Possible Mechanisms of Subsequent Neoplasia Development in Childhood Cancer Survivors: A Review

Kruseová, Jarmila; Vícha, Aleš; Feriančiková, Barbara; Eckschlager, Tomáš

doi:10.3390/cancers13205064

Cited by 6 publications

(2 citation statements)

References 105 publications

(185 reference statements)

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“…Female CCSs are frequently more frail than male CCSs (59,64). This can be partially explained by the sex-dependent acute toxicity of some cytostatics and their late effects (66). Furthermore, in the non-cancer population, frailty is more common in women than in men, which is thought to be due to the lower amount of muscle mass in women (61).…”

Section: Premature Aging In Cancer Survivorsmentioning

confidence: 99%

Premature aging in childhood cancer survivors (Review)

2022

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Progress in medicine has increased the survival time of children suffering from cancer; >80% of patients survive for at least 5 years from the end of treatment. However, there are late effects of anticancer therapy, which accompany this success. Two-thirds of childhood cancer survivors (CCSs) have at least one late effect (any side effects or complications of anticancer treatment that appear months to years after the completion of treatment), e.g. endocrinopathies, cardiovascular diseases or subsequent cancers, and half of these late effects are serious or life threatening. These late consequences of childhood cancer treatment pose a serious health, social and economic problem. A common mechanism for developing a number of late effects is the onset of premature biological aging, which is associated with the early onset of chronic diseases and death. Cellular senescence in cancer survivors is caused by therapy that can induce chromosomal aberrations, mutations, telomere shortening, epigenetic alterations and mitochondrial dysfunctions. The mechanisms of accelerated aging in cancer survivors have not yet been fully clarified. The measurement of biological age in survivors can help improve the understanding of aging mechanisms and identify risk factors for premature aging. However, to the best of our knowledge, no single marker for the evaluation of biological or functional age is known, so it is therefore necessary to measure the consequences of anticancer treatment using complex assessments. The present review presents an overview of premature aging in CCSs and of the mechanisms involved in its development, focusing on the association of senescence and late effects. Contents1. Introduction 2. CCSs and late effects 3. Cell senescence 4. Biological age and its measurement 5. Premature aging in cancer survivors 6. Mechanisms of premature senescence in CCSs 7. Conclusions and future directions

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Section: Premature Aging In Cancer Survivorsmentioning

confidence: 99%

Premature aging in childhood cancer survivors (Review)

2022

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“…Another aspect that should be analyzed—the last but not the least—is the risk that CCS will develop subsequent or secondary malignant neoplasms, namely malignancies that affect children with primary cancer but are histologically different from the original tumor. This “late effect” is more frequent in CCS than in adolescent and young adult cancer survivors, probably because children’s tissues and organs are more sensitive to chemotherapeutic drugs and radiation [ 20 ], and overall, they are more prone to develop a chronic state of inflammation that negatively alters tissue functionality. This problem has a high social, economic and medical impact, hence the necessity to increase the quality of oncological treatments, thus reducing late effects.…”

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confidence: 99%