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p53, stem cell biology and childhood blastomas

Purpose of reviewChildhood blastomas, unlike adult cancers, originate from developing organs in which molecular and cellular features exhibit differentiation arrest and embryonic characteristics. Conventional cancer therapies, which rely on the generalized cytotoxic effect on rapidly dividing cells,...

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Main Authors: Oh, Lixian, Hafsi, Hind, Hainaut, Pierre, Ariffin, Hany
Format: Article
Published: Lippincott, Williams & Wilkins 2019
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R Medicine
Online Access:http://eprints.um.edu.my/23805/
https://doi.org/10.1097/CCO.0000000000000504
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spelling my.um.eprints.238052020-02-17T00:36:51Z http://eprints.um.edu.my/23805/ p53, stem cell biology and childhood blastomas Oh, Lixian Hafsi, Hind Hainaut, Pierre Ariffin, Hany R Medicine Purpose of reviewChildhood blastomas, unlike adult cancers, originate from developing organs in which molecular and cellular features exhibit differentiation arrest and embryonic characteristics. Conventional cancer therapies, which rely on the generalized cytotoxic effect on rapidly dividing cells, may damage delicate organs in young children, leading to multiple late effects. Deep understanding of the biology of embryonal cancers is crucial in reshaping the cancer treatment paradigm for children.Recent findingsp53 plays a major physiological role in embryonic development, by controlling cell proliferation, differentiation and responses to cellular stress. Tumor suppressor function of p53 is commonly lost in adult cancers through genetic alterations. However, both somatic and germline p53 mutations are rare in childhood blastomas, suggesting that in these cancers, p53 may be inactivated through other mechanisms than mutation. In this review, we summarize current knowledge about p53 pathway inactivation in childhood blastomas (specifically neuroblastoma, retinoblastoma and Wilms' tumor) through various upstream mechanisms. Laboratory evidence and clinical trials of targeted therapies specific to exploiting p53 upstream regulators are discussed.SummaryDespite the low rate of inherent TP53 mutations, p53 pathway inactivation is a common denominator in childhood blastomas. Exploiting p53 and its regulators is likely to translate into more effective targeted therapies with minimal late effects for children. (see Video Abstract, Supplemental Digital Content 1, http://links.lww.com/COON/A23). © 2019 Wolters Kluwer Health, Inc. All rights reserved. Lippincott, Williams & Wilkins 2019 Article PeerReviewed Oh, Lixian and Hafsi, Hind and Hainaut, Pierre and Ariffin, Hany (2019) p53, stem cell biology and childhood blastomas. Current Opinion in Oncology, 31 (2). pp. 84-91. ISSN 1040-8746 https://doi.org/10.1097/CCO.0000000000000504 doi:10.1097/CCO.0000000000000504
institution Universiti Malaya
building UM Library
collection Institutional Repository
continent Asia
country Malaysia
content_provider Universiti Malaya
content_source UM Research Repository
url_provider http://eprints.um.edu.my/
topic R Medicine
spellingShingle R Medicine
Oh, Lixian
Hafsi, Hind
Hainaut, Pierre
Ariffin, Hany
p53, stem cell biology and childhood blastomas
description Purpose of reviewChildhood blastomas, unlike adult cancers, originate from developing organs in which molecular and cellular features exhibit differentiation arrest and embryonic characteristics. Conventional cancer therapies, which rely on the generalized cytotoxic effect on rapidly dividing cells, may damage delicate organs in young children, leading to multiple late effects. Deep understanding of the biology of embryonal cancers is crucial in reshaping the cancer treatment paradigm for children.Recent findingsp53 plays a major physiological role in embryonic development, by controlling cell proliferation, differentiation and responses to cellular stress. Tumor suppressor function of p53 is commonly lost in adult cancers through genetic alterations. However, both somatic and germline p53 mutations are rare in childhood blastomas, suggesting that in these cancers, p53 may be inactivated through other mechanisms than mutation. In this review, we summarize current knowledge about p53 pathway inactivation in childhood blastomas (specifically neuroblastoma, retinoblastoma and Wilms' tumor) through various upstream mechanisms. Laboratory evidence and clinical trials of targeted therapies specific to exploiting p53 upstream regulators are discussed.SummaryDespite the low rate of inherent TP53 mutations, p53 pathway inactivation is a common denominator in childhood blastomas. Exploiting p53 and its regulators is likely to translate into more effective targeted therapies with minimal late effects for children. (see Video Abstract, Supplemental Digital Content 1, http://links.lww.com/COON/A23). © 2019 Wolters Kluwer Health, Inc. All rights reserved.
format Article
author Oh, Lixian
Hafsi, Hind
Hainaut, Pierre
Ariffin, Hany
author_facet Oh, Lixian
Hafsi, Hind
Hainaut, Pierre
Ariffin, Hany
author_sort Oh, Lixian
title p53, stem cell biology and childhood blastomas
title_short p53, stem cell biology and childhood blastomas
title_full p53, stem cell biology and childhood blastomas
title_fullStr p53, stem cell biology and childhood blastomas
title_full_unstemmed p53, stem cell biology and childhood blastomas
title_sort p53, stem cell biology and childhood blastomas
publisher Lippincott, Williams & Wilkins
publishDate 2019
url http://eprints.um.edu.my/23805/
https://doi.org/10.1097/CCO.0000000000000504
_version_ 1662755182581121024
score 13.211869

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