scholarly journals Modeling Breast Cancer via an Intraductal Injection of Cre-expressing Adenovirus into the Mouse Mammary Gland

10.3791/59502 ◽  
2019 ◽  
Author(s):  
Dongxi Xiang ◽  
Luwei Tao ◽  
Zhe Li
Keyword(s):  
Breast Cancer ◽  
Mammary Gland ◽  
Mouse Mammary Gland ◽  
Intraductal Injection

scholarly journals A novel and cost-effective ex vivo orthotopic model for the study of human breast cancer in mouse mammary gland organ culture

Biology Open ◽  
2020 ◽  
Vol 9 (5) ◽  
pp. bio051649
Author(s):  
Akash Gupta ◽  
Geetanjali Gupta ◽  
Rajeshwari R. Mehta ◽  
David Z. Ivancic ◽  
Rashidra R. Walker ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Mammary Gland ◽  
Organ Culture ◽  
Human Breast Cancer ◽  
Ex Vivo ◽  
Cost Effective ◽  
Mouse Mammary Gland ◽  
Human Breast ◽  
Orthotopic Model

Antagonistic activity of acolbifene, fulvestrant, tamoxifen, and raloxifene on cancer-associated genes in the mouse mammary gland.

2012 ◽  
Vol 30 (15_suppl) ◽  
pp. 10583-10583
Author(s):  
Ezequiel Calvo ◽  
Van Luu-The ◽  
Céline Martel ◽  
Fernand Labrie
Keyword(s):  
Breast Cancer ◽  
Mammary Gland ◽  
Mouse Mammary Gland ◽  
Antagonistic Activity ◽  
The Other ◽  
Specific Gene ◽  
Good Tolerance ◽  
New Information ◽  
Pure Antiestrogen ◽  
Microarray Screening

10583 Background: The efficacy and exceptionally good tolerance of estrogen blockade in the treatment of breast cancer is well recognized. Acolbifene (ACOL) is a novel and unique SERM completely free of estrogen-like activity in both the mammary gland and uterus. To better understand the specificity of ACOL, we have investigated its effect on the expression of a set of genes modulated by estradiol (E2) in the mouse mammary gland. Methods: ACOL, tamoxifen (TAM), raloxifene (RALOX) and fulvestrant (FULV) were administered (0.01 mg/mouse; sc) to ovariectomized (OVX) mice or to OVX mice simultaneously treated with E2 (0.05 µg/mouse; single sc injection). Microarray screening followed by Q_RTPCR was used to identify a reproducible set of E2 responsive genes. Results: From 128 genes significantly modulated by E2, 108 genes were up-regulated and 20 were down-regulated. Forty-nine of these genes were associated with tumorigenesis while 22 are known to be associated with breast cancer. This set of 49 genes were used to determine the specificity of ACOL compared to another pure antiestrogen in the mammary gland and uterus, namely FULV, as well as to the mixed estrogen antagonists/agonists TAM and RALOX, in their ability to block the effect of E2. Efficacy of reversal of the effect of E2 was 94%, 63%, 45% and 90% for ACOL, FULV, TAM and RALOX, respectively. The overlap between all treatments was 30.6% (15/49). ACOL reversed the effect of E2 on 42 of the 49 (85.7%) cancer-related genes. Between the genes up-regulated by E2 and reversed by ACOL, seven are considered as prognostic markers in breast cancer, namely Fgfr3, Fos12, Junb, Jdp2, Gdf15, Greb1 and Tgm2. On the other hand, two genes down‑regulated by E2, namely Foxa1 and Fgfr2, were restored by ACOL. Conclusions: Taken together, these data offer new information for a better understanding of the previously demonstrated potent tumoricidal action of ACOL in human breast cancer xenografts. The data also suggest, under the tested conditions, superiority of ACOL over TAM and the other compounds to reverse the effect of E2 on specific gene expression, thus supporting the interest of this new 3rd generation SERM for the hormonal therapy and prevention of breast cancer.

A less invasive method for orthotopic injection of breast cancer cells into the mouse mammary gland

2016 ◽  
Vol 51 (1) ◽  
pp. 85-88 ◽  
Author(s):  
Luz E Tavera-Mendoza ◽  
Myles Brown
Keyword(s):  
Breast Cancer ◽  
Mammary Gland ◽  
Cancer Cells ◽  
Cancer Biology ◽  
Mouse Mammary Gland ◽  
Breast Cancers ◽  
Biologically Relevant ◽  
Therapeutic Development ◽  
Invasive Method ◽  
Animal Handling

Breast cancer is the most common type of cancer diagnosed in women, and the second most common cause of cancer-related deaths in women in North America. The use of laboratory mice in research is an essential tool for the study of breast cancer biology and for pre-clinical therapeutic development. While subcutaneous flank injections of cancer cells are widely used for studying breast cancer biology and for exploring novel therapies, orthotopic xenografting of tumors into the mouse mammary gland allow for the study of breast cancers in a biologically relevant microenvironment. In this study we report a modification of the method of orthotopic injections of cancer cells into the mouse mammary gland which greatly reduces the effects of surgery in mice including decreased wound size, procedure time and anesthesia. It also removes the risk of accidentally puncturing the peritoneal cavity. Consequently post-operative animal handling and stress are significantly reduced. All of these advantages are present without compromising procedure success rate. Therefore, this modification makes orthotopic mammary gland injection a more efficient procedure and greatly improves animal welfare.

scholarly journals Annexin A8 Is Up-Regulated During Mouse Mammary Gland Involution and Predicts Poor Survival in Breast Cancer

2005 ◽  
Vol 11 (19) ◽  
pp. 6872-6879 ◽  
Author(s):  
Torsten Stein ◽  
Karen N. Price ◽  
Joanna S. Morris ◽  
Victoria J. Heath ◽  
Roderick K. Ferrier ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Mammary Gland ◽  
Mouse Mammary Gland ◽  
Poor Survival ◽  
Mammary Gland Involution

Intraductal Injection into the Mouse Mammary Gland

2000 ◽  
pp. 259-270 ◽  
Author(s):  
Duy-Ai Nguyen ◽  
Neal Beeman ◽  
Michael Lewis ◽  
Jerome Schaack ◽  
Margaret C. Neville
Keyword(s):  
Mammary Gland ◽  
Mouse Mammary Gland ◽  
Intraductal Injection

The Mouse Mammary Gland: a Tool to Inform Adolescents About Environmental Causes of Breast Cancer

2019 ◽  
Vol 35 (6) ◽  
pp. 1094-1100
Author(s):  
Laura N. Vandenberg ◽  
SriDurgaDevi Kolla ◽  
Charlotte D. LaPlante ◽  
D. Joseph Jerry
Keyword(s):  
Breast Cancer ◽  
Mammary Gland ◽  
Mouse Mammary Gland ◽  
Environmental Causes

scholarly journals Exposure to the Endocrine Disruptor, Propylparaben, During Pregnancy and Lactation, Alters Typical Parity-Induced Reorganization of the Mouse Mammary Gland

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A487-A488
Author(s):  
Joshua Philip Mogus
Keyword(s):  
Breast Cancer ◽  
Mammary Gland ◽  
Cancer Risk ◽  
Immune Cell ◽  
Mammary Glands ◽  
Mouse Mammary Gland ◽  
Receptor Expression ◽  
Intermediate Phenotypes ◽  
Sensitive Organ ◽  
Pregnancy And Lactation

Abstract The mammary gland is a hormone sensitive organ that is susceptible to endocrine disrupting chemicals (EDCs) during several vulnerable periods, including pregnancy and lactation. Mammary gland reorganization during pregnancy and lactation is hormone driven and provides long-term protection against breast cancer risk. It is unknown if EDC exposures during these sensitive windows can alter mammary reorganization to either enhance or offset parity-induced protection against breast cancer. Here, we examined effects of propylparaben (PP), a common preservative used in personal care products and foods with estrogen receptor (ER) agonist properties, on the parous mouse mammary gland. Pregnant BALB/c mice were treated with 0, 20, 100, or 10,000 µg/kg/day PP throughout pregnancy and lactation. These doses were selected for their relevance to human exposures. We also included an unexposed nulliparous female group to evaluate the typical changes associated with parity. Five weeks post-involution (and five weeks after the last PP exposure), mammary glands were collected and assessed for changes in histomorphology, hormone receptor expression, immune cell number, and gene expression. We found that PP reduced many of the typical morphological effects of parity on the mammary gland, resulting in intermediate phenotypes for ductal density and total epithelial structures. Notably, we found increased proliferation in PP-treated mammary glands, despite decreased ductal epithelial volume relative to parous controls. Mammary glands from PP-treated females also had alterations in the expression of ERα-mediated genes, including PgR (the gene that encodes progesterone receptor) and Igf1, with expression levels that were intermediate to both nulliparous and parous control mice. Finally, PP reduced the effect of parity on several immune cell types in the mammary gland including B cells, T-cells, and M2 macrophages. These results suggest that PP, at levels relevant to human exposure, can disrupt the normal response to parity in the mouse mammary gland, including persistent alterations to mammary gland structures. Future studies should address whether PP exposures disturb the protective effects of pregnancy on mammary cancer risk.

scholarly journals The male mammary gland: a novel target of endocrine disrupting chemicals

Reproduction ◽  
2021 ◽  
Author(s):  
Gillian K. Szabo ◽  
Laura N. Vandenberg
Keyword(s):  
Breast Cancer ◽  
Mammary Gland ◽  
Male Breast Cancer ◽  
Male Mouse ◽  
Mouse Mammary Gland ◽  
Male Breast ◽  
Breast Diseases ◽  
Human Populations ◽  
Life Course Studies ◽  
Estrogenic Chemicals

In the past several decades, the incidence of two male breast diseases, gynecomastia and male breast cancer, have increased in human populations. Whereas male breast cancer remains a rare disease, gynecomastia, a condition that arises due to abnormal development and growth of the male breast epithelium, is fairly common. In this review, we present the male mouse mammary gland as a potential model to understand human male breast diseases. Even though the male mouse typically lacks nipples, the male retains a small mammary rudiment with epithelium that is highly sensitive to estrogenic chemicals during the perinatal and peripubertal periods. In just the last few years, our understanding of the biology of the male mouse mammary gland has expanded. Researchers have characterized the complexity and size of the male mammary epithelium across the life course. Studies have documented that the male mouse mammary gland has left-right asymmetric morphologies, as well as asymmetries in the responsiveness of the left and right glands to estrogens. Recent studies have also revealed that the effect of xenoestrogens on the male mammary gland can differ based on the timing of evaluation (prior to puberty, in puberty, and in adulthood) and the administered dose. Based on the available evidence, we argue that there is a strong case that estrogenic chemicals promote the growth of the male mouse epithelium, consistent with human gynecomastia. We also argue that these outcomes should be characterized as adverse effects and should be considered in regulatory decision-making.

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