Ovarian steroids and control of proliferation in the normal human breast

The Breast ◽  
2001 ◽  
Vol 10 (4) ◽  
pp. 273-278 ◽  
Author(s):  
E. Anderson
Keyword(s):  
Human Breast ◽  
Ovarian Steroids ◽  
Normal Human Breast ◽  
Normal Human ◽  
And Control

Unique transcriptomic changes underlie hormonal interactions during mammary histomorphogenesis in female pigs

Endocrinology ◽  
2021 ◽  
Author(s):  
Josephine F Trott ◽  
Anke Schennink ◽  
Katherine C Horigan ◽  
Danielle G Lemay ◽  
Julia R Cohen ◽  
...  
Keyword(s):  
Acid Metabolism ◽  
Human Breast ◽  
Transcriptional Responses ◽  
Ovarian Steroids ◽  
Additional Gene ◽  
Normal Human Breast ◽  
Terminal Ductal Lobular Unit ◽  
Normal Human ◽  
Transcriptomic Changes ◽  
Hormonal Interactions

Abstract Successful lactation and the risk for developing breast cancer depend on growth and differentiation of the mammary gland (MG) epithelium that is regulated by ovarian steroids (17beta-estradiol [E] and progesterone [P]) and pituitary-derived prolactin (PRL). Given that the MG of pigs share histomorphogenic features present in the normal human breast, we sought to define the transcriptional responses within the MG of pigs following exposure to all combinations of these hormones. Hormone-ablated female pigs were administered combinations of E, medroxyprogesterone 17-acetate (source of P), and either haloperidol (to induce PRL) or 2-bromo-α-ergocryptine. We subsequently monitored phenotypic changes in the MG including mitosis, receptors for E and P (ESR1 and PGR), level of phosphorylated STAT5 (pSTAT5), and the frequency of terminal ductal lobular unit (TDLU) subtypes; these changes were then associated with all transcriptomic changes. Estrogen altered the expression of ~20% of all genes that mostly associated with mitosis, whereas PRL stimulated elements of fatty acid metabolism and an inflammatory response. Several outcomes, including increased pSTAT5, highlighted the ability of E to enhance PRL action. Regression of transcriptomic changes against several MG phenotypes revealed 1,669 genes correlated with proliferation, among which 29 were E-inducible. Additional gene expression signatures were associated with TDLU formation and the frequency of ESR1 or PGR. These data provide a link between the hormone-regulated genome and phenome of the MG in a species having a complex histoarchitecture like that in the human breast, and highlight an underexplored synergy between the actions of E and PRL during MG development.

Effects of oestrogen on gene expression in epithelium and stroma of normal human breast tissue

2006 ◽  
Vol 13 (2) ◽  
pp. 617-628 ◽  
Author(s):  
C L Wilson ◽  
A H Sims ◽  
A Howell ◽  
C J Miller ◽  
R B Clarke
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Cell Proliferation ◽  
Breast Tissue ◽  
Epithelial Cell Proliferation ◽  
Human Breast ◽  
Human Breast Tissue ◽  
Tissue Microenvironment ◽  
Normal Human Breast ◽  
Normal Human

Oestrogen (E) is essential for normal and cancer development in the breast, while anti-oestrogens have been shown to reduce the risk of the disease. However, little is known about the effect of E on gene expression in the normal human breast, particularly when the epithelium and stroma are intact. Previous expression profiles of the response to E have been performed on tumour cell lines, in the absence of stroma. We investigated gene expression in normal human breast tissue transplanted into 9–10-week-old female athymic nude (Balb/c nu/nu) mice. After 2 weeks, when epithelial proliferation is minimal, one-third of the mice were treated with 17β-oestradiol (E2) to give human luteal-phase levels in the mouse, which we have previously shown to induce maximal epithelial cell proliferation. RNA was isolated from treated and untreated mice, labelled and hybridized to Affymetrix HG-U133A (human) GeneChips. Gene expression levels were generated using BioConductor implementations of the RMA and MAS5 algorithms. E2 treatment was found to represent the largest source of variation in gene expression and cross-species hybridization of mouse RNA from xenograft samples was demonstrated to be negligible. Known E2-responsive genes (such as TFF1 and AREG), and genes thought to be involved in breast cancer metastasis (including mammoglobin, KRT19 and AGR2), were upregulated in response to E treatment. Genes known to be co-expressed with E receptor α in breast cancer cell lines and tumours were both upregulated (XBP-1 and GREB1) and downregulated (RARRES1 and GATA3). In addition, genes that are normally expressed in the myoepithelium and extracellular matrix that maintain the tissue microenvironment were also differentially expressed. This suggests that the response to oestrogen in normal breast is highly dependent upon epithelial–stromal/myoepithelial interactions which maintain the tissue microenvironment during epithelial cell proliferation.

The Influence of Steroid Hormones and Antihormones on the Growth and Differentiation of Normal Human Breast Cells in Culture

1992 ◽  
pp. 145-156 ◽  
Author(s):  
Frederique Kuttenn ◽  
Anne Gompel ◽  
Catherine Malet ◽  
Etienne Leygue ◽  
Nicole Baudot ◽  
...  
Keyword(s):  
Steroid Hormones ◽  
Human Breast ◽  
Cells In Culture ◽  
Normal Human Breast ◽  
Breast Cells ◽  
Normal Human

Menstrual cycle-dependent variations of breast cyst fluid proteins and sex steroid receptors in the normal human breast

Cancer ◽  
1983 ◽  
Vol 51 (7) ◽  
pp. 1297-1302 ◽  
Author(s):  
John S. Silva ◽  
Gregory S. Georgiade ◽  
William G. Dilley ◽  
Kenneth S. McCarty ◽  
Samuel A. Wells ◽  
...  
Keyword(s):  
Menstrual Cycle ◽  
Steroid Receptors ◽  
Cyst Fluid ◽  
Sex Steroid ◽  
Human Breast ◽  
Breast Cyst Fluid ◽  
Breast Cyst ◽  
Normal Human Breast ◽  
Normal Human ◽  
Cycle Dependent

Clonal analysis of expression of epithelial antigens in cultures of normal human breast

1986 ◽  
Vol 80 (1) ◽  
pp. 91-101
Author(s):  
P.A. Edwards ◽  
I.M. Brooks ◽  
H.J. Bunnage ◽  
A.V. Foster ◽  
M.L. Ellison ◽  
...  
Keyword(s):  
Monoclonal Antibodies ◽  
Epithelial Cells ◽  
Phase Contrast ◽  
Single Cells ◽  
Full Range ◽  
Human Breast ◽  
Intact Tissue ◽  
Normal Human Breast ◽  
Normal Human ◽  
Luminal Epithelial Cells

Cells from normal human breast epithelium were cloned in monolayer culture and the clones were stained with monoclonal antibodies. Tissue was from reduction mammoplasty operations. Cloning efficiencies were 5–30%. Two types of clone were identified: 10 to 30% were of relatively spread cells whose boundaries were often difficult to see by phase-contrast microscopy but where they were visible they appeared as dark lines. The edges of the clones usually appeared to be under tension. These clones were stained by two monoclonal antibodies, LICR-LON-M8 and M24, that stain luminal epithelial cells in the intact tissue, but not myoepithelial or stromal cells. Within a clone the cells showed a full range of antigenic phenotypes. This was confirmed for clones grown from single cells that had been isolated manually. The second type of clone was more compact with little evidence of tension at the edges, and cell boundaries were clearly visible and bright under phase contrast. These clones were not stained by antibodies M8 or M24. Both types of clone stained with a third monoclonal antibody that is specific for luminal epithelial cells in the intact tissue, LICR-LON-M18, but the distribution of staining was different in the different types of clone. The simplest interpretation of the two types of clone is that luminal epithelial cells give rise to the spread type of clone while the myoepithelial cells give rise to the more abundant and vigorous compact clones. Alternatively, the compact clones may be from luminal epithelial cells that have lost differentiated characteristics.

Ultrasonic doppler study of the hormonal response of blood flow in the normal human breast

1987 ◽  
Vol 13 (3) ◽  
pp. 121-129 ◽  
Author(s):  
M. Sambrook ◽  
J.C. Bamber ◽  
H. Minasian ◽  
C.R. Hill
Keyword(s):  
Blood Flow ◽  
Human Breast ◽  
Hormonal Response ◽  
Doppler Study ◽  
Normal Human Breast ◽  
Normal Human
Sign in / Sign up

Export Citation Format

Share Document