Cognitive performance in survivors of breast cancer and markers of biological aging
Background Biological aging pathways accelerated by cancer treatments may be a mechanism for cognitive impairment in cancer survivors. The goal of the current study was to examine whether indicators of biological aging, namely elevated levels of DNA damage, reduced telomerase enzymatic activity, and...
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| Veröffentlicht in: | Cancer 2019-01, Vol.125 (2), p.298-306 |
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| creator | Carroll, Judith E. Van Dyk, Kathleen Bower, Julienne E. Scuric, Zorica Petersen, Laura Schiestl, Robert Irwin, Michael R. Ganz, Patricia A. |
| description | Background
Biological aging pathways accelerated by cancer treatments may be a mechanism for cognitive impairment in cancer survivors. The goal of the current study was to examine whether indicators of biological aging, namely elevated levels of DNA damage, reduced telomerase enzymatic activity, and shorter peripheral blood mononuclear cell (PBMC) telomere length (TL) would be related to cognitive function in a cohort of survivors of breast cancer.
Methods
The authors evaluated a cross‐sectional sample of 94 women aged 36 to 69 years who were treated for early‐stage breast cancer 3 to 6 years previously. Leukocyte DNA damage, PBMC telomerase enzymatic activity, PBMC TL, and the inflammatory marker soluble tumor necrosis factor receptor II (sTNF‐RII) were determined from blood samples. Cognitive function was assessed using a neuropsychological test battery and self‐report. Linear regression models examined the relationship between biological aging predictors and cognitive outcomes.
Results
Both higher DNA damage and lower telomerase were found to be statistically significantly related to lower executive function scores adjusting for age, body mass index, race, years from treatment, and intelligence score (standardized coefficients [B], ‐0.23 and 0.30; all P values |
| doi_str_mv | 10.1002/cncr.31777 |
| format | Article |
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Biological aging pathways accelerated by cancer treatments may be a mechanism for cognitive impairment in cancer survivors. The goal of the current study was to examine whether indicators of biological aging, namely elevated levels of DNA damage, reduced telomerase enzymatic activity, and shorter peripheral blood mononuclear cell (PBMC) telomere length (TL) would be related to cognitive function in a cohort of survivors of breast cancer.
Methods
The authors evaluated a cross‐sectional sample of 94 women aged 36 to 69 years who were treated for early‐stage breast cancer 3 to 6 years previously. Leukocyte DNA damage, PBMC telomerase enzymatic activity, PBMC TL, and the inflammatory marker soluble tumor necrosis factor receptor II (sTNF‐RII) were determined from blood samples. Cognitive function was assessed using a neuropsychological test battery and self‐report. Linear regression models examined the relationship between biological aging predictors and cognitive outcomes.
Results
Both higher DNA damage and lower telomerase were found to be statistically significantly related to lower executive function scores adjusting for age, body mass index, race, years from treatment, and intelligence score (standardized coefficients [B], ‐0.23 and 0.30; all P values <.05). In addition, lower telomerase activity was associated with worse attention and motor speed scores (B values, 0.30 and 0.24; P <.05). sTNF‐RII and TL were found to be unrelated to any of the neurocognitive domains.
Conclusions
The results of the current study suggest a significant association between measures of biological aging and objective measures of cognitive performance in survivors of breast cancer. Future prospective studies are needed to confirm a causal role of biological aging as a driver of declines in cognitive function after cancer treatment.
Among women treated for early‐stage breast cancer an average of 4 years previously, both high DNA damage and low telomerase activity appear to be related to worse executive functioning, high DNA damage is associated with worse memory, and low telomerase activity is associated with worse attention and motor speed. These findings provide initial evidence for a link between markers of biological aging and cognitive performance in survivors of breast cancer.</description><identifier>ISSN: 0008-543X</identifier><identifier>EISSN: 1097-0142</identifier><identifier>DOI: 10.1002/cncr.31777</identifier><identifier>PMID: 30474160</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Adult ; Aged ; Aging ; Aging - physiology ; Bioindicators ; biological aging ; Biomarkers ; Biomarkers - metabolism ; Body mass ; Body mass index ; Body size ; Breast cancer ; Breast Neoplasms - psychology ; Cancer ; Cancer Survivors - psychology ; Cognition ; Cognition - physiology ; Cognitive ability ; Cognitive tasks ; Cohort Studies ; Cross-Sectional Studies ; Damage ; Deoxyribonucleic acid ; DNA ; DNA damage ; DNA Damage - genetics ; Domains ; Enzymatic activity ; Executive function ; Female ; Humans ; Inflammation ; Inflammation - metabolism ; Intelligence ; Leukocytes ; Longitudinal Studies ; Middle Aged ; Neuropsychological Tests ; Oncology ; Peripheral blood mononuclear cells ; Receptors, Tumor Necrosis Factor, Type II - blood ; Regression analysis ; Regression models ; Statistical analysis ; Statistical methods ; survivors ; Telomerase ; Telomere</subject><ispartof>Cancer, 2019-01, Vol.125 (2), p.298-306</ispartof><rights>2018 American Cancer Society</rights><rights>2018 American Cancer Society.</rights><rights>2019 American Cancer Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3937-a719405cd3e591e5cb731d8c14fe186fa3383e9cee22ac4fa6658f6965527f383</citedby><cites>FETCH-LOGICAL-c3937-a719405cd3e591e5cb731d8c14fe186fa3383e9cee22ac4fa6658f6965527f383</cites><orcidid>0000-0003-1500-930X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fcncr.31777$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fcncr.31777$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,1427,27901,27902,45550,45551,46384,46808</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30474160$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Carroll, Judith E.</creatorcontrib><creatorcontrib>Van Dyk, Kathleen</creatorcontrib><creatorcontrib>Bower, Julienne E.</creatorcontrib><creatorcontrib>Scuric, Zorica</creatorcontrib><creatorcontrib>Petersen, Laura</creatorcontrib><creatorcontrib>Schiestl, Robert</creatorcontrib><creatorcontrib>Irwin, Michael R.</creatorcontrib><creatorcontrib>Ganz, Patricia A.</creatorcontrib><title>Cognitive performance in survivors of breast cancer and markers of biological aging</title><title>Cancer</title><addtitle>Cancer</addtitle><description>Background
Biological aging pathways accelerated by cancer treatments may be a mechanism for cognitive impairment in cancer survivors. The goal of the current study was to examine whether indicators of biological aging, namely elevated levels of DNA damage, reduced telomerase enzymatic activity, and shorter peripheral blood mononuclear cell (PBMC) telomere length (TL) would be related to cognitive function in a cohort of survivors of breast cancer.
Methods
The authors evaluated a cross‐sectional sample of 94 women aged 36 to 69 years who were treated for early‐stage breast cancer 3 to 6 years previously. Leukocyte DNA damage, PBMC telomerase enzymatic activity, PBMC TL, and the inflammatory marker soluble tumor necrosis factor receptor II (sTNF‐RII) were determined from blood samples. Cognitive function was assessed using a neuropsychological test battery and self‐report. Linear regression models examined the relationship between biological aging predictors and cognitive outcomes.
Results
Both higher DNA damage and lower telomerase were found to be statistically significantly related to lower executive function scores adjusting for age, body mass index, race, years from treatment, and intelligence score (standardized coefficients [B], ‐0.23 and 0.30; all P values <.05). In addition, lower telomerase activity was associated with worse attention and motor speed scores (B values, 0.30 and 0.24; P <.05). sTNF‐RII and TL were found to be unrelated to any of the neurocognitive domains.
Conclusions
The results of the current study suggest a significant association between measures of biological aging and objective measures of cognitive performance in survivors of breast cancer. Future prospective studies are needed to confirm a causal role of biological aging as a driver of declines in cognitive function after cancer treatment.
Among women treated for early‐stage breast cancer an average of 4 years previously, both high DNA damage and low telomerase activity appear to be related to worse executive functioning, high DNA damage is associated with worse memory, and low telomerase activity is associated with worse attention and motor speed. These findings provide initial evidence for a link between markers of biological aging and cognitive performance in survivors of breast cancer.</description><subject>Adult</subject><subject>Aged</subject><subject>Aging</subject><subject>Aging - physiology</subject><subject>Bioindicators</subject><subject>biological aging</subject><subject>Biomarkers</subject><subject>Biomarkers - metabolism</subject><subject>Body mass</subject><subject>Body mass index</subject><subject>Body size</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - psychology</subject><subject>Cancer</subject><subject>Cancer Survivors - psychology</subject><subject>Cognition</subject><subject>Cognition - physiology</subject><subject>Cognitive ability</subject><subject>Cognitive tasks</subject><subject>Cohort Studies</subject><subject>Cross-Sectional Studies</subject><subject>Damage</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA damage</subject><subject>DNA Damage - genetics</subject><subject>Domains</subject><subject>Enzymatic activity</subject><subject>Executive function</subject><subject>Female</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Inflammation - metabolism</subject><subject>Intelligence</subject><subject>Leukocytes</subject><subject>Longitudinal Studies</subject><subject>Middle Aged</subject><subject>Neuropsychological Tests</subject><subject>Oncology</subject><subject>Peripheral blood mononuclear cells</subject><subject>Receptors, Tumor Necrosis Factor, Type II - blood</subject><subject>Regression analysis</subject><subject>Regression models</subject><subject>Statistical analysis</subject><subject>Statistical methods</subject><subject>survivors</subject><subject>Telomerase</subject><subject>Telomere</subject><issn>0008-543X</issn><issn>1097-0142</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kMtKxDAUhoMoznjZ-AAScCNCx6RpmnYpxRsMCl7AXcmkJyVjpxmT6ci8vakdXbhwdTj8Hz_nfAidUDKhhMSXqlVuwqgQYgeNKclFRGgS76IxISSLeMLeRujA-3lYRczZPhoxkoiEpmSMngtbt2Zl1oCX4LR1C9kqwKbFvnNrs7bOY6vxzIH0K6z60GHZVngh3TtsQ2MbWxslGyxr09ZHaE_LxsPxdh6i15vrl-Iumj7e3hdX00ixnIlICponhKuKAc8pcDUTjFaZookGmqVaMpYxyBVAHEuVaJmmPNNpnnIeCx2yQ3Q-9C6d_ejAr8qF8QqaRrZgO1_GlGWkf5MH9OwPOreda8N1gUpTkmdZTgN1MVDKWe8d6HLpTHh0U1JS9qrLXnX5rTrAp9vKbraA6hf9cRsAOgCfpoHNP1Vl8VA8DaVfJMyIaA</recordid><startdate>20190115</startdate><enddate>20190115</enddate><creator>Carroll, Judith E.</creator><creator>Van Dyk, Kathleen</creator><creator>Bower, Julienne E.</creator><creator>Scuric, Zorica</creator><creator>Petersen, Laura</creator><creator>Schiestl, Robert</creator><creator>Irwin, Michael R.</creator><creator>Ganz, Patricia A.</creator><general>Wiley Subscription Services, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TO</scope><scope>7U7</scope><scope>C1K</scope><scope>H94</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-1500-930X</orcidid></search><sort><creationdate>20190115</creationdate><title>Cognitive performance in survivors of breast cancer and markers of biological aging</title><author>Carroll, Judith E. ; Van Dyk, Kathleen ; Bower, Julienne E. ; Scuric, Zorica ; Petersen, Laura ; Schiestl, Robert ; Irwin, Michael R. ; Ganz, Patricia A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3937-a719405cd3e591e5cb731d8c14fe186fa3383e9cee22ac4fa6658f6965527f383</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Aging</topic><topic>Aging - physiology</topic><topic>Bioindicators</topic><topic>biological aging</topic><topic>Biomarkers</topic><topic>Biomarkers - metabolism</topic><topic>Body mass</topic><topic>Body mass index</topic><topic>Body size</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - psychology</topic><topic>Cancer</topic><topic>Cancer Survivors - psychology</topic><topic>Cognition</topic><topic>Cognition - physiology</topic><topic>Cognitive ability</topic><topic>Cognitive tasks</topic><topic>Cohort Studies</topic><topic>Cross-Sectional Studies</topic><topic>Damage</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>DNA damage</topic><topic>DNA Damage - genetics</topic><topic>Domains</topic><topic>Enzymatic activity</topic><topic>Executive function</topic><topic>Female</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Inflammation - metabolism</topic><topic>Intelligence</topic><topic>Leukocytes</topic><topic>Longitudinal Studies</topic><topic>Middle Aged</topic><topic>Neuropsychological Tests</topic><topic>Oncology</topic><topic>Peripheral blood mononuclear cells</topic><topic>Receptors, Tumor Necrosis Factor, Type II - blood</topic><topic>Regression analysis</topic><topic>Regression models</topic><topic>Statistical analysis</topic><topic>Statistical methods</topic><topic>survivors</topic><topic>Telomerase</topic><topic>Telomere</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Carroll, Judith E.</creatorcontrib><creatorcontrib>Van Dyk, Kathleen</creatorcontrib><creatorcontrib>Bower, Julienne E.</creatorcontrib><creatorcontrib>Scuric, Zorica</creatorcontrib><creatorcontrib>Petersen, Laura</creatorcontrib><creatorcontrib>Schiestl, Robert</creatorcontrib><creatorcontrib>Irwin, Michael R.</creatorcontrib><creatorcontrib>Ganz, Patricia A.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Carroll, Judith E.</au><au>Van Dyk, Kathleen</au><au>Bower, Julienne E.</au><au>Scuric, Zorica</au><au>Petersen, Laura</au><au>Schiestl, Robert</au><au>Irwin, Michael R.</au><au>Ganz, Patricia A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cognitive performance in survivors of breast cancer and markers of biological aging</atitle><jtitle>Cancer</jtitle><addtitle>Cancer</addtitle><date>2019-01-15</date><risdate>2019</risdate><volume>125</volume><issue>2</issue><spage>298</spage><epage>306</epage><pages>298-306</pages><issn>0008-543X</issn><eissn>1097-0142</eissn><abstract>Background
Biological aging pathways accelerated by cancer treatments may be a mechanism for cognitive impairment in cancer survivors. The goal of the current study was to examine whether indicators of biological aging, namely elevated levels of DNA damage, reduced telomerase enzymatic activity, and shorter peripheral blood mononuclear cell (PBMC) telomere length (TL) would be related to cognitive function in a cohort of survivors of breast cancer.
Methods
The authors evaluated a cross‐sectional sample of 94 women aged 36 to 69 years who were treated for early‐stage breast cancer 3 to 6 years previously. Leukocyte DNA damage, PBMC telomerase enzymatic activity, PBMC TL, and the inflammatory marker soluble tumor necrosis factor receptor II (sTNF‐RII) were determined from blood samples. Cognitive function was assessed using a neuropsychological test battery and self‐report. Linear regression models examined the relationship between biological aging predictors and cognitive outcomes.
Results
Both higher DNA damage and lower telomerase were found to be statistically significantly related to lower executive function scores adjusting for age, body mass index, race, years from treatment, and intelligence score (standardized coefficients [B], ‐0.23 and 0.30; all P values <.05). In addition, lower telomerase activity was associated with worse attention and motor speed scores (B values, 0.30 and 0.24; P <.05). sTNF‐RII and TL were found to be unrelated to any of the neurocognitive domains.
Conclusions
The results of the current study suggest a significant association between measures of biological aging and objective measures of cognitive performance in survivors of breast cancer. Future prospective studies are needed to confirm a causal role of biological aging as a driver of declines in cognitive function after cancer treatment.
Among women treated for early‐stage breast cancer an average of 4 years previously, both high DNA damage and low telomerase activity appear to be related to worse executive functioning, high DNA damage is associated with worse memory, and low telomerase activity is associated with worse attention and motor speed. These findings provide initial evidence for a link between markers of biological aging and cognitive performance in survivors of breast cancer.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>30474160</pmid><doi>10.1002/cncr.31777</doi><tpages>0</tpages><orcidid>https://orcid.org/0000-0003-1500-930X</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Aged Aging Aging - physiology Bioindicators biological aging Biomarkers Biomarkers - metabolism Body mass Body mass index Body size Breast cancer Breast Neoplasms - psychology Cancer Cancer Survivors - psychology Cognition Cognition - physiology Cognitive ability Cognitive tasks Cohort Studies Cross-Sectional Studies Damage Deoxyribonucleic acid DNA DNA damage DNA Damage - genetics Domains Enzymatic activity Executive function Female Humans Inflammation Inflammation - metabolism Intelligence Leukocytes Longitudinal Studies Middle Aged Neuropsychological Tests Oncology Peripheral blood mononuclear cells Receptors, Tumor Necrosis Factor, Type II - blood Regression analysis Regression models Statistical analysis Statistical methods survivors Telomerase Telomere |
| title | Cognitive performance in survivors of breast cancer and markers of biological aging |
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