Igf1r is not required for AIB1-induced mammary hyperplasia and ductal branching

10.2741/e564 ◽  
2012 ◽  
Vol E4 (7) ◽  
pp. 2536-2545
Author(s):  
Jaime Font de Mora
Keyword(s):  
Mammary Hyperplasia ◽  
Ductal Branching

scholarly journals A mouse model of Proteus syndrome

2019 ◽  
Vol 28 (17) ◽  
pp. 2920-2936 ◽  
Author(s):  
Marjorie J Lindhurst ◽  
Lauren R Brinster ◽  
Hannah C Kondolf ◽  
Jasmine J Shwetar ◽  
Miranda R Yourick ◽  
...  
Keyword(s):  
Fluorescent Protein ◽  
Vascular Malformations ◽  
Mammary Epithelium ◽  
Benign Tumors ◽  
Proteus Syndrome ◽  
Mosaic Expression ◽  
Mammary Hyperplasia ◽  
Frequent Finding ◽  
Human Disorder ◽  
Green Fluorescent

Abstract Proteus syndrome is a mosaic, progressive overgrowth disorder caused by a somatic activating variant c.49G > A p.(E17K) in AKT1. The presentation in affected individuals is variable, with a diversity of tissues demonstrating abnormalities. Common manifestations include skin and bony overgrowth, vascular malformations (VMs), cysts and benign tumors. We used two methods to create mouse models that had endogenously-regulated mosaic expression of the Proteus syndrome variant. Variant allele fractions (VAFs) ranged from 0% to 50% across numerous tissues in 44 Proteus syndrome mice. Mice were phenotypically heterogeneous with lesions rarely observed before 12 months of age. VMs were the most frequent finding with a total of 69 found in 29 of 44 Proteus syndrome mice. Twenty-eight cysts and ectasia, frequently biliary, were seen in 22 of 44 Proteus syndrome mice. Varying levels of mammary hyperplasia were seen in 10 of 16 female Proteus syndrome mice with other localized regions of hyperplasia and stromal expansion noted in several additional animals. Interestingly, 27 of 31 Proteus syndrome animals had non-zero blood VAF that is in contrast to the human disorder where it is rarely seen in peripheral blood. Identification of variant-positive cells by green fluorescent protein (GFP) staining in chimeric Proteus syndrome mice showed that in some lesions, hyperplastic cells were predominantly GFP/Akt1E17K-positive and showed increased pAKT signal compared to GFP-negative cells. However, hyperplastic mammary epithelium was a mixture of GFP/Akt1E17K-positive and negative cells with some GFP/Akt1E17K-negative cells also having increased pAKT signal suggesting that the variant-positive cells can induce lesion formation in a non-cell autonomous manner.

scholarly journals A MOUSE MODEL OF MAMMARY HYPERPLASIA INDUCED BY ORAL HORMONE ADMINISTRATION

2017 ◽  
Vol 14 (4) ◽  
pp. 247-252
Author(s):  
Li Sun ◽  
Dong-Hui Guo ◽  
Fei Liu ◽  
Qian Liu ◽  
Ning Jiang ◽  
...  
Keyword(s):  
Mouse Model ◽  
Hormone Administration ◽  
Mammary Hyperplasia

Recurrent Mammary Hyperplasia: Current Concepts

2003 ◽  
Vol 111 (1) ◽  
pp. 387-393 ◽  
Author(s):  
Rod J. Rohrich ◽  
James F. Thornton ◽  
Evan S. Sorokin
Keyword(s):  
Mammary Hyperplasia

Abstract 243: Tocopherols inhibit oxidative and nitrosative stress in estrogen-induced early mammary hyperplasia in ACI rats

2014 ◽  
Author(s):  
Soumyasri Das Gupta ◽  
Jae Young So ◽  
Joseph Wahler ◽  
Mao-Jung Lee ◽  
Chung S. Yang ◽  
...  
Keyword(s):  
Nitrosative Stress ◽  
Oxidative And Nitrosative Stress ◽  
Mammary Hyperplasia

Recurrent Mammary Hyperplasia: Current Concepts

2003 ◽  
Vol 111 (1) ◽  
pp. 387-394 ◽  
Author(s):  
Rod J. Rohrich ◽  
James F. Thornton ◽  
Evan S. Sorokin
Keyword(s):  
Mammary Hyperplasia

scholarly journals Temporally regulated overexpression of parathyroid hormone-related protein in the mammary gland reveals distinct fetal and pubertal phenotypes

2001 ◽  
Vol 171 (3) ◽  
pp. 403-416 ◽  
Author(s):  
ME Dunbar ◽  
P Dann ◽  
CW Brown ◽  
J Van Houton ◽  
B Dreyer ◽  
...  
Keyword(s):  
Mammary Gland ◽  
Parathyroid Hormone ◽  
Transgenic Mice ◽  
Mammary Development ◽  
Related Protein ◽  
Parathyroid Hormone Related Protein ◽  
Epithelial Cell Apoptosis ◽  
Ductal Elongation ◽  
Ductal Branching ◽  
Lobuloalveolar Development

We have previously demonstrated that overexpression of parathyroid hormone-related protein (PTHrP) in the mammary glands of transgenic mice results in defects in ductal elongation and branching during puberty and in lobuloalveolar development during pregnancy. In addition, we have shown that PTHrP is necessary for the formation of the initial ductal tree during embryonic mammary development. In order to examine the effect of varying the timing of PTHrP overexpression on mammary development, we created tetracycline-regulated, K14-tTA/Tet(O)-PTHrP double transgenic mice. In this report, we document that this 'tet-off' system directs transgene expression to the mammary gland and that it is fully repressed in the presence of tetracycline. Using these mice, we demonstrate that transient overexpression of PTHrP before birth causes defects in ductal branching during puberty and that overexpression of PTHrP during puberty decreases the rate of ductal elongation. Furthermore, we demonstrate that if PTHrP overexpression is initiated after ductal morphogenesis is completed, lobuloalveolar development is unaffected. Finally, we demonstrate that the impairment in ductal elongation caused by PTHrP is associated with an increase in the basal rate of epithelial cell apoptosis in terminal end buds and a failure to increase end bud cell proliferation and decrease apoptosis in response to estrogen and progesterone.

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