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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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Formato: | Online Artículo Texto |
Lenguaje: | English |
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BioMed Central
2011
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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 |
collection | PubMed |
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. |
format | Online Article Text |
id | pubmed-3236326 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
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 |
work_keys_str_mv | AT clarkerobert cannibalismcellsurvivalandendocrineresistanceinbreastcancer |