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Molecular Mechanisms of Mouse Skin Tumor Promotion

Multiple molecular mechanisms are involved in the promotion of skin carcinogenesis. Induction of sustained proliferation and epidermal hyperplasia by direct activation of mitotic signaling pathways or indirectly in response to chronic wounding and/or inflammation, or due to a block in terminal diffe...

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Detalles Bibliográficos
Autores principales: Rundhaug, Joyce E., Fischer, Susan M.
Formato: Texto
Lenguaje:English
Publicado: Molecular Diversity Preservation International (MDPI) 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3033564/
https://www.ncbi.nlm.nih.gov/pubmed/21297902
http://dx.doi.org/10.3390/cancers2020436
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author Rundhaug, Joyce E.
Fischer, Susan M.
author_facet Rundhaug, Joyce E.
Fischer, Susan M.
author_sort Rundhaug, Joyce E.
collection PubMed
description Multiple molecular mechanisms are involved in the promotion of skin carcinogenesis. Induction of sustained proliferation and epidermal hyperplasia by direct activation of mitotic signaling pathways or indirectly in response to chronic wounding and/or inflammation, or due to a block in terminal differentiation or resistance to apoptosis is necessary to allow clonal expansion of initiated cells with DNA mutations to form skin tumors. The mitotic pathways include activation of epidermal growth factor receptor and Ras/Raf/mitogen-activated protein kinase signaling. Chronic inflammation results in inflammatory cell secretion of growth factors and cytokines such as tumor necrosis factor-α and interleukins, as well as production of reactive oxygen species, all of which can stimulate proliferation. Persistent activation of these pathways leads to tumor promotion.
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spelling pubmed-30335642011-02-04 Molecular Mechanisms of Mouse Skin Tumor Promotion Rundhaug, Joyce E. Fischer, Susan M. Cancers (Basel) Review Multiple molecular mechanisms are involved in the promotion of skin carcinogenesis. Induction of sustained proliferation and epidermal hyperplasia by direct activation of mitotic signaling pathways or indirectly in response to chronic wounding and/or inflammation, or due to a block in terminal differentiation or resistance to apoptosis is necessary to allow clonal expansion of initiated cells with DNA mutations to form skin tumors. The mitotic pathways include activation of epidermal growth factor receptor and Ras/Raf/mitogen-activated protein kinase signaling. Chronic inflammation results in inflammatory cell secretion of growth factors and cytokines such as tumor necrosis factor-α and interleukins, as well as production of reactive oxygen species, all of which can stimulate proliferation. Persistent activation of these pathways leads to tumor promotion. Molecular Diversity Preservation International (MDPI) 2010-04-13 /pmc/articles/PMC3033564/ /pubmed/21297902 http://dx.doi.org/10.3390/cancers2020436 Text en © 2010 by the authors; licensee Molecular Diversity Preservation International, Basel, Switzerland. http://creativecommons.org/licenses/by/3.0/ This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/).
spellingShingle Review
Rundhaug, Joyce E.
Fischer, Susan M.
Molecular Mechanisms of Mouse Skin Tumor Promotion
title Molecular Mechanisms of Mouse Skin Tumor Promotion
title_full Molecular Mechanisms of Mouse Skin Tumor Promotion
title_fullStr Molecular Mechanisms of Mouse Skin Tumor Promotion
title_full_unstemmed Molecular Mechanisms of Mouse Skin Tumor Promotion
title_short Molecular Mechanisms of Mouse Skin Tumor Promotion
title_sort molecular mechanisms of mouse skin tumor promotion
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3033564/
https://www.ncbi.nlm.nih.gov/pubmed/21297902
http://dx.doi.org/10.3390/cancers2020436
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