Search Results
Search for other papers by Vera Cappelletti in
Google Scholar
PubMed
Search for other papers by Luigi Celio in
Google Scholar
PubMed
Search for other papers by Emilio Bajetta in
Google Scholar
PubMed
Search for other papers by Arianna Allevi in
Google Scholar
PubMed
Search for other papers by Raffaella Longarini in
Google Scholar
PubMed
Search for other papers by Patrizia Miodini in
Google Scholar
PubMed
Search for other papers by Raffaella Villa in
Google Scholar
PubMed
Search for other papers by Alessandra Fabbri in
Google Scholar
PubMed
Search for other papers by Luigi Mariani in
Google Scholar
PubMed
Search for other papers by Riccardo Giovanazzi in
Google Scholar
PubMed
Search for other papers by Emanuele Galante in
Google Scholar
PubMed
Search for other papers by Marco Greco in
Google Scholar
PubMed
Search for other papers by Maria Grazia Daidone in
Google Scholar
PubMed
Introduction Most breast tumors express the estrogen receptor (ER), herein referred to as ER-α, which is associated with the likelihood of response to endocrine therapy and is considered, along with the progesterone receptor (PgR
Search for other papers by R J Santen in
Google Scholar
PubMed
Search for other papers by R X Song in
Google Scholar
PubMed
Search for other papers by Z Zhang in
Google Scholar
PubMed
Search for other papers by R Kumar in
Google Scholar
PubMed
Search for other papers by M-H Jeng in
Google Scholar
PubMed
Search for other papers by A Masamura in
Google Scholar
PubMed
Search for other papers by J Lawrence Jr in
Google Scholar
PubMed
Search for other papers by L Berstein in
Google Scholar
PubMed
Search for other papers by W Yue in
Google Scholar
PubMed
initially postulated that enhanced receptor-mediated transcription of genes related to cell proliferation might be involved. Indeed, the levels of estrogen receptor-α (ERα) increased four- to tenfold during long-term estradiol deprivation ( Jeng et al
Search for other papers by Penn Muluhngwi in
Google Scholar
PubMed
Search for other papers by Carolyn M Klinge in
Google Scholar
PubMed
Introduction The sustained exposure to endogenous estrogens is involved in the initiation and progression of breast cancer ( Colditz 1998 ). The cellular effects of estrogens are mediated by estrogen receptors alpha and beta (ERα and ERβ) and their
Search for other papers by Emmanuelle Fleurot in
Google Scholar
PubMed
Search for other papers by Caroline Goudin in
Google Scholar
PubMed
Search for other papers by Vincent Hanoux in
Google Scholar
PubMed
Search for other papers by Pierre-Jacques Bonnamy in
Google Scholar
PubMed
Normandie Univ, UNICAEN, CEA, CNRS, ISTCT/CERVOxy Group, Caen, France
Search for other papers by Jérôme Levallet in
Google Scholar
PubMed
transcription factors ERα and ERβ (encoded by ESR1 and ESR2, respectively) mediate the biological functions of estrogens, directly through binding to estrogen response elements (ERE) of target genes or through binding to transcription factors such as AP-1, SP1
Search for other papers by M Christine Bruce in
Google Scholar
PubMed
Search for other papers by Danielle McAllister in
Google Scholar
PubMed
Search for other papers by Leigh C Murphy in
Google Scholar
PubMed
(p70S6K1) has been shown to phosphorylate ERα ( Yamnik & Holz 2010 ) and under IGF1 stimulation p70S6K1 can be co-immunoprecipitated with ERα in ER+ breast cancer cells ( Becker et al . 2011 ). PPM1D/Wip1 is known for its p53 inhibitory effects and
Search for other papers by A Bardin in
Google Scholar
PubMed
Search for other papers by N Boulle in
Google Scholar
PubMed
Search for other papers by G Lazennec in
Google Scholar
PubMed
Search for other papers by F Vignon in
Google Scholar
PubMed
Search for other papers by P Pujol in
Google Scholar
PubMed
are mediated by estrogen receptor (ER)α and ERβ, which are members of the nuclear steroid receptor superfamily. ERα and ERβ classically mediate their action by ligand-dependent binding to the estrogen-response element (ERE) of target genes, leading to
Search for other papers by Paola Galluzzo in
Google Scholar
PubMed
Search for other papers by Francesco Caiazza in
Google Scholar
PubMed
Search for other papers by Sandra Moreno in
Google Scholar
PubMed
Search for other papers by Maria Marino in
Google Scholar
PubMed
mediated by a complex signaling network rather than a single uniform mechanism. In fact, in addition to its role as gene transcription regulator ( Acevedo & Kraus 2004 ), sustained by the two estrogen receptors (ERα and ERβ ), E2 induces rapid, membrane
Division of Molecular Carcinogenesis, the Netherlands Cancer Institute, Amsterdam, the Netherlands
Search for other papers by Tesa M Severson in
Google Scholar
PubMed
Search for other papers by Wilbert Zwart in
Google Scholar
PubMed
Introduction Male breast cancer is rare, accounting for around 1% of all breast cancers ( Siegel et al. 2016 ) and is frequently positive for ERα (91–95%) and/or PR (80–81%) ( Giordano et al. 2004 , Anderson et al. 2010 , Nilsson et
Search for other papers by Marie Mc Ilroy in
Google Scholar
PubMed
Search for other papers by Fergal J Fleming in
Google Scholar
PubMed
Search for other papers by Yvonne Buggy in
Google Scholar
PubMed
Search for other papers by Arnold D K Hill in
Google Scholar
PubMed
Search for other papers by Leonie S Young in
Google Scholar
PubMed
normal breast development and in the initiation and progression of breast cancer, hence, disruption of ER function is the main therapeutic strategy employed in targeting the disease. The ER is encoded for by two genes, ER-α and ER-β. Variation between the
Search for other papers by Amanda J M O’Donnell in
Google Scholar
PubMed
Search for other papers by Kenneth G Macleod in
Google Scholar
PubMed
Search for other papers by David J Burns in
Google Scholar
PubMed
Search for other papers by John F Smyth in
Google Scholar
PubMed
Search for other papers by Simon P Langdon in
Google Scholar
PubMed
normal ovaries and in the development and progression of ovarian carcinoma, but the mechanisms of action remain unclear. The biological effects of estrogens are mediated by two forms of estrogen receptor (ER) that are encoded by separate genes, ERα and
