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Does autocrine growth factor secretion form part of a mechanism which paradoxically protects against tumour development?

Autocrine growth factor secretion has classically been considered as a mechanism by which tumour cells achieve autonomous growth. However, there is now considerable evidence that autocrine circuits operate in the growth regulation of normal adult tissues. Here we consider the possible advantages to...

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Detalles Bibliográficos
Autores principales: Dawson, T., Wynford-Thomas, D.
Formato: Texto
Lenguaje:English
Publicado: Nature Publishing Group 1995
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2033821/
https://www.ncbi.nlm.nih.gov/pubmed/7779701
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author Dawson, T.
Wynford-Thomas, D.
author_facet Dawson, T.
Wynford-Thomas, D.
author_sort Dawson, T.
collection PubMed
description Autocrine growth factor secretion has classically been considered as a mechanism by which tumour cells achieve autonomous growth. However, there is now considerable evidence that autocrine circuits operate in the growth regulation of normal adult tissues. Here we consider the possible advantages to the normal epithelial cell of utilising such an external growth factor circuit and suggest that autocrine growth factor secretion, when viewed in a multicellular context, could paradoxically form part of a mechanism for preventing tumour development.
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spelling pubmed-20338212009-09-10 Does autocrine growth factor secretion form part of a mechanism which paradoxically protects against tumour development? Dawson, T. Wynford-Thomas, D. Br J Cancer Research Article Autocrine growth factor secretion has classically been considered as a mechanism by which tumour cells achieve autonomous growth. However, there is now considerable evidence that autocrine circuits operate in the growth regulation of normal adult tissues. Here we consider the possible advantages to the normal epithelial cell of utilising such an external growth factor circuit and suggest that autocrine growth factor secretion, when viewed in a multicellular context, could paradoxically form part of a mechanism for preventing tumour development. Nature Publishing Group 1995-06 /pmc/articles/PMC2033821/ /pubmed/7779701 Text en https://creativecommons.org/licenses/by/4.0/This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit https://creativecommons.org/licenses/by/4.0/.
spellingShingle Research Article
Dawson, T.
Wynford-Thomas, D.
Does autocrine growth factor secretion form part of a mechanism which paradoxically protects against tumour development?
title Does autocrine growth factor secretion form part of a mechanism which paradoxically protects against tumour development?
title_full Does autocrine growth factor secretion form part of a mechanism which paradoxically protects against tumour development?
title_fullStr Does autocrine growth factor secretion form part of a mechanism which paradoxically protects against tumour development?
title_full_unstemmed Does autocrine growth factor secretion form part of a mechanism which paradoxically protects against tumour development?
title_short Does autocrine growth factor secretion form part of a mechanism which paradoxically protects against tumour development?
title_sort does autocrine growth factor secretion form part of a mechanism which paradoxically protects against tumour development?
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2033821/
https://www.ncbi.nlm.nih.gov/pubmed/7779701
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