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Cannibalism, cell survival, and endocrine resistance in breast cancer

Breast cancer cells often respond to an endocrine therapy by altering expression of specific estrogen-responsive genes and inducing autophagy, a cannibalistic lysosomal pathway. Autophagy eliminates damaged or other organelles, allowing the recovery of the energy stored in their macromolecules to at...

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Detalles Bibliográficos
Autor principal: Clarke, Robert
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3236326/
https://www.ncbi.nlm.nih.gov/pubmed/21884644
http://dx.doi.org/10.1186/bcr2870
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author Clarke, Robert
author_facet Clarke, Robert
author_sort Clarke, Robert
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description Breast cancer cells often respond to an endocrine therapy by altering expression of specific estrogen-responsive genes and inducing autophagy, a cannibalistic lysosomal pathway. Autophagy eliminates damaged or other organelles, allowing the recovery of the energy stored in their macromolecules to attempt restoration of metabolic homeostasis. Induction of autophagy can result from activation of the unfolded protein response following metabolic stress, the final cell fate often being determined by the extent and duration of autophagy. A study by Gonzalez-Malerva and colleagues builds upon this extensive knowledge, adding HSPB8 to the list of altered genes associated with endocrine resistance in breast cancer and describing the ability of HSPB8 to regulate autophagy and confer tamoxifen resistance.
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spelling pubmed-32363262012-02-12 Cannibalism, cell survival, and endocrine resistance in breast cancer Clarke, Robert Breast Cancer Res Viewpoint Breast cancer cells often respond to an endocrine therapy by altering expression of specific estrogen-responsive genes and inducing autophagy, a cannibalistic lysosomal pathway. Autophagy eliminates damaged or other organelles, allowing the recovery of the energy stored in their macromolecules to attempt restoration of metabolic homeostasis. Induction of autophagy can result from activation of the unfolded protein response following metabolic stress, the final cell fate often being determined by the extent and duration of autophagy. A study by Gonzalez-Malerva and colleagues builds upon this extensive knowledge, adding HSPB8 to the list of altered genes associated with endocrine resistance in breast cancer and describing the ability of HSPB8 to regulate autophagy and confer tamoxifen resistance. BioMed Central 2011 2011-08-12 /pmc/articles/PMC3236326/ /pubmed/21884644 http://dx.doi.org/10.1186/bcr2870 Text en Copyright ©2011 BioMed Central Ltd
spellingShingle Viewpoint
Clarke, Robert
Cannibalism, cell survival, and endocrine resistance in breast cancer
title Cannibalism, cell survival, and endocrine resistance in breast cancer
title_full Cannibalism, cell survival, and endocrine resistance in breast cancer
title_fullStr Cannibalism, cell survival, and endocrine resistance in breast cancer
title_full_unstemmed Cannibalism, cell survival, and endocrine resistance in breast cancer
title_short Cannibalism, cell survival, and endocrine resistance in breast cancer
title_sort cannibalism, cell survival, and endocrine resistance in breast cancer
topic Viewpoint
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3236326/
https://www.ncbi.nlm.nih.gov/pubmed/21884644
http://dx.doi.org/10.1186/bcr2870
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