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Post-menopausal breast cancer: from estrogen to androgen receptor

In the United States, breast cancer is the second leading cause of death among women, and even though different therapies can treat primary breast tumors, most breast cancer-related deaths (>95%) occur due to metastasis. A majority (~70%) of breast tumors are found to express estrogen receptor, a...

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Autores principales: Majumder, Avisek, Singh, Mahavir, Tyagi, Suresh C.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5731994/
https://www.ncbi.nlm.nih.gov/pubmed/29254284
http://dx.doi.org/10.18632/oncotarget.22156
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author Majumder, Avisek
Singh, Mahavir
Tyagi, Suresh C.
author_facet Majumder, Avisek
Singh, Mahavir
Tyagi, Suresh C.
author_sort Majumder, Avisek
collection PubMed
description In the United States, breast cancer is the second leading cause of death among women, and even though different therapies can treat primary breast tumors, most breast cancer-related deaths (>95%) occur due to metastasis. A majority (~70%) of breast tumors are found to express estrogen receptor, and a significant portion (~90%) of ER-positive (ER(+)) breast tumors are also androgen receptor-positive (AR(+)). Although ER is known to promote tumorigenesis, the role and underlying mechanism(s) of AR in these closely knit processes remain controversial. Endocrine therapies are the most commonly used treatment for patients with ER(+) breast tumors; but, ~30%-50% of initially responsive patients develop resistance to these therapies. Whereas 70%–90% of all breast tumors are AR(+) and AR overexpression is correlated with endocrine resistance, but the precise molecular mechanism(s) for this association is yet to be studied. Multiple mechanisms have been proposed to show AR and ER interactions, which indicate that AR may preferentially regulate expression of a subset of ER-responsive genes and that may be responsible for breast cancer and its progression in affected patients. On the other hand, most of the ER(+) breast tumors found in post-menopausal women (~80%); and they have very low 17β-estradiol and high androgen levels, but how these hormonal changes make someone more prone to cancer phenotype has long been a disputed issue. In this study, we have discussed multiple molecular mechanisms that we believe are central to the understanding of the overall contributions of AR in breast cancer and its metastasis in post-menopausal women.
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spelling pubmed-57319942017-12-17 Post-menopausal breast cancer: from estrogen to androgen receptor Majumder, Avisek Singh, Mahavir Tyagi, Suresh C. Oncotarget Review In the United States, breast cancer is the second leading cause of death among women, and even though different therapies can treat primary breast tumors, most breast cancer-related deaths (>95%) occur due to metastasis. A majority (~70%) of breast tumors are found to express estrogen receptor, and a significant portion (~90%) of ER-positive (ER(+)) breast tumors are also androgen receptor-positive (AR(+)). Although ER is known to promote tumorigenesis, the role and underlying mechanism(s) of AR in these closely knit processes remain controversial. Endocrine therapies are the most commonly used treatment for patients with ER(+) breast tumors; but, ~30%-50% of initially responsive patients develop resistance to these therapies. Whereas 70%–90% of all breast tumors are AR(+) and AR overexpression is correlated with endocrine resistance, but the precise molecular mechanism(s) for this association is yet to be studied. Multiple mechanisms have been proposed to show AR and ER interactions, which indicate that AR may preferentially regulate expression of a subset of ER-responsive genes and that may be responsible for breast cancer and its progression in affected patients. On the other hand, most of the ER(+) breast tumors found in post-menopausal women (~80%); and they have very low 17β-estradiol and high androgen levels, but how these hormonal changes make someone more prone to cancer phenotype has long been a disputed issue. In this study, we have discussed multiple molecular mechanisms that we believe are central to the understanding of the overall contributions of AR in breast cancer and its metastasis in post-menopausal women. Impact Journals LLC 2017-10-27 /pmc/articles/PMC5731994/ /pubmed/29254284 http://dx.doi.org/10.18632/oncotarget.22156 Text en Copyright: © 2017 Majumder et al. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (http://creativecommons.org/licenses/by/3.0/) (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Review
Majumder, Avisek
Singh, Mahavir
Tyagi, Suresh C.
Post-menopausal breast cancer: from estrogen to androgen receptor
title Post-menopausal breast cancer: from estrogen to androgen receptor
title_full Post-menopausal breast cancer: from estrogen to androgen receptor
title_fullStr Post-menopausal breast cancer: from estrogen to androgen receptor
title_full_unstemmed Post-menopausal breast cancer: from estrogen to androgen receptor
title_short Post-menopausal breast cancer: from estrogen to androgen receptor
title_sort post-menopausal breast cancer: from estrogen to androgen receptor
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5731994/
https://www.ncbi.nlm.nih.gov/pubmed/29254284
http://dx.doi.org/10.18632/oncotarget.22156
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