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Resistance to endocrine therapy in breast cancer: molecular mechanisms and future goals
Introduction The majority of breast cancers (BCs) are characterized by the expression of estrogen receptor alpha (ERα+). ERα acts as ligand-dependent transcription factor for genes associated with cell survival, proliferation, and tumor growth. Thus, blocking the estrogen agonist effect on ERα is th...
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| Published in: | Breast cancer research and treatment 2019-02, Vol.173 (3), p.489-497 |
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| container_end_page | 497 |
| container_issue | 3 |
| container_start_page | 489 |
| container_title | Breast cancer research and treatment |
| container_volume | 173 |
| creator | Szostakowska, Małgorzata Trębińska-Stryjewska, Alicja Grzybowska, Ewa Anna Fabisiewicz, Anna |
| description | Introduction
The majority of breast cancers (BCs) are characterized by the expression of estrogen receptor alpha (ERα+). ERα acts as ligand-dependent transcription factor for genes associated with cell survival, proliferation, and tumor growth. Thus, blocking the estrogen agonist effect on ERα is the main strategy in the treatment of ERα+ BCs. However, despite the development of targeted anti-estrogen therapies for ER+ BC, around 30–50% of early breast cancer patients will relapse. Acquired resistance to endocrine therapy is a great challenge in ER+ BC patient treatment.
Discussion
Anti-estrogen resistance is a consequence of molecular changes, which allow for tumor growth irrespective of estrogen presence. Those changes may be associated with ERα modifications either at the genetic, regulatory or protein level. Additionally, the activation of alternate growth pathways and/or cell survival mechanisms can lead to estrogen-independence and endocrine resistance.
Conclusion
This comprehensive review summarizes molecular mechanisms associated with resistance to anti-estrogen therapy, focusing on genetic alterations, stress responses, cell survival mechanisms, and cell reprogramming. |
| doi_str_mv | 10.1007/s10549-018-5023-4 |
| format | article |
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The majority of breast cancers (BCs) are characterized by the expression of estrogen receptor alpha (ERα+). ERα acts as ligand-dependent transcription factor for genes associated with cell survival, proliferation, and tumor growth. Thus, blocking the estrogen agonist effect on ERα is the main strategy in the treatment of ERα+ BCs. However, despite the development of targeted anti-estrogen therapies for ER+ BC, around 30–50% of early breast cancer patients will relapse. Acquired resistance to endocrine therapy is a great challenge in ER+ BC patient treatment.
Discussion
Anti-estrogen resistance is a consequence of molecular changes, which allow for tumor growth irrespective of estrogen presence. Those changes may be associated with ERα modifications either at the genetic, regulatory or protein level. Additionally, the activation of alternate growth pathways and/or cell survival mechanisms can lead to estrogen-independence and endocrine resistance.
Conclusion
This comprehensive review summarizes molecular mechanisms associated with resistance to anti-estrogen therapy, focusing on genetic alterations, stress responses, cell survival mechanisms, and cell reprogramming.</description><identifier>ISSN: 0167-6806</identifier><identifier>EISSN: 1573-7217</identifier><identifier>DOI: 10.1007/s10549-018-5023-4</identifier><identifier>PMID: 30382472</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Antiestrogens ; Antineoplastic Agents, Hormonal - administration & dosage ; Antineoplastic Agents, Hormonal - adverse effects ; Antineoplastic Agents, Hormonal - therapeutic use ; Autophagy - drug effects ; Biomarkers, Tumor ; Breast cancer ; Breast Neoplasms - drug therapy ; Breast Neoplasms - etiology ; Breast Neoplasms - metabolism ; Breast Neoplasms - pathology ; Cancer patients ; Cancer research ; Cancer treatment ; Care and treatment ; Cell survival ; Drug Resistance, Neoplasm ; Endocrine therapy ; Estrogen receptors ; Estrogens ; Female ; Genes ; Genetic aspects ; Health aspects ; Humans ; Medicine ; Medicine & Public Health ; Molecular modelling ; Neoplastic Stem Cells - drug effects ; Neoplastic Stem Cells - metabolism ; Oncology ; Patients ; Phenols (Class of compounds) ; Receptors, Estrogen - antagonists & inhibitors ; Receptors, Estrogen - genetics ; Receptors, Estrogen - metabolism ; Recurrence (Disease) ; Review ; Transcription (Genetics) ; Tumors ; Unfolded Protein Response - drug effects</subject><ispartof>Breast cancer research and treatment, 2019-02, Vol.173 (3), p.489-497</ispartof><rights>The Author(s) 2018</rights><rights>COPYRIGHT 2019 Springer</rights><rights>Breast Cancer Research and Treatment is a copyright of Springer, (2018). All Rights Reserved. © 2018. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c568t-247b2153cec5cd5cf2c662663b5b7410bdfcc5f363fedf03910b26168cc4e7563</citedby><cites>FETCH-LOGICAL-c568t-247b2153cec5cd5cf2c662663b5b7410bdfcc5f363fedf03910b26168cc4e7563</cites><orcidid>0000-0002-9334-1773</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27900,27901</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30382472$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Szostakowska, Małgorzata</creatorcontrib><creatorcontrib>Trębińska-Stryjewska, Alicja</creatorcontrib><creatorcontrib>Grzybowska, Ewa Anna</creatorcontrib><creatorcontrib>Fabisiewicz, Anna</creatorcontrib><title>Resistance to endocrine therapy in breast cancer: molecular mechanisms and future goals</title><title>Breast cancer research and treatment</title><addtitle>Breast Cancer Res Treat</addtitle><addtitle>Breast Cancer Res Treat</addtitle><description>Introduction
The majority of breast cancers (BCs) are characterized by the expression of estrogen receptor alpha (ERα+). ERα acts as ligand-dependent transcription factor for genes associated with cell survival, proliferation, and tumor growth. Thus, blocking the estrogen agonist effect on ERα is the main strategy in the treatment of ERα+ BCs. However, despite the development of targeted anti-estrogen therapies for ER+ BC, around 30–50% of early breast cancer patients will relapse. Acquired resistance to endocrine therapy is a great challenge in ER+ BC patient treatment.
Discussion
Anti-estrogen resistance is a consequence of molecular changes, which allow for tumor growth irrespective of estrogen presence. Those changes may be associated with ERα modifications either at the genetic, regulatory or protein level. Additionally, the activation of alternate growth pathways and/or cell survival mechanisms can lead to estrogen-independence and endocrine resistance.
Conclusion
This comprehensive review summarizes molecular mechanisms associated with resistance to anti-estrogen therapy, focusing on genetic alterations, stress responses, cell survival mechanisms, and cell reprogramming.</description><subject>Antiestrogens</subject><subject>Antineoplastic Agents, Hormonal - administration & dosage</subject><subject>Antineoplastic Agents, Hormonal - adverse effects</subject><subject>Antineoplastic Agents, Hormonal - therapeutic use</subject><subject>Autophagy - drug effects</subject><subject>Biomarkers, Tumor</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - drug therapy</subject><subject>Breast Neoplasms - etiology</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>Cancer patients</subject><subject>Cancer research</subject><subject>Cancer treatment</subject><subject>Care and treatment</subject><subject>Cell survival</subject><subject>Drug Resistance, Neoplasm</subject><subject>Endocrine therapy</subject><subject>Estrogen receptors</subject><subject>Estrogens</subject><subject>Female</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Molecular modelling</subject><subject>Neoplastic Stem Cells - drug effects</subject><subject>Neoplastic Stem Cells - metabolism</subject><subject>Oncology</subject><subject>Patients</subject><subject>Phenols (Class of compounds)</subject><subject>Receptors, Estrogen - antagonists & inhibitors</subject><subject>Receptors, Estrogen - genetics</subject><subject>Receptors, Estrogen - metabolism</subject><subject>Recurrence (Disease)</subject><subject>Review</subject><subject>Transcription (Genetics)</subject><subject>Tumors</subject><subject>Unfolded Protein Response - drug effects</subject><issn>0167-6806</issn><issn>1573-7217</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><recordid>eNp1kl1rFTEQhoMo9nj0B3gjAUG82ZqPTbLrRaEUv6AgiOJlyGYnZ1N2k2OyK_Tfm_XUtkc0uRgy88xkZngRek7JKSVEvcmUiLqtCG0qQRiv6gdoQ4XilWJUPUQbQqWqZEPkCXqS8xUhpFWkfYxOOOENqxXboO9fIPs8m2ABzxFD6KNNPpTHAMnsr7EPuEtg8oztCqW3eIoj2GU0CU9gBxN8njI2ocdumZcEeBfNmJ-iR64YeHZjt-jb-3dfLz5Wl58_fLo4v6yskM1clSY6RgW3YIXthXXMSsmk5J3oVE1J1ztrheOSO-gd4W1xMUllY20NSki-RWeHuvulm6C3EOZkRr1PfjLpWkfj9XEk-EHv4k8teVvLsrQten1TIMUfC-RZTz5bGEcTIC5ZM8pUK8pZ0Zd_oVdxSaGM95sSLa1pfUftzAjaBxfLv3Ytqs-FkpTUtOWFOv0HVW4Pk7cxgPPFf5Tw6l7CAGachxzHZfYx5GOQHkCbYs4J3O0yKNGrbPRBNrrIRq-y0WvPL-5v8Tbjj04KwA5ALqGwg3Q3-v-r_gK9asvo</recordid><startdate>20190201</startdate><enddate>20190201</enddate><creator>Szostakowska, Małgorzata</creator><creator>Trębińska-Stryjewska, Alicja</creator><creator>Grzybowska, Ewa Anna</creator><creator>Fabisiewicz, Anna</creator><general>Springer US</general><general>Springer</general><general>Springer Nature B.V</general><scope>C6C</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>K9-</scope><scope>K9.</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-9334-1773</orcidid></search><sort><creationdate>20190201</creationdate><title>Resistance to endocrine therapy in breast cancer: molecular mechanisms and future goals</title><author>Szostakowska, Małgorzata ; Trębińska-Stryjewska, Alicja ; Grzybowska, Ewa Anna ; Fabisiewicz, Anna</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c568t-247b2153cec5cd5cf2c662663b5b7410bdfcc5f363fedf03910b26168cc4e7563</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Antiestrogens</topic><topic>Antineoplastic Agents, Hormonal - administration & dosage</topic><topic>Antineoplastic Agents, Hormonal - adverse effects</topic><topic>Antineoplastic Agents, Hormonal - therapeutic use</topic><topic>Autophagy - drug effects</topic><topic>Biomarkers, Tumor</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - drug therapy</topic><topic>Breast Neoplasms - etiology</topic><topic>Breast Neoplasms - metabolism</topic><topic>Breast Neoplasms - pathology</topic><topic>Cancer patients</topic><topic>Cancer research</topic><topic>Cancer treatment</topic><topic>Care and treatment</topic><topic>Cell survival</topic><topic>Drug Resistance, Neoplasm</topic><topic>Endocrine therapy</topic><topic>Estrogen receptors</topic><topic>Estrogens</topic><topic>Female</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Molecular modelling</topic><topic>Neoplastic Stem Cells - drug effects</topic><topic>Neoplastic Stem Cells - metabolism</topic><topic>Oncology</topic><topic>Patients</topic><topic>Phenols (Class of compounds)</topic><topic>Receptors, Estrogen - antagonists & inhibitors</topic><topic>Receptors, Estrogen - genetics</topic><topic>Receptors, Estrogen - metabolism</topic><topic>Recurrence (Disease)</topic><topic>Review</topic><topic>Transcription (Genetics)</topic><topic>Tumors</topic><topic>Unfolded Protein Response - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Szostakowska, Małgorzata</creatorcontrib><creatorcontrib>Trębińska-Stryjewska, Alicja</creatorcontrib><creatorcontrib>Grzybowska, Ewa Anna</creatorcontrib><creatorcontrib>Fabisiewicz, Anna</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Consumer Health Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>ProQuest Central (New)</collection><collection>ProQuest One Academic (New)</collection><collection>ProQuest Health & Medical Research Collection</collection><collection>ProQuest One Academic Middle East (New)</collection><collection>ProQuest One Health & Nursing</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Breast cancer research and treatment</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Szostakowska, Małgorzata</au><au>Trębińska-Stryjewska, Alicja</au><au>Grzybowska, Ewa Anna</au><au>Fabisiewicz, Anna</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Resistance to endocrine therapy in breast cancer: molecular mechanisms and future goals</atitle><jtitle>Breast cancer research and treatment</jtitle><stitle>Breast Cancer Res Treat</stitle><addtitle>Breast Cancer Res Treat</addtitle><date>2019-02-01</date><risdate>2019</risdate><volume>173</volume><issue>3</issue><spage>489</spage><epage>497</epage><pages>489-497</pages><issn>0167-6806</issn><eissn>1573-7217</eissn><abstract>Introduction
The majority of breast cancers (BCs) are characterized by the expression of estrogen receptor alpha (ERα+). ERα acts as ligand-dependent transcription factor for genes associated with cell survival, proliferation, and tumor growth. Thus, blocking the estrogen agonist effect on ERα is the main strategy in the treatment of ERα+ BCs. However, despite the development of targeted anti-estrogen therapies for ER+ BC, around 30–50% of early breast cancer patients will relapse. Acquired resistance to endocrine therapy is a great challenge in ER+ BC patient treatment.
Discussion
Anti-estrogen resistance is a consequence of molecular changes, which allow for tumor growth irrespective of estrogen presence. Those changes may be associated with ERα modifications either at the genetic, regulatory or protein level. Additionally, the activation of alternate growth pathways and/or cell survival mechanisms can lead to estrogen-independence and endocrine resistance.
Conclusion
This comprehensive review summarizes molecular mechanisms associated with resistance to anti-estrogen therapy, focusing on genetic alterations, stress responses, cell survival mechanisms, and cell reprogramming.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>30382472</pmid><doi>10.1007/s10549-018-5023-4</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0002-9334-1773</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Antiestrogens Antineoplastic Agents, Hormonal - administration & dosage Antineoplastic Agents, Hormonal - adverse effects Antineoplastic Agents, Hormonal - therapeutic use Autophagy - drug effects Biomarkers, Tumor Breast cancer Breast Neoplasms - drug therapy Breast Neoplasms - etiology Breast Neoplasms - metabolism Breast Neoplasms - pathology Cancer patients Cancer research Cancer treatment Care and treatment Cell survival Drug Resistance, Neoplasm Endocrine therapy Estrogen receptors Estrogens Female Genes Genetic aspects Health aspects Humans Medicine Medicine & Public Health Molecular modelling Neoplastic Stem Cells - drug effects Neoplastic Stem Cells - metabolism Oncology Patients Phenols (Class of compounds) Receptors, Estrogen - antagonists & inhibitors Receptors, Estrogen - genetics Receptors, Estrogen - metabolism Recurrence (Disease) Review Transcription (Genetics) Tumors Unfolded Protein Response - drug effects |
| title | Resistance to endocrine therapy in breast cancer: molecular mechanisms and future goals |
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