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Cancer Treatment-Induced Accelerated Aging in Cancer Survivors: Biology and Assessment

SIMPLE SUMMARY: Many modalities used to treat or control cancer lead to accelerated aging in cancer survivors. However, the effects of cancer treatments on aging in individuals with cancer remain poorly studied. In this review, we summarize the possible biological mechanisms of accelerated aging in...

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Autores principales: Wang, Shuo, Prizment, Anna, Thyagarajan, Bharat, Blaes, Anne
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7865902/
https://www.ncbi.nlm.nih.gov/pubmed/33498754
http://dx.doi.org/10.3390/cancers13030427
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author Wang, Shuo
Prizment, Anna
Thyagarajan, Bharat
Blaes, Anne
author_facet Wang, Shuo
Prizment, Anna
Thyagarajan, Bharat
Blaes, Anne
author_sort Wang, Shuo
collection PubMed
description SIMPLE SUMMARY: Many modalities used to treat or control cancer lead to accelerated aging in cancer survivors. However, the effects of cancer treatments on aging in individuals with cancer remain poorly studied. In this review, we summarize the possible biological mechanisms of accelerated aging in cancer survivors induced by cancer treatments. We also discuss the importance of estimating biological age in individuals with cancer and review the methods that can be used to estimate biological age in cancer survivors. ABSTRACT: Rapid improvements in cancer survival led to the realization that many modalities used to treat or control cancer may cause accelerated aging in cancer survivors. Clinically, “accelerated aging” phenotypes in cancer survivors include secondary cancers, frailty, chronic organ dysfunction, and cognitive impairment, all of which can impact long-term health and quality of life in cancer survivors. The treatment-induced accelerated aging in cancer survivors could be explained by telomere attrition, cellular senescence, stem cell exhaustion, DNA damage, and epigenetic alterations. Several aging clocks and biomarkers of aging have been proposed to be potentially useful in estimating biological age, which can provide specific information about how old an individual is biologically independent of chronological age. Measuring biological age in cancer survivors may be important for two reasons. First, it can better predict the risk of cancer treatment-related comorbidities than chronological age. Second, biological age may provide additional value in evaluating the effects of treatments and personalizing cancer therapies to maximize efficacy of treatment. A deeper understanding of treatment-induced accelerated aging in individuals with cancer may lead to novel strategies that reduce the accelerated aging and improve the quality of life in cancer survivors.
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spelling pubmed-78659022021-02-07 Cancer Treatment-Induced Accelerated Aging in Cancer Survivors: Biology and Assessment Wang, Shuo Prizment, Anna Thyagarajan, Bharat Blaes, Anne Cancers (Basel) Review SIMPLE SUMMARY: Many modalities used to treat or control cancer lead to accelerated aging in cancer survivors. However, the effects of cancer treatments on aging in individuals with cancer remain poorly studied. In this review, we summarize the possible biological mechanisms of accelerated aging in cancer survivors induced by cancer treatments. We also discuss the importance of estimating biological age in individuals with cancer and review the methods that can be used to estimate biological age in cancer survivors. ABSTRACT: Rapid improvements in cancer survival led to the realization that many modalities used to treat or control cancer may cause accelerated aging in cancer survivors. Clinically, “accelerated aging” phenotypes in cancer survivors include secondary cancers, frailty, chronic organ dysfunction, and cognitive impairment, all of which can impact long-term health and quality of life in cancer survivors. The treatment-induced accelerated aging in cancer survivors could be explained by telomere attrition, cellular senescence, stem cell exhaustion, DNA damage, and epigenetic alterations. Several aging clocks and biomarkers of aging have been proposed to be potentially useful in estimating biological age, which can provide specific information about how old an individual is biologically independent of chronological age. Measuring biological age in cancer survivors may be important for two reasons. First, it can better predict the risk of cancer treatment-related comorbidities than chronological age. Second, biological age may provide additional value in evaluating the effects of treatments and personalizing cancer therapies to maximize efficacy of treatment. A deeper understanding of treatment-induced accelerated aging in individuals with cancer may lead to novel strategies that reduce the accelerated aging and improve the quality of life in cancer survivors. MDPI 2021-01-23 /pmc/articles/PMC7865902/ /pubmed/33498754 http://dx.doi.org/10.3390/cancers13030427 Text en © 2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Wang, Shuo
Prizment, Anna
Thyagarajan, Bharat
Blaes, Anne
Cancer Treatment-Induced Accelerated Aging in Cancer Survivors: Biology and Assessment
title Cancer Treatment-Induced Accelerated Aging in Cancer Survivors: Biology and Assessment
title_full Cancer Treatment-Induced Accelerated Aging in Cancer Survivors: Biology and Assessment
title_fullStr Cancer Treatment-Induced Accelerated Aging in Cancer Survivors: Biology and Assessment
title_full_unstemmed Cancer Treatment-Induced Accelerated Aging in Cancer Survivors: Biology and Assessment
title_short Cancer Treatment-Induced Accelerated Aging in Cancer Survivors: Biology and Assessment
title_sort cancer treatment-induced accelerated aging in cancer survivors: biology and assessment
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7865902/
https://www.ncbi.nlm.nih.gov/pubmed/33498754
http://dx.doi.org/10.3390/cancers13030427
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