Abstract 2462: Longitudinal change in epigenetic aging and telomere length in breast cancer survivors

Abstract PURPOSE: Cancer treatments may accelerate biological aging, but longitudinal studies of biological markers of aging are needed to better characterize patterns of biological aging over time. METHODS: We followed 184 women with breast cancer (stage 0-III) from diagnosis to 18 months post treatment. We evaluated biological aging in three treatment groups: chemotherapy (with or without radiotherapy), radiotherapy (without chemotherapy), and neither chemotherapy or radiotherapy. Measures of epigenetic age (PCPhenoAge, GrimAge, DunedinPACE) and telomere length were obtained. Linear mixed models estimated within-group change from pre-treatment to immediate post, 6, 12, and 18 months post-treatment. RESULTS: Women who received chemotherapy exhibited increased epigenetic age in PCPhenoAge, GrimAge, and DunedinPACE and shortening of telomere length acutely following treatment (Ps<0.001). The change attenuated but remained significantly different than baseline for GrimAge, DunedinPACE, and telomere length out to 18 months. Women treated with radiotherapy exhibited a trend for increases in PCPhenoAge and significant telomere length shortening 6 months following treatment that remained modified at 18 months (Ps<0.05). There were no significant changes in epigenetic age or telomere length among women who did not receive either chemotherapy or radiation. CONCLUSION: We observed an acceleration of epigenetic age, an increase in the pace of aging, and telomere shortening among women receiving treatment for breast cancer. The effect was predominantly amongst women who received chemotherapy with or without radiation, pointing to this treatment regimen having the most damaging effects. These results support the premise that cancer treatment may accelerate aging and support further research to identify key clinical and biological targets to remediate these effects. Citation Format: Judith E. Carroll, Cynthia Kusters, Catherine M. Crespi, Michael R. Irwin, Patricia A. Ganz, Laura Petersen, Julienne E. Bower. Longitudinal change in epigenetic aging and telomere length in breast cancer survivors [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 2462.

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Journal
Cancer Research
Published
2026-04-03
DOI
https://doi.org/10.1158/1538-7445.am2026-2462
Primary Topic
Telomeres, Telomerase, and Senescence
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article
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article

Abstract 2462: Longitudinal change in epigenetic aging and telomere length in breast cancer survivors

Michael R. Irwin, Judith Carroll, Catherine M. Crespi, Cynthia Kusters et al.
Cancer Research
Telomeres, Telomerase, and Senescence
article

Abstract 2462: Longitudinal change in epigenetic aging and telomere length in breast cancer survivors

Michael R. Irwin, Judith Carroll, Catherine M. Crespi, Cynthia Kusters, Laura Petersen, Julienne E. Bower, Patricia A. Ganz
article en

Abstract

Abstract PURPOSE: Cancer treatments may accelerate biological aging, but longitudinal studies of biological markers of aging are needed to better characterize patterns of biological aging over time. METHODS: We followed 184 women with breast cancer (stage 0-III) from diagnosis to 18 months post treatment. We evaluated biological aging in three treatment groups: chemotherapy (with or without radiotherapy), radiotherapy (without chemotherapy), and neither chemotherapy or radiotherapy. Measures of epigenetic age (PCPhenoAge, GrimAge, DunedinPACE) and telomere length were obtained. Linear mixed models estimated within-group change from pre-treatment to immediate post, 6, 12, and 18 months post-treatment. RESULTS: Women who received chemotherapy exhibited increased epigenetic age in PCPhenoAge, GrimAge, and DunedinPACE and shortening of telomere length acutely following treatment (Ps<0.001). The change attenuated but remained significantly different than baseline for GrimAge, DunedinPACE, and telomere length out to 18 months. Women treated with radiotherapy exhibited a trend for increases in PCPhenoAge and significant telomere length shortening 6 months following treatment that remained modified at 18 months (Ps<0.05). There were no significant changes in epigenetic age or telomere length among women who did not receive either chemotherapy or radiation. CONCLUSION: We observed an acceleration of epigenetic age, an increase in the pace of aging, and telomere shortening among women receiving treatment for breast cancer. The effect was predominantly amongst women who received chemotherapy with or without radiation, pointing to this treatment regimen having the most damaging effects. These results support the premise that cancer treatment may accelerate aging and support further research to identify key clinical and biological targets to remediate these effects. Citation Format: Judith E. Carroll, Cynthia Kusters, Catherine M. Crespi, Michael R. Irwin, Patricia A. Ganz, Laura Petersen, Julienne E. Bower. Longitudinal change in epigenetic aging and telomere length in breast cancer survivors [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 2462.

Cancer ResearchVol. 86(7_Supplement)
APLA Health (US), University of California, Los Angeles (US), UCLA Jonsson Comprehensive Cancer Center
Good health and well-being
Openalex Percentile: Top 29%
Telomeres, Telomerase, and Senescence
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