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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; &gt;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

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • 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