Acceleration of the DNA methylation clock among lynch syndrome-associated mutation carriers

Background DNA methylation (DNAm) age metrics have been widely accepted as an epigenetic biomarker for biological aging and disease. The purpose of this study is to assess whether or not individuals carrying Lynch Syndrome-associated mutations are affected in their rate of biological aging, as measu...
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Autor*in:	Cuadros, Marta [verfasserIn] Cano, Carlos Garcia-Rodriguez, Sonia Martín, José Luis Poyatos-Andujar, Antonio Ruiz-Cabello, Francisco Pedrinaci, Susana Durán, Gema Benavides, Manuel Bautista-Ojeda, María Dolores Pereda, Teresa Benitez-Cantos, Maria Soledad Medina, Pedro Blanco, Armando Gonzalez, Antonio Lizardi, Paul

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2022

Schlagwörter:	DNA methylation Lynch syndrome Epigenetic clock

Anmerkung:	© The Author(s) 2022

Übergeordnetes Werk:	Enthalten in: BMC medical genomics - London : BioMed Central, 2008, 15(2022), 1 vom: 04. März
Übergeordnetes Werk:	volume:15 ; year:2022 ; number:1 ; day:04 ; month:03

Links:	Volltext

DOI / URN:	10.1186/s12920-022-01183-2

Katalog-ID:	SPR050529013

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520			\|a Background DNA methylation (DNAm) age metrics have been widely accepted as an epigenetic biomarker for biological aging and disease. The purpose of this study is to assess whether or not individuals carrying Lynch Syndrome-associated mutations are affected in their rate of biological aging, as measured by the epigenetic clock. Methods Genome-wide bisulfite DNA sequencing data were generated using DNA from CD4 + T-cells obtained from peripheral blood using 27 patient samples from Lynch syndrome families. Horvath’s DNAm age model based on penalized linear regression was applied to estimate DNAm age from patient samples with distinct clinical and genetic characteristics to investigate cancer mutation-related aging effects. Results Both Lynch mutation carriers and controls exhibited high variability in their estimated DNAm age, but regression analysis showed steeper slope for the Lynch mutation carriers. Remarkably, six Lynch Syndrome-associated mutation carriers showed a strong correlation to the control group, and two sisters carrying Lynch Syndrome-associated mutations, with no significant difference in lifestyle and similar chronological age, were assigned very different DNAm age. Conclusions Future studies will be required to explore, in larger patient populations, whether specific epigenetic age acceleration is predictive of time-to-cancer development, treatment response, and survival. Epigenetic clock DNAm metrics may be affected by the presence of cancer mutations in the germline, and thus show promise of potential clinical utility for stratified surveillance strategies based on the relative risk for imminent emergence of tumor lesions in otherwise healthy Lynch Syndrome-associated mutation carriers.
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allfields	10.1186/s12920-022-01183-2 doi (DE-627)SPR050529013 (SPR)s12920-022-01183-2-e DE-627 ger DE-627 rakwb eng Cuadros, Marta verfasserin aut Acceleration of the DNA methylation clock among lynch syndrome-associated mutation carriers 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2022 Background DNA methylation (DNAm) age metrics have been widely accepted as an epigenetic biomarker for biological aging and disease. The purpose of this study is to assess whether or not individuals carrying Lynch Syndrome-associated mutations are affected in their rate of biological aging, as measured by the epigenetic clock. Methods Genome-wide bisulfite DNA sequencing data were generated using DNA from CD4 + T-cells obtained from peripheral blood using 27 patient samples from Lynch syndrome families. Horvath’s DNAm age model based on penalized linear regression was applied to estimate DNAm age from patient samples with distinct clinical and genetic characteristics to investigate cancer mutation-related aging effects. Results Both Lynch mutation carriers and controls exhibited high variability in their estimated DNAm age, but regression analysis showed steeper slope for the Lynch mutation carriers. Remarkably, six Lynch Syndrome-associated mutation carriers showed a strong correlation to the control group, and two sisters carrying Lynch Syndrome-associated mutations, with no significant difference in lifestyle and similar chronological age, were assigned very different DNAm age. Conclusions Future studies will be required to explore, in larger patient populations, whether specific epigenetic age acceleration is predictive of time-to-cancer development, treatment response, and survival. Epigenetic clock DNAm metrics may be affected by the presence of cancer mutations in the germline, and thus show promise of potential clinical utility for stratified surveillance strategies based on the relative risk for imminent emergence of tumor lesions in otherwise healthy Lynch Syndrome-associated mutation carriers. DNA methylation (dpeaa)DE-He213 Lynch syndrome (dpeaa)DE-He213 Epigenetic clock (dpeaa)DE-He213 Cano, Carlos aut Garcia-Rodriguez, Sonia aut Martín, José Luis aut Poyatos-Andujar, Antonio aut Ruiz-Cabello, Francisco aut Pedrinaci, Susana aut Durán, Gema aut Benavides, Manuel aut Bautista-Ojeda, María Dolores aut Pereda, Teresa aut Benitez-Cantos, Maria Soledad aut Medina, Pedro aut Blanco, Armando aut Gonzalez, Antonio aut Lizardi, Paul aut Enthalten in BMC medical genomics London : BioMed Central, 2008 15(2022), 1 vom: 04. März (DE-627)559080824 (DE-600)2411865-5 1755-8794 nnns volume:15 year:2022 number:1 day:04 month:03 https://dx.doi.org/10.1186/s12920-022-01183-2 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2022 1 04 03
spelling	10.1186/s12920-022-01183-2 doi (DE-627)SPR050529013 (SPR)s12920-022-01183-2-e DE-627 ger DE-627 rakwb eng Cuadros, Marta verfasserin aut Acceleration of the DNA methylation clock among lynch syndrome-associated mutation carriers 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2022 Background DNA methylation (DNAm) age metrics have been widely accepted as an epigenetic biomarker for biological aging and disease. The purpose of this study is to assess whether or not individuals carrying Lynch Syndrome-associated mutations are affected in their rate of biological aging, as measured by the epigenetic clock. Methods Genome-wide bisulfite DNA sequencing data were generated using DNA from CD4 + T-cells obtained from peripheral blood using 27 patient samples from Lynch syndrome families. Horvath’s DNAm age model based on penalized linear regression was applied to estimate DNAm age from patient samples with distinct clinical and genetic characteristics to investigate cancer mutation-related aging effects. Results Both Lynch mutation carriers and controls exhibited high variability in their estimated DNAm age, but regression analysis showed steeper slope for the Lynch mutation carriers. Remarkably, six Lynch Syndrome-associated mutation carriers showed a strong correlation to the control group, and two sisters carrying Lynch Syndrome-associated mutations, with no significant difference in lifestyle and similar chronological age, were assigned very different DNAm age. Conclusions Future studies will be required to explore, in larger patient populations, whether specific epigenetic age acceleration is predictive of time-to-cancer development, treatment response, and survival. Epigenetic clock DNAm metrics may be affected by the presence of cancer mutations in the germline, and thus show promise of potential clinical utility for stratified surveillance strategies based on the relative risk for imminent emergence of tumor lesions in otherwise healthy Lynch Syndrome-associated mutation carriers. DNA methylation (dpeaa)DE-He213 Lynch syndrome (dpeaa)DE-He213 Epigenetic clock (dpeaa)DE-He213 Cano, Carlos aut Garcia-Rodriguez, Sonia aut Martín, José Luis aut Poyatos-Andujar, Antonio aut Ruiz-Cabello, Francisco aut Pedrinaci, Susana aut Durán, Gema aut Benavides, Manuel aut Bautista-Ojeda, María Dolores aut Pereda, Teresa aut Benitez-Cantos, Maria Soledad aut Medina, Pedro aut Blanco, Armando aut Gonzalez, Antonio aut Lizardi, Paul aut Enthalten in BMC medical genomics London : BioMed Central, 2008 15(2022), 1 vom: 04. März (DE-627)559080824 (DE-600)2411865-5 1755-8794 nnns volume:15 year:2022 number:1 day:04 month:03 https://dx.doi.org/10.1186/s12920-022-01183-2 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2022 1 04 03
allfields_unstemmed	10.1186/s12920-022-01183-2 doi (DE-627)SPR050529013 (SPR)s12920-022-01183-2-e DE-627 ger DE-627 rakwb eng Cuadros, Marta verfasserin aut Acceleration of the DNA methylation clock among lynch syndrome-associated mutation carriers 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2022 Background DNA methylation (DNAm) age metrics have been widely accepted as an epigenetic biomarker for biological aging and disease. The purpose of this study is to assess whether or not individuals carrying Lynch Syndrome-associated mutations are affected in their rate of biological aging, as measured by the epigenetic clock. Methods Genome-wide bisulfite DNA sequencing data were generated using DNA from CD4 + T-cells obtained from peripheral blood using 27 patient samples from Lynch syndrome families. Horvath’s DNAm age model based on penalized linear regression was applied to estimate DNAm age from patient samples with distinct clinical and genetic characteristics to investigate cancer mutation-related aging effects. Results Both Lynch mutation carriers and controls exhibited high variability in their estimated DNAm age, but regression analysis showed steeper slope for the Lynch mutation carriers. Remarkably, six Lynch Syndrome-associated mutation carriers showed a strong correlation to the control group, and two sisters carrying Lynch Syndrome-associated mutations, with no significant difference in lifestyle and similar chronological age, were assigned very different DNAm age. Conclusions Future studies will be required to explore, in larger patient populations, whether specific epigenetic age acceleration is predictive of time-to-cancer development, treatment response, and survival. Epigenetic clock DNAm metrics may be affected by the presence of cancer mutations in the germline, and thus show promise of potential clinical utility for stratified surveillance strategies based on the relative risk for imminent emergence of tumor lesions in otherwise healthy Lynch Syndrome-associated mutation carriers. DNA methylation (dpeaa)DE-He213 Lynch syndrome (dpeaa)DE-He213 Epigenetic clock (dpeaa)DE-He213 Cano, Carlos aut Garcia-Rodriguez, Sonia aut Martín, José Luis aut Poyatos-Andujar, Antonio aut Ruiz-Cabello, Francisco aut Pedrinaci, Susana aut Durán, Gema aut Benavides, Manuel aut Bautista-Ojeda, María Dolores aut Pereda, Teresa aut Benitez-Cantos, Maria Soledad aut Medina, Pedro aut Blanco, Armando aut Gonzalez, Antonio aut Lizardi, Paul aut Enthalten in BMC medical genomics London : BioMed Central, 2008 15(2022), 1 vom: 04. März (DE-627)559080824 (DE-600)2411865-5 1755-8794 nnns volume:15 year:2022 number:1 day:04 month:03 https://dx.doi.org/10.1186/s12920-022-01183-2 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2022 1 04 03
allfieldsGer	10.1186/s12920-022-01183-2 doi (DE-627)SPR050529013 (SPR)s12920-022-01183-2-e DE-627 ger DE-627 rakwb eng Cuadros, Marta verfasserin aut Acceleration of the DNA methylation clock among lynch syndrome-associated mutation carriers 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2022 Background DNA methylation (DNAm) age metrics have been widely accepted as an epigenetic biomarker for biological aging and disease. The purpose of this study is to assess whether or not individuals carrying Lynch Syndrome-associated mutations are affected in their rate of biological aging, as measured by the epigenetic clock. Methods Genome-wide bisulfite DNA sequencing data were generated using DNA from CD4 + T-cells obtained from peripheral blood using 27 patient samples from Lynch syndrome families. Horvath’s DNAm age model based on penalized linear regression was applied to estimate DNAm age from patient samples with distinct clinical and genetic characteristics to investigate cancer mutation-related aging effects. Results Both Lynch mutation carriers and controls exhibited high variability in their estimated DNAm age, but regression analysis showed steeper slope for the Lynch mutation carriers. Remarkably, six Lynch Syndrome-associated mutation carriers showed a strong correlation to the control group, and two sisters carrying Lynch Syndrome-associated mutations, with no significant difference in lifestyle and similar chronological age, were assigned very different DNAm age. Conclusions Future studies will be required to explore, in larger patient populations, whether specific epigenetic age acceleration is predictive of time-to-cancer development, treatment response, and survival. Epigenetic clock DNAm metrics may be affected by the presence of cancer mutations in the germline, and thus show promise of potential clinical utility for stratified surveillance strategies based on the relative risk for imminent emergence of tumor lesions in otherwise healthy Lynch Syndrome-associated mutation carriers. DNA methylation (dpeaa)DE-He213 Lynch syndrome (dpeaa)DE-He213 Epigenetic clock (dpeaa)DE-He213 Cano, Carlos aut Garcia-Rodriguez, Sonia aut Martín, José Luis aut Poyatos-Andujar, Antonio aut Ruiz-Cabello, Francisco aut Pedrinaci, Susana aut Durán, Gema aut Benavides, Manuel aut Bautista-Ojeda, María Dolores aut Pereda, Teresa aut Benitez-Cantos, Maria Soledad aut Medina, Pedro aut Blanco, Armando aut Gonzalez, Antonio aut Lizardi, Paul aut Enthalten in BMC medical genomics London : BioMed Central, 2008 15(2022), 1 vom: 04. März (DE-627)559080824 (DE-600)2411865-5 1755-8794 nnns volume:15 year:2022 number:1 day:04 month:03 https://dx.doi.org/10.1186/s12920-022-01183-2 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2022 1 04 03
allfieldsSound	10.1186/s12920-022-01183-2 doi (DE-627)SPR050529013 (SPR)s12920-022-01183-2-e DE-627 ger DE-627 rakwb eng Cuadros, Marta verfasserin aut Acceleration of the DNA methylation clock among lynch syndrome-associated mutation carriers 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2022 Background DNA methylation (DNAm) age metrics have been widely accepted as an epigenetic biomarker for biological aging and disease. The purpose of this study is to assess whether or not individuals carrying Lynch Syndrome-associated mutations are affected in their rate of biological aging, as measured by the epigenetic clock. Methods Genome-wide bisulfite DNA sequencing data were generated using DNA from CD4 + T-cells obtained from peripheral blood using 27 patient samples from Lynch syndrome families. Horvath’s DNAm age model based on penalized linear regression was applied to estimate DNAm age from patient samples with distinct clinical and genetic characteristics to investigate cancer mutation-related aging effects. Results Both Lynch mutation carriers and controls exhibited high variability in their estimated DNAm age, but regression analysis showed steeper slope for the Lynch mutation carriers. Remarkably, six Lynch Syndrome-associated mutation carriers showed a strong correlation to the control group, and two sisters carrying Lynch Syndrome-associated mutations, with no significant difference in lifestyle and similar chronological age, were assigned very different DNAm age. Conclusions Future studies will be required to explore, in larger patient populations, whether specific epigenetic age acceleration is predictive of time-to-cancer development, treatment response, and survival. Epigenetic clock DNAm metrics may be affected by the presence of cancer mutations in the germline, and thus show promise of potential clinical utility for stratified surveillance strategies based on the relative risk for imminent emergence of tumor lesions in otherwise healthy Lynch Syndrome-associated mutation carriers. DNA methylation (dpeaa)DE-He213 Lynch syndrome (dpeaa)DE-He213 Epigenetic clock (dpeaa)DE-He213 Cano, Carlos aut Garcia-Rodriguez, Sonia aut Martín, José Luis aut Poyatos-Andujar, Antonio aut Ruiz-Cabello, Francisco aut Pedrinaci, Susana aut Durán, Gema aut Benavides, Manuel aut Bautista-Ojeda, María Dolores aut Pereda, Teresa aut Benitez-Cantos, Maria Soledad aut Medina, Pedro aut Blanco, Armando aut Gonzalez, Antonio aut Lizardi, Paul aut Enthalten in BMC medical genomics London : BioMed Central, 2008 15(2022), 1 vom: 04. März (DE-627)559080824 (DE-600)2411865-5 1755-8794 nnns volume:15 year:2022 number:1 day:04 month:03 https://dx.doi.org/10.1186/s12920-022-01183-2 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2022 1 04 03
language	English
source	Enthalten in BMC medical genomics 15(2022), 1 vom: 04. März volume:15 year:2022 number:1 day:04 month:03
sourceStr	Enthalten in BMC medical genomics 15(2022), 1 vom: 04. März volume:15 year:2022 number:1 day:04 month:03
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author	Cuadros, Marta
spellingShingle	Cuadros, Marta misc DNA methylation misc Lynch syndrome misc Epigenetic clock Acceleration of the DNA methylation clock among lynch syndrome-associated mutation carriers
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topic_title	Acceleration of the DNA methylation clock among lynch syndrome-associated mutation carriers DNA methylation (dpeaa)DE-He213 Lynch syndrome (dpeaa)DE-He213 Epigenetic clock (dpeaa)DE-He213
topic	misc DNA methylation misc Lynch syndrome misc Epigenetic clock
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title	Acceleration of the DNA methylation clock among lynch syndrome-associated mutation carriers
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title_full	Acceleration of the DNA methylation clock among lynch syndrome-associated mutation carriers
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author_browse	Cuadros, Marta Cano, Carlos Garcia-Rodriguez, Sonia Martín, José Luis Poyatos-Andujar, Antonio Ruiz-Cabello, Francisco Pedrinaci, Susana Durán, Gema Benavides, Manuel Bautista-Ojeda, María Dolores Pereda, Teresa Benitez-Cantos, Maria Soledad Medina, Pedro Blanco, Armando Gonzalez, Antonio Lizardi, Paul
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title_sort	acceleration of the dna methylation clock among lynch syndrome-associated mutation carriers
title_auth	Acceleration of the DNA methylation clock among lynch syndrome-associated mutation carriers
abstract	Background DNA methylation (DNAm) age metrics have been widely accepted as an epigenetic biomarker for biological aging and disease. The purpose of this study is to assess whether or not individuals carrying Lynch Syndrome-associated mutations are affected in their rate of biological aging, as measured by the epigenetic clock. Methods Genome-wide bisulfite DNA sequencing data were generated using DNA from CD4 + T-cells obtained from peripheral blood using 27 patient samples from Lynch syndrome families. Horvath’s DNAm age model based on penalized linear regression was applied to estimate DNAm age from patient samples with distinct clinical and genetic characteristics to investigate cancer mutation-related aging effects. Results Both Lynch mutation carriers and controls exhibited high variability in their estimated DNAm age, but regression analysis showed steeper slope for the Lynch mutation carriers. Remarkably, six Lynch Syndrome-associated mutation carriers showed a strong correlation to the control group, and two sisters carrying Lynch Syndrome-associated mutations, with no significant difference in lifestyle and similar chronological age, were assigned very different DNAm age. Conclusions Future studies will be required to explore, in larger patient populations, whether specific epigenetic age acceleration is predictive of time-to-cancer development, treatment response, and survival. Epigenetic clock DNAm metrics may be affected by the presence of cancer mutations in the germline, and thus show promise of potential clinical utility for stratified surveillance strategies based on the relative risk for imminent emergence of tumor lesions in otherwise healthy Lynch Syndrome-associated mutation carriers. © The Author(s) 2022
abstractGer	Background DNA methylation (DNAm) age metrics have been widely accepted as an epigenetic biomarker for biological aging and disease. The purpose of this study is to assess whether or not individuals carrying Lynch Syndrome-associated mutations are affected in their rate of biological aging, as measured by the epigenetic clock. Methods Genome-wide bisulfite DNA sequencing data were generated using DNA from CD4 + T-cells obtained from peripheral blood using 27 patient samples from Lynch syndrome families. Horvath’s DNAm age model based on penalized linear regression was applied to estimate DNAm age from patient samples with distinct clinical and genetic characteristics to investigate cancer mutation-related aging effects. Results Both Lynch mutation carriers and controls exhibited high variability in their estimated DNAm age, but regression analysis showed steeper slope for the Lynch mutation carriers. Remarkably, six Lynch Syndrome-associated mutation carriers showed a strong correlation to the control group, and two sisters carrying Lynch Syndrome-associated mutations, with no significant difference in lifestyle and similar chronological age, were assigned very different DNAm age. Conclusions Future studies will be required to explore, in larger patient populations, whether specific epigenetic age acceleration is predictive of time-to-cancer development, treatment response, and survival. Epigenetic clock DNAm metrics may be affected by the presence of cancer mutations in the germline, and thus show promise of potential clinical utility for stratified surveillance strategies based on the relative risk for imminent emergence of tumor lesions in otherwise healthy Lynch Syndrome-associated mutation carriers. © The Author(s) 2022
abstract_unstemmed	Background DNA methylation (DNAm) age metrics have been widely accepted as an epigenetic biomarker for biological aging and disease. The purpose of this study is to assess whether or not individuals carrying Lynch Syndrome-associated mutations are affected in their rate of biological aging, as measured by the epigenetic clock. Methods Genome-wide bisulfite DNA sequencing data were generated using DNA from CD4 + T-cells obtained from peripheral blood using 27 patient samples from Lynch syndrome families. Horvath’s DNAm age model based on penalized linear regression was applied to estimate DNAm age from patient samples with distinct clinical and genetic characteristics to investigate cancer mutation-related aging effects. Results Both Lynch mutation carriers and controls exhibited high variability in their estimated DNAm age, but regression analysis showed steeper slope for the Lynch mutation carriers. Remarkably, six Lynch Syndrome-associated mutation carriers showed a strong correlation to the control group, and two sisters carrying Lynch Syndrome-associated mutations, with no significant difference in lifestyle and similar chronological age, were assigned very different DNAm age. Conclusions Future studies will be required to explore, in larger patient populations, whether specific epigenetic age acceleration is predictive of time-to-cancer development, treatment response, and survival. Epigenetic clock DNAm metrics may be affected by the presence of cancer mutations in the germline, and thus show promise of potential clinical utility for stratified surveillance strategies based on the relative risk for imminent emergence of tumor lesions in otherwise healthy Lynch Syndrome-associated mutation carriers. © The Author(s) 2022
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title_short	Acceleration of the DNA methylation clock among lynch syndrome-associated mutation carriers
url	https://dx.doi.org/10.1186/s12920-022-01183-2
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author2	Cano, Carlos Garcia-Rodriguez, Sonia Martín, José Luis Poyatos-Andujar, Antonio Ruiz-Cabello, Francisco Pedrinaci, Susana Durán, Gema Benavides, Manuel Bautista-Ojeda, María Dolores Pereda, Teresa Benitez-Cantos, Maria Soledad Medina, Pedro Blanco, Armando Gonzalez, Antonio Lizardi, Paul
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up_date	2024-07-03T16:07:06.921Z
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The purpose of this study is to assess whether or not individuals carrying Lynch Syndrome-associated mutations are affected in their rate of biological aging, as measured by the epigenetic clock. Methods Genome-wide bisulfite DNA sequencing data were generated using DNA from CD4 + T-cells obtained from peripheral blood using 27 patient samples from Lynch syndrome families. Horvath’s DNAm age model based on penalized linear regression was applied to estimate DNAm age from patient samples with distinct clinical and genetic characteristics to investigate cancer mutation-related aging effects. Results Both Lynch mutation carriers and controls exhibited high variability in their estimated DNAm age, but regression analysis showed steeper slope for the Lynch mutation carriers. Remarkably, six Lynch Syndrome-associated mutation carriers showed a strong correlation to the control group, and two sisters carrying Lynch Syndrome-associated mutations, with no significant difference in lifestyle and similar chronological age, were assigned very different DNAm age. Conclusions Future studies will be required to explore, in larger patient populations, whether specific epigenetic age acceleration is predictive of time-to-cancer development, treatment response, and survival. 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Acceleration of the DNA methylation clock among lynch syndrome-associated mutation carriers

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