Co-expression of steroid receptors (estrogen receptor alpha and/or progesterone receptors) and Her-2/neu: Clinical implications

2006 ◽  
Vol 102 (1-5) ◽  
pp. 32-40 ◽  
Author(s):  
Daniel R. Ciocca ◽  
Francisco E. Gago ◽  
Mariel A. Fanelli ◽  
Stuart K. Calderwood
Keyword(s):  
Estrogen Receptor ◽  
Estrogen Receptor Alpha ◽  
Steroid Receptors ◽  
Progesterone Receptors ◽  
Clinical Implications ◽  
Receptor Alpha ◽  
Her 2

scholarly journals Association of genetic polymorphisms of estrogen and progesterone receptors and endometriosis: Meta-analysis

2019 ◽  
Vol 11 (1) ◽  
pp. 25-36
Author(s):  
Priscila Prais Carneiro ◽  
Bruna Vicente de Oliveira ◽  
Antonio Marcio Teodoro Cordeiro Silva
Keyword(s):  
Estrogen Receptor ◽  
Progesterone Receptor ◽  
Estrogen Receptor Alpha ◽  
Meta Analysis ◽  
Estrogen Receptor Beta ◽  
Progesterone Receptors ◽  
Estrogen And Progesterone Receptors ◽  
Receptor Alpha ◽  
Pubmed Database ◽  
Receptor Beta

Purpose: To investigate the association between polymorphisms in the genes of estrogen receptor alpha, estrogen receptor beta, and progesterone receptor and the genesis of endometriosis. Methods: Systematic review and meta-analysis of articles published fully in the PubMed database, in Portuguese, English, or Spanish, from 2006 to 2017, using the descriptors: “endometriosis,” “polymorphism,” “ESR1,” “ESR2,” “PROGINS,” “rs9340799,” “rs4986938,” and “rs1042838.” Results: A total of 20 studies were included based on the criterion of search for susceptibility to endometriosis related to polymorphisms of estrogen receptor alpha, estrogen receptor beta, and progesterone receptor genes. Analysis of all polymorphisms found no association with endometriosis. Conclusion: This meta-analysis showed that estrogen receptor alpha, estrogen receptor beta, and progesterone receptor polymorphisms are not related to susceptibility to endometriosis. However, such results may be able to provide more detailed interpretations of how they influence the pathogenesis of endometriosis.

scholarly journals Spontaneous Basaloid Adenomas of the Mammary Gland in Four Dogs: Clinicopathologic and Immunohistochemical Features

2002 ◽  
Vol 39 (6) ◽  
pp. 739-743 ◽  
Author(s):  
J. Martín de las Mulas ◽  
J. Ordás ◽  
M. Y. Millán ◽  
A. Espinosa de los Monteros ◽  
C. Reymundo
Keyword(s):  
Estrogen Receptor ◽  
Mammary Gland ◽  
Epithelial Cells ◽  
Tumor Cells ◽  
Basal Cell ◽  
Estrogen Receptor Alpha ◽  
Progesterone Receptors ◽  
Receptor Alpha ◽  
Contraceptive Steroids

Spontaneous basaloid adenomas occurred in four out of 354 dogs with mammary tumors. Affected dogs were pure-bred, intact females between 6 and 8 years of age. Three dogs were nuliparous, two had pseudopregnancies, and none had received contraceptive steroids. The tumors were multiple (three cases) or unique, less than 1 cm in diameter, well delineated, and composed of uniform cords and clusters of monomorphic epithelial cells with focal signs of squamous or glandular differentiation. A basal cell immunophenotype (cytokeratins 5 and 14 positive) without either glandular epithelial (cytokeratins 8, 18, and 19 negative) or myoepithelial (calponin negative) differentiation was observed in the majority of tumor cells. No recurrence or metastasis was recorded after follow-up periods between 3 and 24 months. In spite of the hormone-dependent nature of this tumor in female Beagles given experimental contraceptive steroids, spontaneous basaloid adenomas lacked estrogen receptor alpha and progesterone receptors.

Progesterone receptors A and B and estrogen receptor alpha expression in normal breast tissue and fibroadenomas

Endocrine ◽  
2009 ◽  
Vol 35 (3) ◽  
pp. 459-466 ◽  
Author(s):  
Gisele Branchini ◽  
Lolita Schneider ◽  
Rodrigo Cericatto ◽  
Edison Capp ◽  
Ilma Simoni Brum
Keyword(s):  
Estrogen Receptor ◽  
Estrogen Receptor Alpha ◽  
Breast Tissue ◽  
Normal Breast Tissue ◽  
Progesterone Receptors ◽  
Normal Breast ◽  
Receptor Alpha

scholarly journals Estrogen Receptor Alpha Mediates Progestin-Induced Mammary Tumor Growth by Interacting with Progesterone Receptors at the Cyclin D1/MYC Promoters

2012 ◽  
Vol 72 (9) ◽  
pp. 2416-2427 ◽  
Author(s):  
Sebastián Giulianelli ◽  
José P. Vaqué ◽  
Rocío Soldati ◽  
Victoria Wargon ◽  
Silvia I. Vanzulli ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Tumor Growth ◽  
Cyclin D1 ◽  
Mammary Tumor ◽  
Estrogen Receptor Alpha ◽  
Progesterone Receptors ◽  
Receptor Alpha ◽  
Mammary Tumor Growth

scholarly journals Forkhead Box Transcription Factor FOXO3a Regulates Estrogen Receptor Alpha Expression and Is Repressed by the Her-2/neu/Phosphatidylinositol 3-Kinase/Akt Signaling Pathway

2004 ◽  
Vol 24 (19) ◽  
pp. 8681-8690 ◽  
Author(s):  
Shangqin Guo ◽  
Gail E. Sonenshein
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Estrogen Receptor Alpha ◽  
Breast Cancer Cell Lines ◽  
Phosphatidylinositol 3 Kinase ◽  
Receptor Alpha ◽  
Forkhead Box ◽  
Green Tea Polyphenol ◽  
Her 2 ◽  
Phosphatidylinositol 3

ABSTRACT The expression status of the estrogen receptor alpha (ERα) and that of the epidermal growth factor receptor Her-2/neu frequently correlate inversely in breast cancers. While ERα-dependent cancers respond to antiestrogen therapy, Her-2/neu-overexpressing cancers typically display resistance to antiestrogens and poor prognosis. In this report we have explored the mechanism linking the loss of expression of ERα in breast cancer cells with overexpression of Her-2/neu, which signals constitutively via a phosphatidylinositol 3-kinase (PI3K)/Akt kinase pathway. We identify for the first time the Forkhead box protein FOXO3a (formerly termed FKHRL-1), which is inactivated by Akt, as a key regulator of ERα gene transcription. In breast cancer cell lines, expression of ERα was correlated with active FOXO3a levels. Ectopic FOXO3a expression induced ERα protein levels and promoter activity, while a dominant negative FOXO3a decreased ERα levels. By using transient transfection, mobility shift assays, and site-directed mutagenesis, two major functional Forkhead binding sites were identified in the human ERα promoter B. A chromatin immunoprecipitation assay confirmed FOXO3a binding at these two sites. Ectopic FOXO3a induced estrogen response element-driven reporter activity and expression of ERα target genes. The constitutively activated myristylated Akt reduced ERα expression, whereas agents that negatively affect the PI3K/Akt pathway, i.e., wortmannin, celecoxib, and the green tea polyphenol epigallocatechin-3 gallate, induced ERα. Thus, FOXO3a represents an important intracellular mediator of ERα expression, suggesting possible therapeutic intervention strategies for Her-2/neu-overexpressing refractory breast tumors.

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