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Asymmetric cell division of stem and progenitor cells during homeostasis and cancer

Stem and progenitor cells are characterized by their ability to self-renew and produce differentiated progeny. A fine balance between these processes is achieved through controlled asymmetric divisions and is necessary to generate cellular diversity during development and to maintain adult tissue ho...

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Detalles Bibliográficos
Autores principales: Gómez-López, Sandra, Lerner, Robin G., Petritsch, Claudia
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Basel 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3901929/
https://www.ncbi.nlm.nih.gov/pubmed/23771628
http://dx.doi.org/10.1007/s00018-013-1386-1
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author Gómez-López, Sandra
Lerner, Robin G.
Petritsch, Claudia
author_facet Gómez-López, Sandra
Lerner, Robin G.
Petritsch, Claudia
author_sort Gómez-López, Sandra
collection PubMed
description Stem and progenitor cells are characterized by their ability to self-renew and produce differentiated progeny. A fine balance between these processes is achieved through controlled asymmetric divisions and is necessary to generate cellular diversity during development and to maintain adult tissue homeostasis. Disruption of this balance may result in premature depletion of the stem/progenitor cell pool, or abnormal growth. In many tissues, including the brain, dysregulated asymmetric divisions are associated with cancer. Whether there is a causal relationship between asymmetric cell division defects and cancer initiation is as yet not known. Here, we review the cellular and molecular mechanisms that regulate asymmetric cell divisions in the neural lineage and discuss the potential connections between this regulatory machinery and cancer.
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spelling pubmed-39019292014-01-30 Asymmetric cell division of stem and progenitor cells during homeostasis and cancer Gómez-López, Sandra Lerner, Robin G. Petritsch, Claudia Cell Mol Life Sci Review Stem and progenitor cells are characterized by their ability to self-renew and produce differentiated progeny. A fine balance between these processes is achieved through controlled asymmetric divisions and is necessary to generate cellular diversity during development and to maintain adult tissue homeostasis. Disruption of this balance may result in premature depletion of the stem/progenitor cell pool, or abnormal growth. In many tissues, including the brain, dysregulated asymmetric divisions are associated with cancer. Whether there is a causal relationship between asymmetric cell division defects and cancer initiation is as yet not known. Here, we review the cellular and molecular mechanisms that regulate asymmetric cell divisions in the neural lineage and discuss the potential connections between this regulatory machinery and cancer. Springer Basel 2013-06-15 2014 /pmc/articles/PMC3901929/ /pubmed/23771628 http://dx.doi.org/10.1007/s00018-013-1386-1 Text en © The Author(s) 2013 https://creativecommons.org/licenses/by/2.0/ Open AccessThis article is distributed under the terms of the Creative Commons Attribution License which permits any use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited.
spellingShingle Review
Gómez-López, Sandra
Lerner, Robin G.
Petritsch, Claudia
Asymmetric cell division of stem and progenitor cells during homeostasis and cancer
title Asymmetric cell division of stem and progenitor cells during homeostasis and cancer
title_full Asymmetric cell division of stem and progenitor cells during homeostasis and cancer
title_fullStr Asymmetric cell division of stem and progenitor cells during homeostasis and cancer
title_full_unstemmed Asymmetric cell division of stem and progenitor cells during homeostasis and cancer
title_short Asymmetric cell division of stem and progenitor cells during homeostasis and cancer
title_sort asymmetric cell division of stem and progenitor cells during homeostasis and cancer
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3901929/
https://www.ncbi.nlm.nih.gov/pubmed/23771628
http://dx.doi.org/10.1007/s00018-013-1386-1
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