Evidence shows that there is a synergistic, bidirectional association between cancer and aging with many shared traits. Age itself is a risk factor for the onset of most cancers while evidence suggests that cancer and its treatments might accelerate aging by causing genotoxic and cytotoxic insults. Aging has been associated with a series of alterations that can be linked to cancer: i) genomic instability caused by DNA damage or epigenetic alterations coupled with repair errors, which lead to progressive accumulation of mutations; ii) telomere attrition with possible impairment of telomerase, shelterin complex, or the trimeric complex (Cdc13, Stn1 and Ten1 - CST) activities associated with abnormalities in DNA replication and repair; iii) altered proteostasis especially when leading to an augmented proteasome, chaperon and autophagy-lysosome activity; iv) mitochondrial dysfunction causing oxidative stress; v) cellular senescence; vi) stem cells exhaustion, intercellular altered communication and deregulated nutrient sensing which are associated with microenvironmental modifications which may facilitate the subsequential role of cancer stem cells. Nowadays anti-growth factor agents and epigenetic therapies seem to assume an increasing role to fight aging-related diseases, especially cancer. This report aims to discuss the impact of age on cancer growth.

Characteristic hallmarks of aging and the impact on carcinogenesis / Terracina, Sergio; Ferraguti, Giampiero; Petrella, Carla; Bruno, SABINA MARIA; Blaconà, Giovanna; Grazia Di Certo, Maria; Minni, Antonio; Greco, Antonio; Musacchio, Angela; Ralli, Massimo; Tarani, Luigi; Ceccanti, Mauro; Polimeni, Antonella; Triaca, Viviana; Fiore, Marco. - In: CURRENT CANCER DRUG TARGETS. - ISSN 1568-0096. - 23:2(2023), pp. 87-102. [10.2174/1568009622666220816120353]

Characteristic hallmarks of aging and the impact on carcinogenesis

Sergio Terracina
Primo
;
Giampiero Ferraguti
Secondo
;
Carla Petrella;Sabina Maria Bruno;Giovanna Blaconà;Antonio Minni;Antonio Greco;Angela Musacchio;Massimo Ralli;Luigi Tarani;Mauro Ceccanti;Antonella Polimeni;
2023

Abstract

Evidence shows that there is a synergistic, bidirectional association between cancer and aging with many shared traits. Age itself is a risk factor for the onset of most cancers while evidence suggests that cancer and its treatments might accelerate aging by causing genotoxic and cytotoxic insults. Aging has been associated with a series of alterations that can be linked to cancer: i) genomic instability caused by DNA damage or epigenetic alterations coupled with repair errors, which lead to progressive accumulation of mutations; ii) telomere attrition with possible impairment of telomerase, shelterin complex, or the trimeric complex (Cdc13, Stn1 and Ten1 - CST) activities associated with abnormalities in DNA replication and repair; iii) altered proteostasis especially when leading to an augmented proteasome, chaperon and autophagy-lysosome activity; iv) mitochondrial dysfunction causing oxidative stress; v) cellular senescence; vi) stem cells exhaustion, intercellular altered communication and deregulated nutrient sensing which are associated with microenvironmental modifications which may facilitate the subsequential role of cancer stem cells. Nowadays anti-growth factor agents and epigenetic therapies seem to assume an increasing role to fight aging-related diseases, especially cancer. This report aims to discuss the impact of age on cancer growth.
2023
aging; cancer; epigenetic; genomic instability; microenvironment; oxidative stress
01 Pubblicazione su rivista::01g Articolo di rassegna (Review)
Characteristic hallmarks of aging and the impact on carcinogenesis / Terracina, Sergio; Ferraguti, Giampiero; Petrella, Carla; Bruno, SABINA MARIA; Blaconà, Giovanna; Grazia Di Certo, Maria; Minni, Antonio; Greco, Antonio; Musacchio, Angela; Ralli, Massimo; Tarani, Luigi; Ceccanti, Mauro; Polimeni, Antonella; Triaca, Viviana; Fiore, Marco. - In: CURRENT CANCER DRUG TARGETS. - ISSN 1568-0096. - 23:2(2023), pp. 87-102. [10.2174/1568009622666220816120353]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/1652245
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