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Stem cells in cancer initiation and progression

While standard therapies can lead to an initial remission of aggressive cancers, they are often only a transient solution. The resistance and relapse that follows is driven by tumor heterogeneity and therapy-resistant populations that can reinitiate growth and promote disease progression. There is t...

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Detalles Bibliográficos
Autores principales: Bajaj, Jeevisha, Diaz, Emily, Reya, Tannishtha
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Rockefeller University Press 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7039188/
https://www.ncbi.nlm.nih.gov/pubmed/31874116
http://dx.doi.org/10.1083/jcb.201911053
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author Bajaj, Jeevisha
Diaz, Emily
Reya, Tannishtha
author_facet Bajaj, Jeevisha
Diaz, Emily
Reya, Tannishtha
author_sort Bajaj, Jeevisha
collection PubMed
description While standard therapies can lead to an initial remission of aggressive cancers, they are often only a transient solution. The resistance and relapse that follows is driven by tumor heterogeneity and therapy-resistant populations that can reinitiate growth and promote disease progression. There is thus a significant need to understand the cell types and signaling pathways that not only contribute to cancer initiation, but also those that confer resistance and drive recurrence. Here, we discuss work showing that stem cells and progenitors may preferentially serve as a cell of origin for cancers, and that cancer stem cells can be key in driving the continued growth and  functional heterogeneity of established cancers. We also describe emerging evidence for the role of developmental signals in cancer initiation, propagation, and therapy resistance and discuss how targeting these pathways may be of therapeutic value.
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spelling pubmed-70391882020-07-06 Stem cells in cancer initiation and progression Bajaj, Jeevisha Diaz, Emily Reya, Tannishtha J Cell Biol Reviews While standard therapies can lead to an initial remission of aggressive cancers, they are often only a transient solution. The resistance and relapse that follows is driven by tumor heterogeneity and therapy-resistant populations that can reinitiate growth and promote disease progression. There is thus a significant need to understand the cell types and signaling pathways that not only contribute to cancer initiation, but also those that confer resistance and drive recurrence. Here, we discuss work showing that stem cells and progenitors may preferentially serve as a cell of origin for cancers, and that cancer stem cells can be key in driving the continued growth and  functional heterogeneity of established cancers. We also describe emerging evidence for the role of developmental signals in cancer initiation, propagation, and therapy resistance and discuss how targeting these pathways may be of therapeutic value. Rockefeller University Press 2019-12-24 /pmc/articles/PMC7039188/ /pubmed/31874116 http://dx.doi.org/10.1083/jcb.201911053 Text en © 2019 Bajaj et al. http://www.rupress.org/terms/https://creativecommons.org/licenses/by-nc-sa/4.0/This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms/). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 International license, as described at https://creativecommons.org/licenses/by-nc-sa/4.0/).
spellingShingle Reviews
Bajaj, Jeevisha
Diaz, Emily
Reya, Tannishtha
Stem cells in cancer initiation and progression
title Stem cells in cancer initiation and progression
title_full Stem cells in cancer initiation and progression
title_fullStr Stem cells in cancer initiation and progression
title_full_unstemmed Stem cells in cancer initiation and progression
title_short Stem cells in cancer initiation and progression
title_sort stem cells in cancer initiation and progression
topic Reviews
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7039188/
https://www.ncbi.nlm.nih.gov/pubmed/31874116
http://dx.doi.org/10.1083/jcb.201911053
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