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Abstract
Simple SummaryAround 80% of children treated for childhood cancer become long-term survivors. Although chemotherapy and radiotherapy improve survival of these patients, they cause a low-grade chronic inflammation (inflamm-aging) which induces premature aging processes and vital organ failure, a condition known as frailty. Understanding frailty’s biological and molecular mechanisms and identifying inflamm-aging key biomarkers in childhood cancer survivors could be useful to facilitate the screening of comorbidities and to understand whether treatments, used to counteract inflamm-aging, may prevent side effects.Anti-cancer treatments improve survival in children with cancer. A total of 80% of children treated for childhood cancer achieve 5-year survival, becoming long-term survivors. However, they undergo several chronic late effects related to treatments. In childhood cancer survivors a chronic low-grade inflammation, known as inflamm-aging, is responsible for frailty, a condition characterized by vital organ failure and by premature aging processes. Inflamm-aging is closely related to chemotherapy and radiotherapy, which induce inflammation, accumulation of senescent cells, DNA mutations, and the production of reactive oxygen species. All these conditions are responsible for the onset of secondary diseases, such as osteoporosis, cardiovascular diseases, obesity, and infertility. Considering that the pathobiology of frailty among childhood cancer survivors is still unknown, investigations are needed to better understand frailty’s biological and molecular processes and to identify inflamm-aging key biomarkers in order to facilitate the screening of comorbidities and to clarify whether treatments, normally used to modulate inflamm-aging, may be beneficial. This review offers an overview of the possible biological mechanisms involved in the development of inflamm-aging, focusing our attention on immune system alteration, oxidative stress, cellular senescence, and therapeutic strategies.
Highlights
This article is an open access articleOne of the greatest medical successes over the past five decades is the improvement in survival among children with cancer
Exposure to oncogenic insults leads to inflammation, the accumulation of senescent cells, and the increasing of reactive oxygen species (ROS) and DNA mutations [12,13]
This review offers an overview of the possible biological mechanisms involved in the development of chronic systemic inflammation, focusing our attention on immune system alteration, oxidative stress, cellular senescence, and therapeutic strategies
Summary
One of the greatest medical successes over the past five decades is the improvement in survival among children with cancer. Increase over time and influence the physiological aging process, resulting in a premature alteration of vital organ system function during adulthood and predispose individuals to a major risk to prematurely develop chronic age-related health conditions, frequent hospitalization, and early mortality. This condition is known as frailty [6,7]. Metabolic syndrome pathophysiology is related to lifestyle factors, like reduced physical activity and incorrect diet, which are responsible for an increase of BMI and, low-grade inflammation [20,24]. This review offers an overview of the possible biological mechanisms involved in the development of chronic systemic inflammation, focusing our attention on immune system alteration, oxidative stress, cellular senescence, and therapeutic strategies
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