Premature aging in childhood cancer survivors (Review)
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00064203%3A_____%2F23%3A10452799" target="_blank" >RIV/00064203:_____/23:10452799 - isvavai.cz</a>
Alternative codes found
RIV/00216208:11130/23:10452799
Result on the web
<a href="https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=5F7e9btDAv" target="_blank" >https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=5F7e9btDAv</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.3892/ol.2022.13629" target="_blank" >10.3892/ol.2022.13629</a>
Alternative languages
Result language
angličtina
Original language name
Premature aging in childhood cancer survivors (Review)
Original language description
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.
Czech name
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Czech description
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Classification
Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
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OECD FORD branch
30204 - Oncology
Result continuities
Project
<a href="/en/project/NV19-03-00245" target="_blank" >NV19-03-00245: Signs of accelerated aging as late effect of therapy for childhood cancer and as risk factor of subsequent malignant neoplasms.</a><br>
Continuities
P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)
Others
Publication year
2023
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Oncology Letters
ISSN
1792-1074
e-ISSN
1792-1082
Volume of the periodical
25
Issue of the periodical within the volume
2
Country of publishing house
GR - GREECE
Number of pages
8
Pages from-to
43
UT code for WoS article
000907283500001
EID of the result in the Scopus database
2-s2.0-85144533829