Macias-Gómez, Adrià Fernández-Pérez, Isabel Vallverdú-Prats, Marta Cuadrado-Godia, Elisa Giralt-Steinhauer, Eva Campanale, Maia Guisado-Alonso, Daniel Rodríguez-Campello, Ana Jiménez-Balado, Joan Jiménez Conde, Jordi Ois Santiago, Angel Javier |
| author_role |
author |
| author2 |
Macias-Gómez, Adrià Fernández-Pérez, Isabel Vallverdú-Prats, Marta Cuadrado-Godia, Elisa Giralt-Steinhauer, Eva Campanale, Maia Guisado-Alonso, Daniel Rodríguez-Campello, Ana Jiménez-Balado, Joan Jiménez Conde, Jordi Ois Santiago, Angel Javier |
| author2_role |
author author author author author author author author author author author |
| dc.subject.none.fl_str_mv |
Aging Cancer DNA methylation Epigenetic clock Stroke |
| topic |
Aging Cancer DNA methylation Epigenetic clock Stroke |
| description |
Background: The association between increased cancer risk following a cerebrovascular event (CVE) has been previously reported. We hypothesize that biological age (B-age) acceleration is involved in this association. Our study aims to examine B-age as a novel contributing factor to cancer development post-CVE. Methods: From our prospective stroke registry (BasicMar), we selected 940 cases with epigenetic data. For this study, we specifically analyzed 648 of these patients who had available data, no prior history of cancer, and a minimum follow-up of 3 months. The primary outcome was cancer incidence. B-age was estimated using DNA methylation data derived from whole blood samples obtained within 24 h of stroke onset, employing various epigenetic clocks (including Hannum, Horvath, PhenoAge, Zhang, Zhang, and the mitotic epiTOC). Extrinsic epigenetic age acceleration (EEAA) was calculated as the residuals from the regression of B-age against chronological age (C-age). For epiTOC, the age-adjusted values were obtained by regressing out the effect of age from the raw epiTOC measurements. Estimated white cell counts were derived from DNA methylation data, and these cell fractions were used to compute the intrinsic epigenetic age acceleration (IEAA). Subsequently, we evaluated the independent association between EEAA, IEAA, and cancer incidence while controlling for potential confounding variables. Results: Among 648 patients with a median follow-up of 8.15 years, 83 (12.8%) developed cancer. Cox multivariable analyses indicated significant associations between Hannum, Zhang, and epiTOC EEAA and the risk of cancer after CVE. After adjusting for multiple testing and competing risks, EEAA measured by Hannum clock maintained an independent association with cancer risk. Specifically, for each year increase in Hannum's EEAA, we observed a 6.0% increased incidence of cancer (HR 1.06 [1.02-1.10], p value = 0.002). Conclusions: Our findings suggest that epigenetic accelerated aging, as indicated by Hannum's EEAA, may play a significant role in the increased cancer risk observed in CVE survivors. |
| publishDate |
2024 |
| dc.date.none.fl_str_mv |
2024 2025 2025 2025 |
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info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion |
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article |
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publishedVersion |
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http://hdl.handle.net/10230/71920 http://dx.doi.org/10.1186/s13073-024-01408-2 http://hdl.handle.net/10230/71920 |
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http://hdl.handle.net/10230/71920 http://dx.doi.org/10.1186/s13073-024-01408-2 |
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Inglés |
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Inglés |
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Genome Medicine. 2024;16(1):135 |
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http://creativecommons.org/licenses/by-nc-nd/4.0/ info:eu-repo/semantics/openAccess |
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http://creativecommons.org/licenses/by-nc-nd/4.0/ |
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openAccess |
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application/pdf application/pdf |
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BioMed Central |
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BioMed Central |
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reponame:Recercat. Dipósit de la Recerca de Catalunya instname:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya) |
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Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya) |
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Recercat. Dipósit de la Recerca de Catalunya |
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Recercat. Dipósit de la Recerca de Catalunya |
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1869406078622498816 |
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Epigenetic age and long-term cancer risk following a strokeSuárez-Pérez, AntoniMacias-Gómez, AdriàFernández-Pérez, IsabelVallverdú-Prats, MartaCuadrado-Godia, ElisaGiralt-Steinhauer, EvaCampanale, MaiaGuisado-Alonso, DanielRodríguez-Campello, AnaJiménez-Balado, JoanJiménez Conde, JordiOis Santiago, Angel JavierAgingCancerDNA methylationEpigenetic clockStrokeBackground: The association between increased cancer risk following a cerebrovascular event (CVE) has been previously reported. We hypothesize that biological age (B-age) acceleration is involved in this association. Our study aims to examine B-age as a novel contributing factor to cancer development post-CVE. Methods: From our prospective stroke registry (BasicMar), we selected 940 cases with epigenetic data. For this study, we specifically analyzed 648 of these patients who had available data, no prior history of cancer, and a minimum follow-up of 3 months. The primary outcome was cancer incidence. B-age was estimated using DNA methylation data derived from whole blood samples obtained within 24 h of stroke onset, employing various epigenetic clocks (including Hannum, Horvath, PhenoAge, Zhang, Zhang, and the mitotic epiTOC). Extrinsic epigenetic age acceleration (EEAA) was calculated as the residuals from the regression of B-age against chronological age (C-age). For epiTOC, the age-adjusted values were obtained by regressing out the effect of age from the raw epiTOC measurements. Estimated white cell counts were derived from DNA methylation data, and these cell fractions were used to compute the intrinsic epigenetic age acceleration (IEAA). Subsequently, we evaluated the independent association between EEAA, IEAA, and cancer incidence while controlling for potential confounding variables. Results: Among 648 patients with a median follow-up of 8.15 years, 83 (12.8%) developed cancer. Cox multivariable analyses indicated significant associations between Hannum, Zhang, and epiTOC EEAA and the risk of cancer after CVE. After adjusting for multiple testing and competing risks, EEAA measured by Hannum clock maintained an independent association with cancer risk. Specifically, for each year increase in Hannum's EEAA, we observed a 6.0% increased incidence of cancer (HR 1.06 [1.02-1.10], p value = 0.002). Conclusions: Our findings suggest that epigenetic accelerated aging, as indicated by Hannum's EEAA, may play a significant role in the increased cancer risk observed in CVE survivors.BioMed Central2025202520242025info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfapplication/pdfhttp://hdl.handle.net/10230/71920http://dx.doi.org/10.1186/s13073-024-01408-2http://hdl.handle.net/10230/71920reponame:Recercat. Dipósit de la Recerca de Catalunyainstname:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)InglésGenome Medicine. 2024;16(1):135© The Author(s) 2024. Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by-nc-nd/4.0/.http://creativecommons.org/licenses/by-nc-nd/4.0/info:eu-repo/semantics/openAccessoai:recercat.cat:10230/719202026-05-29T05:05:01Z |
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