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<title lang=en>Modulation of estrogen receptor alpha activity and expression during breast cancer progression.</title>
<creator>Kerdivel, Gwenneg</creator>
<creator>Flouriot, Gilles</creator>
<creator>Pakdel, Farzad</creator>
<contributor>TREC : Transcription, Environment and Cancer ; Institut de recherche, santé, environnement et travail [Rennes] (Irset) ; Université d'Angers (UA) - Université des Antilles et de la Guyane (UAG) - Université de Rennes 1 (UR1) - École des Hautes Études en Santé Publique [EHESP] (EHESP) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ) - Université d'Angers (UA) - Université des Antilles et de la Guyane (UAG) - Université de Rennes 1 (UR1) - École des Hautes Études en Santé Publique [EHESP] (EHESP) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )</contributor>
<description>International audience</description>
<source>ISSN: 0083-6729</source>
<source>Vitamins and hormones</source>
<publisher>Elsevier</publisher>
<identifier>hal-00874313</identifier>
<identifier>https://hal.archives-ouvertes.fr/hal-00874313</identifier>
<source>https://hal.archives-ouvertes.fr/hal-00874313</source>
<source>Vitamins and hormones, Elsevier, 2013, 93, pp.135-60. 〈10.1016/B978-0-12-416673-8.00004-6〉</source>
<identifier>DOI : 10.1016/B978-0-12-416673-8.00004-6</identifier>
<relation>info:eu-repo/semantics/altIdentifier/doi/10.1016/B978-0-12-416673-8.00004-6</relation>
<identifier>PUBMED : 23810005</identifier>
<relation>info:eu-repo/semantics/altIdentifier/pmid/23810005</relation>
<language>en</language>
<subject lang=en>Breast cancer</subject>
<subject lang=en>Estrogen receptor</subject>
<subject lang=en>Endocrine resistance</subject>
<subject lang=en>Estrogen</subject>
<subject lang=en>Hormone dependence</subject>
<subject lang=en>Growth factor signaling</subject>
<subject lang=en>Cross talk</subject>
<subject lang=en>Hormonal therapy</subject>
<subject lang=en>Proliferation</subject>
<subject lang=en>Epigenetic</subject>
<subject>[SDV.CAN] Life Sciences [q-bio]/Cancer</subject>
<type>info:eu-repo/semantics/article</type>
<type>Journal articles</type>
<description lang=en>Seventy percent of breast tumors express the estrogen receptor (ER), which is generally considered to predict a better outcome relative to ER-negative tumors, as they often respond to antiestrogen therapies. During cancer progression, mammary tumors can escape from estrogen control, resulting in the acquisition of invasive properties and resistance to treatment. ER expression is a dynamic phenomenon and is finely regulated at numerous levels, including the gene, mRNA, and protein levels. As a consequence, many molecular mechanisms have been implicated in modulating ER activity and estrogen signaling in mammary cancer. In fact, one-third of ER-positive breast cancer cells do not respond to first-line endocrine therapies, and a large subset of relapsing tumors retain ER expression. Increased knowledge of these mechanisms has led to the development of better prognostic methods and targeted therapies for patients; however, additional research is still needed to improve patient survival. In this chapter, we focus on the signaling pathways leading to changes in or loss of ER activity in breast cancer progression.</description>
<date>2013</date>
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