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Journal articles on the topic 'Human Mammary Glands'
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1
Li, Xiangdong, Anni Wärri, Sari Mäkelä, Tommi Ahonen, Tomi Streng, Risto Santti, and Matti Poutanen. "Mammary Gland Development in Transgenic Male Mice Expressing Human P450 Aromatase." Endocrinology 143, no. 10 (October 1, 2002): 4074–83. http://dx.doi.org/10.1210/en.2002-220181.
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Abstract We recently generated a transgenic mouse strain that expresses the human aromatase gene under the ubiquitin C promoter (AROM+). We have previously shown that in these mice the serum estradiol concentration is highly elevated, whereas the testosterone concentration is decreased. In the present study we examined mammary gland development in AROM+ male mice at different ages and found that the mammary glands of AROM+ males undergo ductal and alveolar development morphologically resembling that of terminally differentiated female mammary glands, expressing mRNA for a milk protein gene (β-casein). The male mammary glands also express multiple hormone receptors typical for female mammary gland: estrogen receptor α and β, progesterone receptor, and PRL receptor. Furthermore, data showed activation of the Stat5 (signal transducer and activator of transcription 5) signaling pathway in the AROM+ male mammary gland. Interestingly, the phenotype observed is in part reversible. Treatment with finrozole, a specific aromatase inhibitor, caused an involution of the differentiated phenotype of the mammary gland, marked by the disappearance of alveolar structures and the majority of the tertiary side branches of the ducts. The present animal model is a valuable tool for better understanding the cellular and molecular mechanisms involved in the development of gynecomastia.
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Mogus, Joshua Philip. "Exposure to the Endocrine Disruptor, Propylparaben, During Pregnancy and Lactation, Alters Typical Parity-Induced Reorganization of the Mouse Mammary Gland." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A487—A488. http://dx.doi.org/10.1210/jendso/bvab048.997.
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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.
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Lee, Sungin, Seulji Lee, Aeri Lee, Hun Ju Sim, Geon A. Kim, Byung-Jae Kang, and Wan Hee Kim. "The Presence and Distribution of TRPM7 in the Canine Mammary Glands." Animals 10, no. 3 (March 11, 2020): 466. http://dx.doi.org/10.3390/ani10030466.
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The transient receptor potential melastatin-subfamily member 7 (TRPM7) cation channel is a bifunctional ion channel with intrinsic kinase activity and is ubiquitously expressed in the animal/human body. Accumulated knowledge of TRPM7 suggests that it plays an essential role in normal physiological processes, including the development, survival, proliferation, differentiation, and migration of cells. The aim of this study was to demonstrate the presence and expression patterns of TRPM7 in normal canine mammary glands using reverse transcription-polymerase chain reaction (RT-PCR), Western blotting, and immunohistochemistry. Normal mammary gland tissue samples were obtained from five female beagle dogs. RT-PCR and sequencing of the amplified PCR products demonstrated the presence of TRPM7 mRNA in normal mammary glands, and the presence of TRPM7 protein was confirmed by Western blotting. Immunohistochemical investigations demonstrated the expression of TRPM7 in the apical membrane of acinar and ductal epithelial cells in the canine mammary glands. These results provide the first evidence of the presence and distribution of TRPM7 in the canine mammary gland and could help explain the physiological and pathological roles of TRPM7 in the canine mammary gland; however, additional studies are required to elucidate these roles.
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Parmar, Hema, and Gerald R. Cunha. "Epithelial–stromal interactions in the mouse and human mammary gland in vivo." Endocrine-Related Cancer 11, no. 3 (September 2004): 437–58. http://dx.doi.org/10.1677/erc.1.00659.
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This review deals with the development and hormonal responses of mouse and human mammary glands. A major focus of the review is the role of mesenchymal–epithelial interactions in embryonic mammary development and the role of stromal–epithelial interactions in mammary gland biology. Finally, we present a new model for studying growth, differentiation and hormonal response in human breast epithelium grown in vivo in nude mouse hosts. This new model involves the construction of tissue recombinants composed of human or mouse mammary fibroblasts plus human breast epithelium in polymerized collagen gels. In the model, mouse mammary fibroblasts and human breast fibroblasts appear to support the normal differentiation and growth of human breast epithelium equally. This observation raises the possibility of using mouse mammary fibroblasts from various mutant mice to assess the role of specific paracrine-acting gene products in human mammary gland biology and carcinogenesis.
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Zhao, Yan, Carina Johansson, Thai Tran, Ryan Bettencourt, Yoko Itahana, Pierre-Yves Desprez, and Stephen F. Konieczny. "Identification of a Basic Helix-Loop-Helix Transcription Factor Expressed in Mammary Gland Alveolar Cells and Required for Maintenance of the Differentiated State." Molecular Endocrinology 20, no. 9 (September 1, 2006): 2187–98. http://dx.doi.org/10.1210/me.2005-0214.
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Abstract The development of mammary glands relies on complicated signaling pathways that control cell proliferation, differentiation, and apoptotic events through transcriptional regulatory circuits. A key family of transcription factors used in mammary gland development is the helix-loop-helix/basic helix-loop-helix (HLH/bHLH) protein family. In this study, we identify Mist1 as a tissue-restricted Class II bHLH transcription factor expressed in lactating mammary glands. Mouse and human mammary glands accumulated Mist1 protein exclusively in secretory alveolar cells, and Mist1 transcripts were differentially expressed in mouse SCp2 cells induced to differentiate by addition of lactogenic hormones. Mist1 null (Mist1KO) lactating mammary glands were defective in normal lobuloalveolar organization, exhibiting shedding of cells into the alveolus lumen and premature activation of the signal transducer and activator of transcription 3 signaling pathway. These cells also failed to maintain expression of the gap junction proteins connexin26 and connexin32, leading to the loss of gap junctions. Our findings suggest that loss of Mist1 impairs the maintenance of the fully differentiated alveolar state and, for the first time, places Mist1 within the hierarchy of known HLH/bHLH proteins that control mammary epithelial cell development.
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Myal, Y., B. Iwasiow, H. Cosby, A. Yarmill, A. Blanchard, D. Tsuyuki, A. Fresnoza, ML Duckworth, and RP Shiu. "Analysis of tissue- and hormone-specific regulation of the human prolactin-inducible protein/gross cystic disease fluid protein-15 gene in transgenic mice." Journal of Molecular Endocrinology 21, no. 2 (October 1, 1998): 217–23. http://dx.doi.org/10.1677/jme.0.0210217.
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The human prolactin-inducible protein/gross cystic disease fluid protein-15 (PIP/GCDFP-15) gene is expressed in more than 90% of human breast cancer biopsies but not in the normal mammary gland. However, it is expressed in several normal human apocrine glands such as the lacrimal and salivary glands. In human breast cancer cell lines, the gene is regulated by a number of hormones including androgen and prolactin. It is not known whether gene expression in normal tissues is under similar hormonal control. To understand the mechanisms by which hormone- and tissue-specific expression of the human PIP/GCDFP-15 gene are regulated in vivo, we generated transgenic mice using a 13.7 kb genomic DNA fragment containing the entire 7 kb human gene, together with 2.9 kilobases of 5' and 3.8 kilobases of 3' flanking sequences. The human PIP/GCDFP-15 transgene was found to be expressed in both the lacrimal and salivary glands but was not expressed in the mammary glands of transgenic mice. This tissue-specific pattern of the transgene expression in the mouse was very similar to that of the endogenous human PIP/GCDFP-15 gene, and to the endogenous mouse,gene. In the mouse salivary glands, the transgene expression was highest in the parotid, considerably less in the submaxillary (submandibular) and absent in the sublingual glands. In the mouse lacrimal gland, as in the human breast cancer cell lines, the human PIP/GCDFP-15 transgene was also up-regulated by androgen. These studies demonstrate that the human gene with its 6.3 kb flanking sequences is able to confer gene expression in vivo in a tissue-specific and hormone-responsive manner.
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Welsch, Ulrich, Pia Unterberger, Eugen Höfter, Frank Cuttitta, and Alfredo Martínez. "Adrenomedullin in mammalian and human skin glands including the mammary gland." Acta Histochemica 104, no. 1 (January 2002): 65–72. http://dx.doi.org/10.1078/0065-1281-00623.
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Kudo, H., G. Ohshio, K. Ogawa, Y. Wakatsuki, M. Inada, Y. Hamashima, and T. Miyake. "Distribution of vitamin B12 R binder in normal human tissues: an immunohistochemical study." Journal of Histochemistry & Cytochemistry 35, no. 8 (August 1987): 855–59. http://dx.doi.org/10.1177/35.8.3298426.
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We studied the distribution of vitamin B12 R binder in various normal human tissues by use of an immunoperoxidase technique. Positive staining for R binder was observed in almost all glandular epithelia of digestive system, bronchial glands, renal proximal tubules, prostate, uterus, Fallopian tube, mammary gland, and sweat glands. The distribution of R binder was similar to that of lactoferrin and secretory component. These findings support the hypothesis that R binder plays a role in the local defense mechanism.
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Järvensivu, Päivi, Taija Heinosalo, Janne Hakkarainen, Pauliina Kronqvist, Niina Saarinen, and Matti Poutanen. "HSD17B1 expression induces inflammation-aided rupture of mammary gland myoepithelium." Endocrine-Related Cancer 25, no. 4 (April 2018): 393–406. http://dx.doi.org/10.1530/erc-17-0476.
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Hydroxysteroid (17-beta) dehydrogenase type 1 (HSD17B1) converts low-active estrogen estrone to highly active estradiol. Estradiol is necessary for normal postpubertal mammary gland development; however, elevated estradiol levels increase mammary tumorigenesis. To investigate the significance of the human HSD17B1 enzyme in the mammary gland, transgenic mice universally overexpressing human HSD17B1 were used (HSD17B1TG mice). Mammary glands obtained from HSD17B1TG females at different ages were investigated for morphology and histology, and HSD17B1 activity and estrogen receptor activation in mammary gland tissue were assessed. To study the significance of HSD17B1 enzyme expression locally in mammary gland tissue, HSD17B1-expressing mammary epithelium was transplanted into cleared mammary fat pads of wild-type females, and the effects on mammary gland estradiol production, epithelial cells and the myoepithelium were investigated. HSD17B1TG females showed increased estrone to estradiol conversion and estrogen-response element-driven estrogen receptor signaling in mammary gland tissue, and they showed extensive lobuloalveolar development that was further enhanced by age along with an increase in serum prolactin concentrations. At old age, HSD17B1TG females developed mammary cancers. Mammary-restricted HSD17B1 expression induced lesions at the sites of ducts and alveoli, accompanied by peri- and intraductal inflammation and disruption of the myoepithelial cell layer. The lesions were shown to be estrogen dependent, as treatment with an antiestrogen, ICI 182,780, starting when lesions were already established reversed the phenotype. These data elucidate the ability of human HSD17B1 to enhance estrogen action in the mammary glandin vivoand indicate that HSD17B1 is a factor inducing phenotypic alterations associated with mammary tumorigenesis.
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Chung, Heaji, Sungin Lee, Geon A. Kim, and Wan Hee Kim. "Down-expression of klotho in canine mammary gland tumors and its prognostic significance." PLOS ONE 17, no. 6 (June 6, 2022): e0265248. http://dx.doi.org/10.1371/journal.pone.0265248.
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Since the discovery of klotho as an anti-aging gene, its association with tumors has been studied. Several previous studies have reported the down-expression of klotho in various human cancers, and much of its mechanism has been revealed. Nonetheless, the significance of klotho in canine mammary gland tumors is not yet known. This study aimed to determine whether klotho is expressed within normal canine mammary glands and whether the expression changes in benign and malignant tumors. Using immunohistochemistry, the experiment was conducted on eight normal canine mammary gland tissues and 55 mammary gland tumor samples. Additionally, the correlation between the Ki-67 proliferation index and clinicopathological features, such as age, tumor size, tumor grade, histologic type, and metastasis, was evaluated. All eight normal mammary gland tissues showed immunohistochemistry expression of klotho, and the expression significantly decreased as malignancy increased. Among the samples, 11% (3/28) of benign tumors and 26% (7/27) of malignant tumors showed negative klotho expression. Furthermore, higher Ki-67 expression, higher grades, and metastasis were confirmed to be associated with the negative klotho expression. Analysis of the survival curve for dogs with malignant tumors revealed that negative klotho expression was significantly associated with poor overall survival and disease-free survival. These results indicate that klotho is expressed in normal canine mammary glands and that negative klotho expression in canine mammary gland tumors is positively correlated with poor prognosis.
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Groneberg, David A., Frank Döring, Stephan Theis, Monika Nickolaus, Axel Fischer, and Hannelore Daniel. "Peptide transport in the mammary gland: expression and distribution of PEPT2 mRNA and protein." American Journal of Physiology-Endocrinology and Metabolism 282, no. 5 (May 1, 2002): E1172—E1179. http://dx.doi.org/10.1152/ajpendo.00381.2001.
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The lactating mammary gland utilizes free plasma amino acids as well as those derived by hydrolysis from circulating short-chain peptides for protein synthesis. Apart from the major route of amino acid nitrogen delivery to the gland by the various transporters for free amino acids, it has been suggested that dipeptides may also be taken up in intact form to serve as a source of amino acids. The identification of peptide transporters in the mammary gland may therefore provide new insights into protein metabolism and secretion by the gland. The expression and distribution of the high-affinity type proton-coupled peptide transporter PEPT2 were investigated in rat lactating mammary gland as well as in human epithelial cells derived from breast milk. By use of RT-PCR, PEPT2 mRNA was detected in rat mammary gland extracts and human milk epithelial cells. The expression pattern of PEPT2 mRNA revealed a localization in epithelial cells of ducts and glands by nonisotopic high resolution in situ hybridization. In addition, immunohistochemistry was carried out and showed transporter immunoreactivity in the same epithelial cells of the glands and ducts. In addition, two-electrode voltage clamp recordings using PEPT2-expressing Xenopus laevis oocytes demonstrated positive inward currents induced by selected dipeptides that may play a role in aminonitrogen handling in mammalian mammary gland. Taken together, these data suggest that PEPT2 is expressed in mammary gland epithelia, in which it may contribute to the reuptake of short-chain peptides derived from hydrolysis of milk proteins secreted into the lumen. Whereas PEPT2 also transports a variety of drugs, such as selected β-lactams, angiotensin-converting enzyme inhibitors, and antiviral and anticancer metabolites, their efficient reabsorption via PEPT2 may reduce the burden of xenobiotics in milk.
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Torres, L. N., J. M. Matera, C. H. Vasconcellos, J. L. Avanzo, F. J. Hernandez-Blazquez, and M. L. Z. Dagli. "Expression of Connexins 26 and 43 in Canine Hyperplastic and Neoplastic Mammary Glands." Veterinary Pathology 42, no. 5 (September 2005): 633–41. http://dx.doi.org/10.1354/vp.42-5-633.
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Gap junctions are the only communicating junctions found in animal tissues and are composed of proteins known as connexins. Alterations in connexin expression have been associated with oncogenesis; reported studies in rodent and human mammary glands, which normally express connexins 26 and 43, confirm these alterations in malignancies. Mammary neoplasms represent the second most frequent neoplasm in dogs, and since there are no reports on the study of connexins in canine mammary glands, the present study investigated the expression of connexins 26 and 43 in normal, hyperplastic, and neoplastic mammary glands of this species, to verify if altered patterns of connexin staining are related to higher cell proliferation and malignant phenotypes. A total of 4 normal, 8 hyperplastic mammary glands, 9 benign, and 51 malignant mammary gland neoplasms were submitted for the immunostaining of connexins 26 and 43, E-cadherin, and proliferating cell nuclear antigen (PCNA). Normal, hyperplastic, and benign neoplastic mammary glands showed a punctate pattern for connexin 26 and 43 staining and an intercellular E-cadherin staining. Malignant neoplasms, especially the most aggressive cases with high cell proliferation rates, presented either fewer gap junction spots on the cell membranes or increased cytoplasmic immunostaining. Malignant tumors also expressed a less intense immunostaining of E-cadherin; the expression of this adhesion molecule is important for the transportation of connexins to cell membranes and in forming communicating gap junctions. Deficient expression of E-cadherin could be related to the aberrant connexin localization and may contribute to the malignant phenotype. In conclusion, the expression and distribution of connexins and E-cadherin are inversely correlated to cell proliferation in malignant mammary neoplasms of dogs and may well be related to their more aggressive histologic type and biologic behavior.
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Grönberg, Malin, Rose-Marie Amini, Mats Stridsberg, Eva T. Janson, and Jan Saras. "Neuroendocrine markers are expressed in human mammary glands." Regulatory Peptides 160, no. 1-3 (February 2010): 68–74. http://dx.doi.org/10.1016/j.regpep.2009.12.011.
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Li, Lan, Wei Shen, Lingjiang Min, Huansheng Dong, Yujiang Sun, and Qingjie Pan. "Human lactoferrin transgenic rabbits produced efficiently using dimethylsulfoxide - sperm-mediated gene transfer." Reproduction, Fertility and Development 18, no. 6 (2006): 689. http://dx.doi.org/10.1071/rd06001.
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Transgenic animal mammary gland bioreactors are used to produce recombinant proteins. However, it is difficult to validate whether these transgenic domestic animals are able to express the recombinant protein efficiently in their mammary glands before the birth of transgenic offspring. In the present study, a simple and efficient method was established to evaluate the functionality of animal mammary gland tissue-expressed cassettes. The gene transfer vector pGBC2LF was constructed, and the expression of human lactoferrin (LF) gene was controlled by the goat β-casein gene 5′ flanking sequence. To obtain the most efficient transfection, the influence of DNA concentration, dimethylsulfoxide (DMSO) concentration, and the ratio of linear-to-circular DNA required for associating DNA with spermatozoa were evaluated. Transfection of exogenous DNA into rabbit spermatozoa was found to be efficient using 30 μg mL–1 DNA, DMSO at a final concentration of 3%, and a 3 : 1 ratio of linear-to-circular DNA, with 29 of 85 (34.1%) in vitro-fertilised embryos being transgenic. Using DMSO–sperm-mediated gene transfer (DMSO-SMGT), 89 rabbit offspring were produced, with 46 of these (57.1%) being transgenic. As mammary gland bioreactor models, 17 of 21 (81%) transgenic female rabbits could express human LF protein in their glands. During lactation of the transgenic rabbits, the highest level of human LF protein expressed was 153 ± 31 μg mL–1, and the mean expression level in all of the transgenic rabbits was 103 ± 20 μg mL–1 in the third week, declining gradually after this time. Our results demonstrate that transgenic rabbits produced by DMSO–SMGT were able to express human LF protein in the correct tissue.
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Suarez-Cabrera, Cristian, Isabel Ojeda-Perez, Raquel Sanchez-Baltasar, Angustias Page, Ana Bravo, Manuel Navarro, and Angel Ramirez. "ERAS, a Member of the Ras Superfamily, Acts as an Oncoprotein in the Mammary Gland." Cancers 13, no. 21 (November 8, 2021): 5588. http://dx.doi.org/10.3390/cancers13215588.
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ERAS is a relatively uncharacterized gene of the Ras superfamily. It is expressed in ES cells and in the first stages of embryonic development; later on, it is silenced in the majority of cell types and tissues. Although there are several reports showing ERAS expression in tumoral cell lines and human tumor samples, it is unknown if ERAS deregulated expression is enough to drive tumor development. In this report, we have generated transgenic mice expressing ERAS in myoepithelial basal cells of the mammary gland and in basal cells of stratified epithelia. In spite of the low level of ERAS expression, these transgenic mice showed phenotypic alterations resembling overgrowth syndromes caused by the activation of the AKT-PI3K pathway. In addition, their mammary glands present developmental and functional disabilities accompanied by morphological and biochemical alterations in the myoepithelial cells. These mice suffer from tumoral transformation in the mammary glands with high incidence. These mammary tumors resemble, both histologically and by the expression of differentiation markers, malignant adenomyoepitheliomas. In sum, our results highlight the importance of ERAS silencing in adult tissues and define a truly oncogenic role for ERAS in mammary gland cells when inappropriately expressed.
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Bortner, D. M., and M. P. Rosenberg. "Induction of mammary gland hyperplasia and carcinomas in transgenic mice expressing human cyclin E." Molecular and Cellular Biology 17, no. 1 (January 1997): 453–59. http://dx.doi.org/10.1128/mcb.17.1.453.
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Deregulated expression of several cell cycle regulatory genes has been demonstrated to be associated with cancer. In particular, a strong correlation has been established between inappropriate cyclin E expression and human breast cancer. To determine the ability of cyclin E to play a causative role in mammary tumorigenesis, regulatory sequences from the ovine beta-lactoglobulin gene were utilized to specifically target expression of human cyclin E to the mammary glands of pregnant and lactating mice. Lactating mammary glands of transgenic mice expressing cyclin E contained areas of hyperplasia, primarily papillary projections of hyperplastic cells, which were rarely observed in lactating glands of control mice. Over 10% of female cyclin E transgenic mice have developed mammary carcinomas, with latencies ranging from 8 to 13 months. Tumor analysis revealed the presence of transgene-specific cyclin E RNA and protein, as well as cyclin E- and cdk2-associated kinase activity, suggesting that cyclin E is likely a contributing component of tumorigenic progression in this model system.
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Sassi, Francesco, Giuseppe Sarli, Barbara Brunetti, Federico Morandi, and Cinzia Benazzi. "Immunohistochemical Characterization of Mammary Squamous Cell Carcinoma of the Dog." Journal of Veterinary Diagnostic Investigation 20, no. 6 (November 2008): 766–73. http://dx.doi.org/10.1177/104063870802000608.
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Squamous cell carcinoma of the mammary gland is rare in both veterinary and human medicine. Whereas human metaplastic and squamous variants are known, the objectives of the current study were to ascertain the presence of such entities in canine mammary tumors and to distinguish them from other (epidermal, sweat gland) squamous tumors that may develop in the same area. A panel of antibodies (anticytokeratin [CK] 19, CK 14, CK 5/6, pancytokeratin, and vimentin) was used on 18 mammary gland malignancies with squamous features and 16 malignant skin tumors (11 squamous cell carcinomas of the skin and 5 sweat glands). Fifteen of the 18 mammary carcinomas were classified as metaplastic carcinomas, and the remaining 3 were classified as squamous cell carcinomas. The 2 most useful markers to establish the histogenesis of mammary tumors were pancytokeratin and CK 19. All other antibodies were equally expressed (CK 14 and 5/6) in all histotypes. The antibody panel discriminated primary epidermal squamous tumors (pancytokeratin positive and CK 19 negative) from gland-derived squamous neoplasms (pancytokeratin positive and CK 19 positive) but failed to distinguish primary mammary tumors from other squamous tumors of glandular origin.
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Manhès, Caroline, Christine Kayser, Philippe Bertheau, Bruce Kelder, John J. Kopchick, Paul A. Kelly, Philippe Touraine, and Vincent Goffin. "Local over-expression of prolactin in differentiating mouse mammary gland induces functional defects and benign lesions, but no carcinoma." Journal of Endocrinology 190, no. 2 (August 2006): 271–85. http://dx.doi.org/10.1677/joe.1.06829.
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Experimental, clinical, and epidemiological data support the growth-promoting role of endocrine prolactin (PRL) in mammary tumors. PRL is also produced by the breast, where it is now recognized to act as a growth/survival factor via autocrine/paracrine mechanisms. Recent transgenic (Tg) mouse models have revealed the pro-oncogenic effect of PRL over-expression in virgin mammary glands. To address the question whether PRL tumorigenicity was maintained on differentiated mammary glands, we generated mammary-specific Tg mice expressing human (h)PRL under the control of the milk whey acidic protein promoter, which directs autocrine hPRL over-expression in late gestation throughout lactation. Minimal levels of transgene expression were detected in the mammary glands of virgin animals, which at best induced partial ductal branching and lobulo-alveolar structures in older nulliparous females. As expected, expression of mammary hPRL dramatically increased at the end of first pregnancy, and from this point it never returned to baseline, although it peaked at each gestation/lactation cycle. Over-expression of hPRL that starts when the gland is already well into the differentiation process led to various morphological mammary alterations, including abnormally differentiated epithelium, atropy of the myoepithelial layer, dilated ducts, cysts, and lymphocytic infiltrates. These phenotypes tended to worsen with successive pregnancies, also reflecting cumulative damage of failure of involution. Although some older, multiparous females developed benign tumors (papillomas and metaplasias), none of the animals studied developed mammary carcinomas. In addition, we noticed that half of the Tg females exhibited lactation defects, leading to significantly increased pup mortality. This phenotype was due neither to failure of milk production nor to modification of its protein content, but rather it was correlated to lipid enrichment of the milk, which, in combination with profoundly altered morphology of the gland, led to impaired milk extrusion through the nipple. In summary, these data show that over-expression of autocrine hPRL in a differentiating mammary gland induces dramatic functional and morphological defects, but not carcinoma. This deserves further investigations on the emerging concept that autocrine PRL may have different effects on pathological development of the mammary gland depending on the differentiation state of the latter.
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Kett, K., P. Brandtzaeg, J. Radl, and J. J. Haaijman. "Different subclass distribution of IgA-producing cells in human lymphoid organs and various secretory tissues." Journal of Immunology 136, no. 10 (May 15, 1986): 3631–35. http://dx.doi.org/10.4049/jimmunol.136.10.3631.
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Abstract A highly reproducible paired immunofluorescence staining method was used to map the relative distribution of IgA1- and IgA2-producing cells in peripheral lymphoid organs and various secretory tissues. Spleen, peripheral lymph nodes, and tonsils all contained a marked predominance (91 to 95%) of IgA1 immunocytes. However, striking variations were demonstrated among the secretory tissues with regard to the median proportion of IgA1-producing cells: nasal mucosa, 96%; lacrimal glands, 81%; major salivary glands, 66%; mammary glands, 63%; gastric and proximal small intestinal mucosa, 84 to 77%; ileum, 55%; and large bowel, 41%. Thus, IgA2 production is relatively enhanced mainly in the distal gut and in mammary and salivary glands, in that order.
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Hubert, Chiche, Legros, Jeannin, Montange, Gessain, Ceccaldi, and Vidy. "Productive Infection of Mouse Mammary Glands and Human Mammary Epithelial Cells by Zika Virus." Viruses 11, no. 10 (October 15, 2019): 950. http://dx.doi.org/10.3390/v11100950.
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Zika virus (ZIKV) belongs to the large category of arboviruses. Surprisingly, several human-to-human transmissions of ZIKV have been notified, either following sexual intercourse or from the mother to fetus during pregnancy. Importantly, high viral loads have been detected in the human breast milk of infected mothers, and the existence of breastfeeding as a new mode of mother-to-child transmission of ZIKV was recently hypothesized. However, the maternal origin of infectious particles in breast milk is currently unknown. Here, we show that ZIKV disseminates to the mammary glands of infected mice after both systemic and local exposure with differential kinetics. Ex vivo, we demonstrate that primary human mammary epithelial cells were sensitive and permissive to ZIKV infection in this study. Moreover, by using in vitro models, we prove that mammary luminal- and myoepithelial-phenotype cell lines are both able to produce important virus progeny after ZIKV exposure. Our data suggest that the dissemination of ZIKV to the mammary glands and subsequent infection of the mammary epithelium could be one mechanism of viral excretion in human breast milk.
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Jousset, V., B. Legendre, P. Besnard, N. Segond, A. Jullienne, and J. M. Garel. "Calcitonin-like immunoreactivity and calcitonin gene expression in the placenta and in the mammary gland of the rat." Acta Endocrinologica 119, no. 3 (November 1988): 443–51. http://dx.doi.org/10.1530/acta.0.1190443.
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Abstract. Recently, the presence of monomeric CT in plasma and milk was reported by others in a lactating woman surgically thyroidectomized. Similarly, the placenta was thought to be a possible source of CT. Since such findings were based exclusively on immunological arguments, we have investigated the CT gene expression in these rat tissues. CT mRNAs were detected by dot-blot hybridization of total RNAs extracted from rat tissues with a 32P-labelled human CT cDNA probe. Subcellular fractions of each tissue were screened for CT-like immunoreactivity using two different antibodies. With one antibody, extracts of the mammary gland and placenta both produced full displacement of labelled human CT from the antiserum and serial dilutions of the extracts gave displacement curves parallel to that of synthetic human CT, which suggests immunological similarity. However, dilution curves were not parallel for the second antibody, and for both antisera, CT-like immunoreactivity was found in all subsellular fractions from nuclei to cytosols. Immunoprecipitation of translation products from poly (A)+RNAs of placenta showed two major bands around 30 kD. Under stringent conditions, the weak hybridization of placental RNAs seen by dot-blot under less stringent conditions disappeared. Northern analyses of total RNAs from the placenta failed to detect mRNA of 1 k base size like in thyroid glands, but hybridization under weak stringent conditions occurred with larger mRNAs (around 4.4 and 2.4 k bases). Immunoprecipitation of translation products from mRNAs of rat mammary glands showed three major bands around 46, 30 and 20 kD. Dot-blot hybridization of total RNAs extracted from mammary glands was also negative. In conelusion, our results suggest that the CT gene is not expressed in the rat placenta and in rat mammary gland, since CT mRNAs were not detected in either tissues.
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Robichaux, Jacqulyne P., John W. Fuseler, Shrusti S. Patel, Steven W. Kubalak, Adam Hartstone-Rose, and Ann F. Ramsdell. "Left–right analysis of mammary gland development in retinoid X receptor-α +/− mice." Philosophical Transactions of the Royal Society B: Biological Sciences 371, no. 1710 (December 19, 2016): 20150416. http://dx.doi.org/10.1098/rstb.2015.0416.
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Left–right (L–R) differences in mammographic parenchymal patterns are an early predictor of breast cancer risk; however, the basis for this asymmetry is unknown. Here, we use retinoid X receptor alpha heterozygous null (RXRα +/− ) mice to propose a developmental origin: perturbation of coordinated anterior–posterior (A–P) and L–R axial body patterning. We hypothesized that by analogy to somitogenesis—in which retinoic acid (RA) attenuation causes anterior somite pairs to develop L–R asynchronously—that RA pathway perturbation would likewise result in asymmetric mammary development. To test this, mammary glands of RXRα +/− mice were quantitatively assessed to compare left- versus right-side ductal epithelial networks. Unlike wild-type controls, half of the RXRα +/− thoracic mammary gland (TMG) pairs exhibited significant L–R asymmetry, with left-side reduction in network size. In RXRα +/− TMGs in which symmetry was maintained, networks had bilaterally increased size, with left networks showing greater variability in area and pattern. Reminiscent of posterior somites, whose bilateral symmetry is refractory to RA attenuation, inguinal mammary glands (IMGs) also had bilaterally increased network size, but no loss of symmetry. Together, these results demonstrate that mammary glands exhibit differential A–P sensitivity to RXRα heterozygosity, with ductal network symmetry markedly compromised in anterior but not posterior glands. As TMGs more closely model human breast development than IMGs, these findings raise the possibility that for some women, breast cancer risk may initiate with subtle axial patterning defects that result in L–R asymmetric growth and pattern of the mammary ductal epithelium. This article is part of the themed issue ‘Provocative questions in left–right asymmetry’.
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Nagasawa, H., M. Mizuno, M. Hasegawa, and T. Harigaya. "Variable expression of human transgenes in SHN mice." Laboratory Animals 30, no. 2 (April 1, 1996): 127–31. http://dx.doi.org/10.1258/002367796780865727.
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The mouse mammary tumour virus/human transforming growth factor α (MMTV/hTGF α) gene or the mouse whey acidic protein/human growth hormone (mWAP/hGH) gene was introduced to a high mammary tumour strain of SHN virgin females by mating with males bearing each gene. We maintained transgenic mice by backcrossing males with the hTGF α transgene or high serum hGH levels (>50 ng/ml) to SHN virgins in the subsequent generations. Expression of the transgenes was examined at each generation. At the first and the second generations of backcrossing (N1 and N2), females showed hTGF α mRNA in the mammary glands associated with a marked outgrowth of the glands. Both females and males had high hGH levels in the circulation, but these characteristics disappeared completely after the third generation (N3). All findings indicate that SHN mice are specific in the resistance to the expression of some human transgenes.
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Kuorelahti, Aino, Susana Rulli, Ilpo Huhtaniemi, and Matti Poutanen. "Human Chorionic Gonadotropin (hCG) Up-Regulates wnt5b and wnt7b in the Mammary Gland, and hCGβ Transgenic Female Mice Present with Mammary Gland Tumors Exhibiting Characteristics of the Wnt/β-Catenin Pathway Activation." Endocrinology 148, no. 8 (August 1, 2007): 3694–703. http://dx.doi.org/10.1210/en.2007-0249.
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Transgenic (TG) mice expressing human chorionic gonadotropin (hCG) β-subunit under the ubiquitin C promoter, presenting with a moderately elevated level of LH/hCG bioactivity develop multiple neoplasms secondary to the endocrine abnormalities, including mammary gland tumors after the age of 9 months. The increased levels of circulating estradiol, progesterone, and prolactin of the TG females after puberty boost the lobuloalveolar development in the mammary gland resulting ultimately in the formation of estrogen and progesterone receptor-negative, malignant tumors. These tumors have a similar histopathology with those observed in TG mice with activated wnt/β-catenin pathway, showing increased expression of β-catenin, also a common finding in human breast tumors. Transdifferentiation is observed in mammary tumors of the hCGβ TG mice, accompanied by abnormal expression of the Wnt genes in the tumorous and nontumorous mammary gland tissue. Specifically we found increased expression of Wnt5b in the TG mammary glands at the age of 3 months and up-regulation of Wnt7b and -5b in the subsequently appearing tumors. Importantly, hCG was found to up-regulate these wnt ligands in mouse mammary gland, independent of the changes in ovarian steroidogenesis. Thus, the hCGβ-overexpressing TG mice represent a novel model that links enhanced hCG action to dysregulated wnt signaling in the mammary gland, resulting in β-catenin-stabilizing mammary tumorigenesis. The novel finding of hCG up-regulating wnt7b and wnt5b could contribute to pregnancy-induced breast cancer in humans.
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Kazakov, Dmitry V., Jana Nemcova, Iva Mikyskova, Irena E. Belousova, Marina Vazmitel, and Michal Michal. "Human Papillomavirus in Lesions of Anogenital Mammary-Like Glands." International Journal of Gynecological Pathology 26, no. 4 (October 2007): 475–80. http://dx.doi.org/10.1097/pgp.0b013e31803104af.
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Jensen, Vivi Flou Hjorth, Peter R. Brinck, Jette Nowak, Inger Thorup, Ingrid Sjögren, and Anne-Marie Mølck. "Evaluation of Cell Proliferation in Rat Mammary Glands Is Not Predictive of the Carcinogenic Potential of Insulin In Vivo." International Journal of Toxicology 39, no. 6 (July 29, 2020): 560–76. http://dx.doi.org/10.1177/1091581820941776.
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For nonclinical safety-assessment of insulin analogues in vivo, mitogenic effects are compared to that of human insulin. Besides histopathologic evaluation, this usually includes assessment of cell proliferation (CP) in mammary glands. Insulin analogue X10 is recommended as positive control, due to its known carcinogenic effect in rat mammary glands. Here, we discuss the mitogenic effect of insulin in vivo and use of X10 as positive control. We present results from 4 nonclinical rat studies evaluating effects of repeated dosing with insulin detemir (≤26 weeks) or degludec (52 weeks) in mammary glands. Studies included human insulin-dosed groups as comparators, CP, and histopathologic evaluation. One study included an X10-dosed group (26 weeks), another ≤3 weeks of dosing with X10 or human insulin evaluating effects of these comparators. Neither human insulin, insulin detemir, degludec, nor X10 induced mammary tumors or increased CP in the studies. The CP marker proliferating cell nuclear antigen varied within/between studies and was not correlated with the remaining markers or CP fluctuations during estrous cycle, whereas the other CP markers, Ki-67 and 5-bromo-2′-deoxyuridine (BrdU), correlated with estrous cycle changes and each other. In conclusion, we propose that the mitogenic effect of insulin in rat mammary glands is weak in vivo. Cell proliferation evaluation in nonclinical safety assessment studies is not predictive of the carcinogenic potential of insulin, thus, the value of including this end point is debatable. Moreover, X10 is not recommended as positive control, due to lack of proliferative effects. Typical CP markers vary greatly in quality, BrdU seemingly most reliable.
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Magi, Gian Enrico, Francesca Mariotti, Lorenzo Pallotta, Alessandro Di Cerbo, and Franco Maria Venanzi. "Immunohistochemical Expression of p62 in Feline Mammary Carcinoma and Non-Neoplastic Mammary Tissue." Animals 12, no. 15 (August 2, 2022): 1964. http://dx.doi.org/10.3390/ani12151964.
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The p62 protein, also called sequestosome 1 (SQSTM1), is a ubiquitin-binding scaffold protein. In human oncology, although the interest in the function of this protein is recent, the knowledge is now numerous, but its role in tumorigenesis is not yet clear. This preliminary study aims to evaluate the immunohistochemical expression of p62 in 38 cases of feline mammary carcinoma with different grades of differentiation and in 12 non-neoplastic mammary gland tissues, to assess the expression level and a possible correlation with malignancy. The expression of p62 was statistically higher in carcinoma compared to non-neoplastic mammary glands: 28 feline mammary carcinomas (73.7%) had a high p62 expression score, three (7.9%) had a moderate expression, while seven cases (18.4%) had a low expression. The grade of the differentiation of the carcinoma was not correlated with the p62 expression. This study represents the first approach in feline oncology that correlates p62 expression in feline mammary carcinoma. Our results, although preliminary, are similar to the results of human breast cancer, therefore, also in the cat, p62 could be considered a possible oncotarget.
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Romieu-Mourez, Raphaëlle, Dong W. Kim, Sang Min Shin, Elizabeth G. Demicco, Esther Landesman-Bollag, David C. Seldin, Robert D. Cardiff, and Gail E. Sonenshein. "Mouse Mammary Tumor Virus c-rel Transgenic Mice Develop Mammary Tumors." Molecular and Cellular Biology 23, no. 16 (August 15, 2003): 5738–54. http://dx.doi.org/10.1128/mcb.23.16.5738-5754.2003.
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ABSTRACT Amplification, overexpression, or rearrangement of the c-rel gene, encoding the c-Rel NF-κB subunit, has been reported in solid and hematopoietic malignancies. For example, many primary human breast cancer tissue samples express high levels of nuclear c-Rel. While the Rev-T oncogene v-rel causes tumors in birds, the ability of c-Rel to transform in vivo has not been demonstrated. To directly test the role of c-Rel in breast tumorigenesis, mice were generated in which overexpression of mouse c-rel cDNA was driven by the hormone-responsive mouse mammary tumor virus long terminal repeat (MMTV-LTR) promoter, and four founder lines identified. In the first cycle of pregnancy, the expression of transgenic c-rel mRNA was observed, and levels of c-Rel protein were increased in the mammary gland. Importantly, 31.6% of mice developed one or more mammary tumors at an average age of 19.9 months. Mammary tumors were of diverse histology and expressed increased levels of nuclear NF-κB. Analysis of the composition of NF-κB complexes in the tumors revealed aberrant nuclear expression of multiple subunits, including c-Rel, p50, p52, RelA, RelB, and the Bcl-3 protein, as observed previously in human primary breast cancers. Expression of the cancer-related NF-κB target genes cyclin D1, c-myc, and bcl-xl was significantly increased in grossly normal transgenic mammary glands starting the first cycle of pregnancy and increased further in mammary carcinomas compared to mammary glands from wild-type mice or virgin transgenic mice. In transient transfection analysis in untransformed breast epithelial cells, c-Rel-p52 or -p50 heterodimers either potently or modestly induced cyclin D1 promoter activity, respectively. Lastly, stable overexpression of c-Rel resulted in increased cyclin D1 and NF-κB p52 and p50 subunit protein levels. These results indicate for the first time that dysregulated expression of c-Rel, as observed in breast cancers, is capable of contributing to mammary tumorigenesis.
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Ren, Xiaoli, Yuying Fan, Yongqi Li, Dongmei Shi, and Yun Liu. "Clinicopathological analysis of expression of enhancer of zeste homologue 2 in canine mammary carcinoma." Journal of Veterinary Research 66, no. 2 (June 1, 2022): 267–72. http://dx.doi.org/10.2478/jvetres-2022-0033.
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Abstract Introduction Enhancer of zeste homologue 2 (EZH2) is the human homologue of Drosophila zeste gene enhancer. The aim of this study was to determine the expression of EZH2 in canine mammary carcinomas (CMCs) and its relationship with clinicopathological features. Material and Methods The expression of EZH2 mRNA and protein in 53 CMC tissue and 8 normal mammary gland tissue samples was measured by quantitative real-time PCR and immunohistochemical staining assay, respectively. The relationship between EZH2 protein expression and clinicopathological features was analysed by χ2 test to further explore the clinical significance of EZH2 in CMCs. Results Compared with normal mammary gland tissues, EZH2 mRNA expressions were significantly increased in CMC tissues (P < 0.01). Moreover, normal mammary glands did not express the EZH2 protein but carcinomic glands did, and expression increased in CMCs with high histological grades, especially in histological grade II (P < 0.05). However, EZH2 expression was not related to age, tumour size, or metastasis (P > 0.05). The expression of EZH2 in one type of CMC was not significantly different from the expression in any other type (P > 0.05). Conclusion EZH2 is highly expressed in CMCs, indicating that it can be used as a molecular marker for early diagnosis, prognosis, or therapy of CMCs.
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Kudo, Yasusei, Daniele Guardavaccaro, Patricia G. Santamaria, Ryo Koyama-Nasu, Esther Latres, Roderick Bronson, Lili Yamasaki, and Michele Pagano. "Role of F-Box Protein βTrcp1 in Mammary Gland Development and Tumorigenesis." Molecular and Cellular Biology 24, no. 18 (September 15, 2004): 8184–94. http://dx.doi.org/10.1128/mcb.24.18.8184-8194.2004.
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ABSTRACT The F-box protein βTrcp1 controls the stability of several crucial regulators of proliferation and apoptosis, including certain inhibitors of the NF-κB family of transcription factors. Here we show that mammary glands of βTrcp1−/− female mice display a hypoplastic phenotype, whereas no effects on cell proliferation are observed in other somatic cells. To investigate further the role of βTrcp1 in mammary gland development, we generated transgenic mice expressing human βTrcp1 targeted to epithelial cells under the control of the mouse mammary tumor virus (MMTV) long terminal repeat promoter. Compared to controls, MMTV βTrcp1 mammary glands display an increase in lateral ductal branching and extensive arrays of alveolus-like protuberances. The mammary epithelia of MMTV βTrcp1 mice proliferate more and show increased NF-κB DNA binding activity and higher levels of nuclear NF-κB p65/RelA. In addition, 38% of transgenic mice develop tumors, including mammary, ovarian, and uterine carcinomas. The targeting of βTrcp1 to lymphoid organs produces no effects on these tissues. In summary, our results support the notion that βTrcp1 positively controls the proliferation of breast epithelium and indicate that alteration of βTrcp1 function and expression may contribute to malignant behavior of breast tumors, at least in part through NF-κB transactivation.
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Kawaguchi, H., Y. Umekita, K. Fukuzaki, H. Maeda, H. Miyajima, R. Nagata, and H. Yoshida. "Expression of Androgen Receptor in Mammary Glands in Ovariectomized Cynomolgus Monkeys." Veterinary Pathology 46, no. 3 (January 27, 2009): 526–30. http://dx.doi.org/10.1354/vp.08-vp-0134-k-am.
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This study investigated structural alterations and the immunohistochemical expression of androgen receptor (AR), estrogen receptor (ER), and progesterone receptor (PgR) in the mammary glands from surgically postmenopausal cynomolgus monkeys ( Macaca fascicularis). Fourteen animals were divided into 2 groups. Seven animals underwent an ovariectomy (OVX), and the other 7 animals underwent a sham operation (sham). The in-life phase of study was 78 weeks. Atrophy in the mammary glands of OVX monkeys was similar to early postmenopausal atrophy of the human breast. The proportion of AR-positive cells in the OVX group was significantly higher than in the sham group, but the proportion of ER and PgR-positive cells was significantly lower. These results suggest that use of a primate model for hormone receptor expression has potential applications in basic human endocrinology, particularly in research in hormone receptor expression in mammary glands (both normal and neoplastic).
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Dinjens, W. N., J. ten Kate, E. P. van der Linden, J. T. Wijnen, P. M. Khan, and F. T. Bosman. "Distribution of adenosine deaminase complexing protein (ADCP) in human tissues." Journal of Histochemistry & Cytochemistry 37, no. 12 (December 1989): 1869–75. http://dx.doi.org/10.1177/37.12.2573631.
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The normal distribution of adenosine deaminase complexing protein (ADCP) in the human body was investigated quantitatively by ADCP-specific radioimmunoassay (RIA) and qualitatively by immunohistochemistry. In these studies we used a specific rabbit anti-human ADCP antiserum. In all 19 investigated tissues, except erythrocytes, ADCP was found by RIA in the soluble and membrane fractions. From all tissues the membrane fractions contained more ADCP (expressed per mg protein) than the soluble fractions. High membrane ADCP concentrations were found in skin, renal cortex, gastrointestinal tract, and prostate. Immunoperoxidase staining confirmed the predominant membrane-associated localization of the protein. In serous sweat glands, convoluted tubules of renal cortex, bile canaliculi, gastrointestinal tract, lung, pancreas, prostate gland, salivary gland, gallbladder, mammary gland, and uterus, ADCP immunoreactivity was found confined to the luminal membranes of the epithelial cells. These data demonstrate that ADCP is present predominantly in exocrine glands and absorptive epithelia. The localization of ADCP at the secretory or absorptive apex of the cells suggests that the function of ADCP is related to the secretory and/or absorptive process.
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Tada, T., I. Ohkubo, M. Niwa, M. Sasaki, H. Tateyama, and T. Eimoto. "Immunohistochemical localization of Zn-alpha 2-glycoprotein in normal human tissues." Journal of Histochemistry & Cytochemistry 39, no. 9 (September 1991): 1221–26. http://dx.doi.org/10.1177/39.9.1918940.
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The Zn-alpha 2-glycoprotein (Zn-alpha 2-GP) is present at a high concentration in the seminal plasma and at significant levels in other human body fluids. Its precise localization, however, has remained unclear, as well as its physiological and pathological significance. The present study reports the immunohistochemical localization of this protein in normal adult human tissues. Localization of the reactive product to anti-human plasma Zn-alpha 2-GP antibody was demonstrated in the following cells: luminal and basal cells of the prostate gland, luminal epithelial cells of the acini and of some ducts of the mammary glands, luminal cells of the secretory portion of the eccrine and apocrine sweat glands, serous cells of the salivary, tracheal, and bronchial glands, acinar cells of the esophageal glands, exocrine acinar cells of the pancreas, hepatocytes of the liver, and epithelial cells of the proximal and distal tubules in the kidney. The present results suggest that Zn-alpha 2-GP exerts some unknown but fairly widespread exocrine function and may be produced in the various epithelial cells tested. Hepatocytes are also suggested to be a source of the protein in the blood plasma.
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Palmieri, C., S. Saji, H. Sakaguchi, G. Cheng, A. Sunters, MJ O'Hare, M. Warner, JA Gustafsson, RC Coombes, and EW Lam. "The expression of oestrogen receptor (ER)-beta and its variants, but not ERalpha, in adult human mammary fibroblasts." Journal of Molecular Endocrinology 33, no. 1 (August 1, 2004): 35–50. http://dx.doi.org/10.1677/jme.0.0330035.
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Whilst oestrogen receptor (ER)-alpha and ERbeta have been shown to be important in the development of the mammary gland, the cell-specific expression pattern of these two receptors within the human breast is not clear. Although it is well established that in the developing rodent mammary gland stromal ERalpha mediates the secretion of growth factors which stimulate the proliferation of the ductal epithelium, the expression of ERalpha in human adult breast stromal fibroblasts is controversial, and the expression of ERbeta has not been properly defined. In the present study, we have evaluated the expression of ERalpha and ERbeta by immunohistochemistry in normal tissue samples, and in purified human breast fibroblasts by Western blotting, RT-PCR analysis and ligand-binding sucrose gradient assay. Our data clearly demonstrated that ERbeta variants, including ERbeta1, ERbeta2, ERbeta5, ERbetadelta and ERbetains, but not ERalpha, are expressed in human adult mammary fibroblasts. These results are supported by the findings that an ERbeta-selective ligand, BAG, but not the ERalpha high-affinity ligand oestradiol, can induce fibroblast growth factor-7 release and activate transcription from an oestrogen-responsive element promoter in these adult human mammary fibroblasts. Together, these observations revealed that, in the adult breast and in breast cancer, the proliferative signals derived from the stroma of adult mammary glands in response to oestrogen are not mediated by ERalpha and provide new insights into the nature of stromal-epithelial interactions in the adult mammary gland. In addition, the expression of these ERbeta variants in cells where there is no ERalpha suggested that these ERbeta splice forms may have functions other than that of modulating ERalpha activity.
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Farke, Carolin, Heinrich H. D. Meyer, Rupert M. Bruckmaier, and Christiane Albrecht. "Differential expression of ABC transporters and their regulatory genes during lactation and dry period in bovine mammary tissue." Journal of Dairy Research 75, no. 4 (August 14, 2008): 406–14. http://dx.doi.org/10.1017/s002202990800335x.
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ATP-binding cassette (ABC) transporters play a pivotal role in human physiology, and mutations in these genes often result in severe hereditary diseases. ABC transporters are expressed in the bovine mammary gland but their physiological role in this organ remains elusive. Based on findings in the context of human disorders we speculated that candidate ABC transporters are implicated in lipid and cholesterol transport in the mammary gland. Therefore we investigated the expression pattern of selected genes that are associated with sterol transport in lactating and nonlactating mammary glands of dairy cows. mRNA levels from mammary gland biopsies taken during lactation and in the first and second week of the dry period were analysed using quantitative PCR. Five ABC transporter genes, namely ABCA1, ABCA7, ABCG1, ABCG2 and ABCG5, their regulating genes LXRα, PPARγ, SREBP1 and the milk proteins lactoferrin and α-lactalbumin were assessed. A significantly enhanced expression in the dry period was observed for ABCA1 while a significant decrease of expression in this period was detected for ABCA7, ABCG2, SREBP1 and α-lactalbumin. ABCG1, ABCG5, LXRα, PPARγ and lactoferrin expression was not altered between lactation and dry period. These results indicate that candidate ABC transporters involved in lipid and cholesterol transport show differential mRNA expression between lactation and the dry period. This may be due to physiological changes in the mammary gland such as immigration of macrophages or the accumulation of fat due to the loss of liquid in the involuting mammary gland. The current mRNA expression analysis of transporters in the mammary gland is the prerequisite for elucidating novel molecular mechanisms underlying cholesterol and lipid transfer into milk.
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Gwyther, J., H. M. Gehring, and L. J. Parry. "282.Differential expression of the relaxin receptor (LGR7) in the mammary apparatus of the lactating tammar wallaby (Macropus eugenii)." Reproduction, Fertility and Development 16, no. 9 (2004): 282. http://dx.doi.org/10.1071/srb04abs282.
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Growth and development of the mammary apparatus (nipple and mammary gland) are important aspects of lactation. Macropodid marsupials can suckle young of two different ages simultaneously, a phenomenon known as asynchronous lactation. As a result, the type of milk produced and the structure of the two mammary glands supporting young of different ages vary considerably. A role for the peptide hormone relaxin in lactation has been demonstrated in relaxin receptor (LGR7)-deficient mice, which fail to deliver milk to their offspring due to impaired nipple development (1). This study investigated the distribution of LGR7 in the different mammary glands and nipples during asynchronous lactation in the tammar wallaby. The specific aim was to determine if the age of the pouch young influences LGR7 gene expression. Tissues were collected from the mammary apparatus sustaining the neonate and an older pouch young in the same mother, between Days 0 and 21 of lactation (n = 5/stage). A partial sequence (250-bp) of the tammar LGR7 was first obtained from a region close to the N-terminus of the soluble ectodomain, with 82% amino acid homology compared to the human LGR7 sequence. LGR7 gene expression was then measured by quantitative-PCR, using a TaqMan probe in the Opticon 2 thermal cycler (MJ Research, GeneWorks). Expression of LGR7 was upregulated in both the nipple and mammary gland supporting the neonate between 5 and 11 days after birth. There was no difference in LGR7 expression between these two tissues. However, LGR7 mRNA concentrations were significantly (P < 0.05: paired t-test) higher in the mammary apparatus supporting the neonate compared with that of the older young. These data suggest that a local stimulus, such as the continuous sucking by the neonate, may influence LGR7 expression in the mammary apparatus. (1) Krajnc-Franken et al. (2004) Mol. Cell. Biol. 24, 687–696.
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Hernandez, Laura L., Sean W. Limesand, Jayne L. Collier, Nelson D. Horseman, and Robert J. Collier. "The bovine mammary gland expresses multiple functional isoforms of serotonin receptors." Journal of Endocrinology 203, no. 1 (August 4, 2009): 123–31. http://dx.doi.org/10.1677/joe-09-0187.
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Recent studies in dairy cows have demonstrated that serotonergic ligands affect milk yield and composition. Correspondingly, serotonin (5-HT) has been demonstrated to be an important local regulator of lactational homeostasis and involution in mouse and human mammary cells. We determined the mRNA expression of bovine 5-HT receptor (HTR) subtypes in bovine mammary tissue (BMT) and used pharmacological agents to evaluate functional activities of 5-HT receptors. The mRNAs for five receptor isoforms (HTR1B, 2A, 2B, 4, and 7) were identified by conventional real-time (RT)-PCR, RT quantitative PCR, and in situ hybridization in BMT. In addition to luminal mammary epithelial cell expression, HTR4 was expressed in myoepithelium, and HTR1B, 2A, and 2B were expressed in small mammary blood vessels. Serotonin suppressed milk protein mRNA expression (α-lactalbumin and β-casein mRNA) in lactogen-treated primary bovine mammary epithelial cell (BMEC) cultures. To probe the functional activities of individual receptors, caspase-3 activity and expression of α-lactalbumin and β-casein were measured. Both SB22489 (1B antagonist) and ritanserin (2A antagonist) increased caspase-3 activity. Expression of α-lactalbumin and β-casein mRNA levels in BMEC were stimulated by low concentrations of SB224289, ritanserin, or pimozide. These results demonstrate that there are multiple 5-HT receptor isoforms in the bovine mammary gland, and point to profound differences between serotonergic systems of the bovine mammary gland and the human and mouse mammary glands. Whereas human and mouse mammary epithelial cells express predominately the protein for the 5-HT7 receptor, cow mammary epithelium expresses multiple receptors that have overlapping, but not identical, functional activities.
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Gong, Gui-Hua, Shu Han, Xiao-Ling Huang, Li-Ping Xie, Wei Zhang, Lei Xu, and You-Jia Hu. "The Expression of Recombinant Human Serum Albumin in the Mammary Gland of Transgenic Mice." Pharmaceutical Fronts 03, no. 01 (March 2021): e30-e37. http://dx.doi.org/10.1055/s-0041-1730985.
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AbstractHuman serum albumin (HSA) is widely used in the clinic for the treatment of several diseases in large amount each year. With the increasing demands of HSA in clinic and limited blood resource, recombinant HSA (rHSA) is becoming an attractive and alternative source for HSA production. In this study, we aimed to express rHSA in the mammary glands of transgenic mice by using a tissue-specific promoter and other regulatory elements. An rHSA expression vector was constructed bearing the cDNA and first intron of HSA under the control of bovine αs1-casein promoter with a 2 × chicken β-globin insulator in the front. Transgenic mice were generated and reverse transcription polymerase chain reaction showed that rHSA was expressed only in the mammary gland, indicating the tissue specificity of the bovine αs1-casein promoter in directing transgene transcription in transgenic mice. Enzyme-linked immunosorbent assay test showed that rHSA was successfully secreted into the milk of transgenic mice with the highest level at 1.98 ± 0.12 g/L. Our results indicate the ability of the bovine αs1-casein promoter to induce successful expression of rHSA in the mammary gland of transgenic mice.
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Vasiu, Iosif, Gabriele Meroni, Roman Dąbrowski, Piera Anna Martino, Asta Tvarijonaviciute, Mariola Bochniarz, Raul Alexandru Pop, Florinel Gheorghe Brudaşcă, and Nicodim Iosif Fiţ. "Aerobic Isolates from Gestational and Non-Gestational Lactating Bitches (Canis lupus familiaris)." Animals 11, no. 11 (November 14, 2021): 3259. http://dx.doi.org/10.3390/ani11113259.
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Mastitis is a complex and well-defined mammary gland pathology, and an emergency in bitches. In dogs, its prevalence is about 1% of all reported diseases and about 5.3% of all reproductive pathologies. Lactating bitches are naturally prone to developing mastitis since puppies can easily overstimulate the epidermal layer of nipples during feeding, facilitating bacterial colonization of the glands. This study aimed to describe the aerobic bacterial flora isolated from milk samples derived from a cohort of patients (n = 87) diagnosed with clinical mastitis (n = 29), subclinical mastitis (n = 17) and healthy mammary glands (n = 46). All of the patients underwent a gynecology consultation to diagnose mammary gland afflictions; physical examination results were coupled with traditional hematological findings. The milk samples were plated on specific microbiological media for bacterial isolation. Among the 162 milk samples analyzed, 93.2% (151/162) had a positive microbiological result, while 6.8% (11/162) were sterile. The bacteriological profile of the milk samples showed 47 different species. The most common bacterial families detected in healthy bitches and bitches with subclinical and clinical mastitis were the Staphylococcaceae, Enterobacteriaceae and Enterococcaceae families. The results indicated that half of the isolated bacteria are novel findings in dogs and that some of them are normal components of human milk.
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Sugino, Hitomi, and Yu Sawada. "Influence of S100A2 in Human Diseases." Diagnostics 12, no. 7 (July 20, 2022): 1756. http://dx.doi.org/10.3390/diagnostics12071756.
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S100 proteins are a family of low-molecular-weight proteins characterized by two calcium-binding sites with a helix-loop-helix (“EF-hand-type”) domain. The S100 family of proteins is distributed across various organs and can interact with diverse molecules. Among the proteins of the S100 family, S100 calcium-binding protein A2 (S100A2) has been identified in mammary epithelial cells, glands, lungs, kidneys, and prostate gland, exhibiting various physiological and pathological actions in human disorders, such as inflammatory diseases and malignant tumors. In this review, we introduce basic knowledge regarding S100A2 regulatory mechanisms. Although S100A2 is a tumor suppressor, we describe the various influences of S100A2 on cancer and inflammatory diseases.
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Espinosa de los Monteros, A., M. Y. Millán, J. Ordás, L. Carrasco, C. Reymundo, and J. Martín de las Mulas. "Immunolocalization of the Smooth Muscle-Specific Protein Calponin in Complex and Mixed Tumors of the Mammary Gland of the Dog: Assessment of the Morphogenetic Role of the Myoepithelium." Veterinary Pathology 39, no. 2 (March 2002): 247–56. http://dx.doi.org/10.1354/vp.39-2-247.
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The immunohistochemical expression of the smooth muscle-specific protein calponin was studied to assess the contribution of myoepithelial cells to the histogenesis of spindle cells of complex and mixed tumors of the mammary gland of the dog and the origin of cartilage and bone in mixed tumors. Formalin-fixed tissues from 55 benign and malignant tumors (49 also containing surrounding normal mammary gland) were evaluated. Periacinar and periductal myoepithelial cells of all the 49 normal mammary glands were diffusely stained by the anti-human calponin monoclonal antibody. Calponin was found in 53 (98%) of the tumors studied, reacting with the myoepithelium-like cells of 86% of benign tumors and their remnants in 85% of malignant tumors. Five different types of calponin-immunoreactive myoepithelial cells were identified: hypertrophic myoepithelial cells, fusiform cells, stellate myoepithelial cells, rounded (myoepithelial) cells, and chondroblasts. Differences in staining intensity and staining pattern among these five types of cells suggested a transition of myoepithelial cells to chondroblasts. Stromal myofibroblasts also showed calponin immunoreactivity, but they did not react with a cytokeratin 14 monoclonal antibody, which recognizes myoepithelial cells in mammary gland. Calponin appears to be a very sensitive marker of normal and neoplastic myoepithelium in the canine mammary gland, and its identification in different cell types of complex and mixed tumors of the mammary gland of the dog suggests a major histogenetic role for myoepithelial cells.
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Lopez, Veronica, and Shannon L. Kelleher. "Zinc transporter-2 (ZnT2) variants are localized to distinct subcellular compartments and functionally transport zinc." Biochemical Journal 422, no. 1 (July 29, 2009): 43–52. http://dx.doi.org/10.1042/bj20081189.
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ZnT2 (zinc transporter-2) expression is restricted to tissues with unique zinc requirements such as mammary and prostate glands. We previously determined that ZnT2 plays a major role in zinc export from mammary glands, as women with a mutation in the gene encoding ZnT2 (SLC30A2) had an ∼75% reduction in milk zinc concentration. Two distinct human ZnT2 isoforms (∼42 and 35 kDa) are predicted to result from alternative splicing of SLC30A2. We examined the localization and function of each ZnT2 isoform, in cells generated to express ZnT2–HA (haemagglutinin) fusion proteins. The 42 kDa isoform was localized primarily to the endosomal/secretory compartment and overexpression resulted in increased zinc vesicularization. In contrast, the 35 kDa isoform is associated with the plasma membrane. Importantly, zinc transport was higher in cells over-expressing each isoform, indicating that both proteins are functional. Endogenous expression of the secretory vesicle-associated ZnT2 isoform predominates in mammary cells and expression is higher in secreting cells, whereas the smaller isoform plays a minor role in zinc export, directly reflecting the secretory function of the mammary gland. Together our data shed further light on the complex integration of cellular zinc transport mechanisms, which may be facilitated by multiple isoforms of specific zinc transporters with unique cellular functions.
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Sfacteria, A., G. Mazzullo, C. Bertani, P. Calabrò, G. De Vico, and B. Macrì. "Erythropoietin Receptor Expression in Canine Mammary Tumor: An Immunohistochemical Study." Veterinary Pathology 42, no. 6 (November 2005): 837–40. http://dx.doi.org/10.1354/vp.42-6-837.
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Erythropoietin (EPO) is a cytokine primarily involved in the regulation of the erythropoiesis. Recently, it has been demonstrated that EPO and its receptor (EPOR) are expressed in several neoplastic cell lines and solid tumors. Furthermore, in vitro and in vivo studies have shown that EPO could promote human breast carcinoma growth by means of the binding with its receptor, although a clear function for EPO in this setting has not been yet established. While the human medical literature has been accumulating strong evidence on EPO's role in oncogenesis, to date, there are no veterinary reports focusing on such an issue. The aim of the present study was to investigate the immunohistochemical expression of EPOR in canine mammary gland dysplastic and neoplastic lesions. Our results show a weak to moderate EPOR expression in dysplastic glands, being immunoreactivity enhanced as the lesion shows an increasing malignant pattern. On the basis of these findings, this study describes, for the first time, the evidence for EPOR expression in canine mammary gland tumor and suggests a feasible EPO's role for canine mammary tumor progression.
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Blanchard, Anne, Barbara Iwasiow, Alison Yarmill, Agnes Fresnosa, Josef Silha, Yvonne Myal, Leigh C. Murphy, Michel Chrétien, Nabil Seidah, and Robert P. C. Shiu. "Targeted production of proprotein convertase PC1 enhances mammary development and tumorigenesis in transgenic miceThis article is one of a selection of papers published in a special issue celebrating the 125th anniversary of the Faculty of Medicine at the University of Manitoba." Canadian Journal of Physiology and Pharmacology 87, no. 10 (October 2009): 831–38. http://dx.doi.org/10.1139/y09-073.
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Elevated production of proprotein convertases (PCs), proteolytic enzymes that posttranslationally modify the biological activities of diverse groups of cellular proteins, is a common occurrence in human breast carcinomas. A transgenic mouse model was developed to gain insight into the significance of PC production in breast development and neoplasia. Mammary epithelium-specific and early expression of PC1 was targeted by the use of the mouse mammary tumor virus promoter/enhancer. Whole-mount examinations revealed that the mammary glands of 83-day-old virgin PC1 transgenic mice exhibited an accelerated lobuloalveolar development compared with that of age-matched wild-type mice (p < 0.001). This phenotypic change was accompanied by extensive alterations in gene expression assessed by gene expression microarray analyses. Pathway analysis of PC1-induced alterations in gene expression has revealed possible mechanism of action of PC1 in the mammary gland. PC1 expression alone, however, did not promote spontaneous mammary tumorigenesis in the transgenic mice. PC1 transgene expression resulted in a significantly higher incidence (p = 0.008) and accelerated growth (p = 0.023) of 7,12-dimethylbenz[a]anthracene (DMBA)-induced mammary adenocarcinomas. The present study therefore shows that PC1 expression can promote normal and neoplastic mammary development and growth and suggests that proprotein convertases may be important etiological factors in human breast neoplasia.
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Lanz, Rainer B., Steven S. Chua, Niall Barron, Bettina M. Söder, Francesco DeMayo, and Bert W. O'Malley. "Steroid Receptor RNA Activator Stimulates Proliferation as Well as Apoptosis In Vivo." Molecular and Cellular Biology 23, no. 20 (October 15, 2003): 7163–76. http://dx.doi.org/10.1128/mcb.23.20.7163-7176.2003.
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ABSTRACT Steroid receptor RNA activator (SRA) is an RNA that coactivates steroid hormone receptor-mediated transcription in vitro. Its expression is strongly up-regulated in many human tumors of the breast, uterus, and ovary, suggesting a potential role in pathogenesis. To assess SRA function in vivo, a transgenic-mouse model was generated to enable robust human SRA expression by using the transcriptional activity of the mouse mammary tumor virus long terminal repeat. Transgenic SRA was expressed in the nuclei of luminal epithelial cells of the mammary gland and tissues of the male accessory sex glands. Distinctive evidence for SRA function in vivo was obtained from the elevated levels of estrogen-controlled expression of progesterone receptor in transgenic mammary glands. Although overexpression of SRA showed strong promoting activities on cellular proliferation and differentiation, no alterations progressed to malignancy. Epithelial hyperplasia was accompanied by increased apoptosis, and preneoplastic lesions were cleared by focal degenerative transformations. In bitransgenic mice, SRA also antagonized ras-induced tumor formation. This work indicates that although coactivation of steroid-dependent transcription by SRA is accompanied by a proliferative response, overexpression is not in itself sufficient to induce turmorigenesis. Our results underline an intricate relationship between the different physiological roles of steroid receptors in conjunction with the RNA activator in the regulation of development, tissue homeostasis, and reproduction.
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Fidianingsih, Ika, Teguh Aryandono, Sitarina Widyarini, and Sri Herwiyanti. "Profile of Histopathological Type and Molecular Subtypes of Mammary Cancer of DMBA-induced Rat and its Relevancy to Human Breast Cancer." Open Access Macedonian Journal of Medical Sciences 10, A (January 18, 2022): 71–78. http://dx.doi.org/10.3889/oamjms.2022.7975.
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BACKGROUND: Animal models with mammary cancer that closely mimic human breast cancer for treatment development purposes are still required. Induction of 7,12-dimethylbenzanthracene (DMBA) to rats shows the histopathological features and mammary cancer characterization similar to humans. Examinations of estrogen receptor (ER), progesterone receptor (PR), human epidermal growth factor receptor 2 (HER2), and Ki67 expressions are crucial in deciding the treatment and prognosis of breast cancer. AIM: This research aimed to view histopathology images of mammary glands and expressions of ER, PR, Ki67, and HER2 of DMBA-induced rats. METHODS: After 1-week adaptation, 11 5-weeks-old female rats were induced with 20 mg/kg body weight (BW) of DMBA 2 times a week for 5 weeks. On week 29, nodules taken from the mammary gland were examined for hematoxylin-eosin staining and immunohistochemistry with p63, ER, PR, HER2, and Ki67 antibodies. The grading score used the Nottingham Grading System and molecular classifications based on St. Gallen 2013. RESULTS: Six rats had nodules, but the histopathologic features of one nodule showed normal mammary gland without cancer. The histopathological type of mammary cancer was cribriform carcinoma, comedo carcinoma, lipid-rich carcinoma, adenocarcinoma squamous, and adenomyepithelioma. Histopathological grading showed 60% of grade 3 and 40% of grade 2. P63 expression showed 60% positive and 40% negative. The frequency of ER, PR, HER2, and Ki67 of five nodules showed positivity: 40%, 60%, 60%, and 60%, respectively. Molecular subtypes of Luminal A, B, HER2, and triple-negative were 0%, 60%, 20%, and 20%, respectively. CONCLUSION: Histopathological features and molecular subtype of mammary cancer on rats induced with 20 mg/kg BW of DMBA showed similarity to human breast cancer.
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Kalirai, H., and R. B. Clarke. "Review of: Proliferation of estrogen receptor-alpha-positive mammary epithelial cells is restrained by transforming growth factor-beta1 in adult mice." Breast Cancer Online 9, no. 6 (May 12, 2006): 1–3. http://dx.doi.org/10.1017/s1470903106005086.
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Citation of original article:K. B. Ewan, H. A. Oketch-Rabah, S. A. Ravani, G. Shyamala, H. L. Moses, M. H. Barcellos-Hoff. Proliferation of estrogen receptor-alpha-positive mammary epithelial cells is restrained by transforming growth factor-beta1 in adult mice.American Journal of Pathology2005;167(2): 409–17.Abstract of the original article:Transforming growth factor (TGF)-beta1 is a potent inhibitor of mammary epithelial proliferation. In human breast, estrogen receptor (ER)-alpha cells rarely co-localize with markers of proliferation, but their increased frequency correlates with breast cancer risk. To determine whether TGF-beta1 is necessary for the quiescence of ER-alpha-positive populations, we examined mouse mammary epithelial glands at estrus. Approximately, 35% of epithelial cells showed TGF-beta1 activation, which co-localized with nuclear receptor-phosphorylated Smad 2/3, indicating that TGF-beta signaling is autocrine. Nuclear Smad co-localized with nuclear ER-alpha. To test whether TGF-beta inhibits proliferation, we examined genetically engineered mice with different levels of TGF-beta1. ER-alpha co-localization with markers of proliferation (i.e., Ki-67 or bromodeoxyuridine) at estrus was significantly increased in the mammary glands of TGF-beta1 C57/bl/129SV heterozygote mice. This relationship was maintained after pregnancy but was absent at puberty. Conversely, mammary epithelial expression of constitutively active TGF-beta1 via the MMTV promoter suppressed proliferation of ER-alpha-positive cells. Thus, TGF-beta1 activation functionally restrains ER-alpha-positive cells from proliferating in adult mammary gland. Accordingly, we propose that TGF-beta1 dysregulation may promote proliferation of ER-alpha-positive cells associated with breast cancer risk in humans.
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Zaichick, V., and G. A. Davydov. "MEASUREMENT OF SOME CHEMICAL ELEMENTS IN NORMAL HUMAN BREAST TISSUE BY NEUTRON-ACTIVATION ANALYSIS." MEDICAL RADIOLOGY AND RADIATION SAFETY 67, no. 2 (April 2022): 64–68. http://dx.doi.org/10.33266/1024-6177-2022-67-2-64-68.
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Purpose: To develop the method of chemical element (ChE) content measurement in samples of breast tissue (BT) using the activation by neutrons of nuclear reactor combined with the high-resolution spectrometry of gamma-radiation of short-lived radionuclides (INAA-SLR), and to investigate ChE contents in normal human mammary gland. Material and methods: In the samples of BT taken from female with intact mammary glands (mostly died from trauma, n = 38) the contents of calcium (Ca), chlorine (Cl), iodine (I), potassium (K), magnesium (Mg), manganese (Mn), sodium (Na), and strontium (Sr) were measured. To determine these element contents, the method of INAA-SLR was developed. Results: The accuracy of the developed method and the reliability of the results obtained in the study were confirmed by the measurements of international certified reference material IAEA H-4 Animal Muscles and the good agreement with data of its certificate. The main statistic parameters, including, arithmetic mean, standard deviation, standard error of mean, minimum and maximum values, median, percentiles with 0.025 and 0.975 levels was calculated for ChE contents in the normal BT. It was shown, for example, that means of mass fractions ± standard errors of means (M±SEM, mg/kg dry tissue) in normal human mammary gland were: Ca 128±14, Cl 1014±146, I 0,82±0,11, K 196±20, Mg 80,0±9,4, Mn 0,27±0,04, Na 665±71 и Sr 5,20±0,75. It was found that the Ca, Cl, I, K, Mg, Mn, Na и Sr contents in human mammary gland very differ from the normal level of these elements in whole blood, muscle and adipose tissue, particularly in contents of I and Sr. Conclusion: The method of INAA-SLR allow to obtain the representative data on Ca, Cl, I, K, Mg, Mn, Na и Sr contents in human BT specimen. It was shown, that such trace elements as I and Sr may be directly involved in the mammary gland function.
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Della Libera, A. M. M. P., W. P. de Araújo, M. G. Blagitz, C. R. Bastos, M. R. Azedo, and A. de S. Traldi. "MASTITIS AFTER INDUCED MAMMOGENESIS IN A NULLIPAROUS GOAT." Arquivos do Instituto Biológico 74, no. 1 (January 3, 2007): 29–31. http://dx.doi.org/10.1590/1808-1657v74p0292007.
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ABSTRACT This is a case report on a nulliparous Toggenbourg goat, one year of age that, after being submitted to superovulation with human menopause gonadotrophin, presented mammogenesis and lactogenesis. Both neoformed mammary glands were naturally infected with β-hemolytic Staphylococcus aureus and evolved clinically in different forms. The left half evolved to acute catarrhal mastitis that responded positively to treatment using sodium cloxacillin, whereas right mammary gland evolved to phlegmonous gangrenous mastitis, with teat loss. The mammary tissue remaining had to be surgically removed. The present report emphasizes that multi-tissue effect should not be ignored when hormonal therapy is used. The potential risk of induced mammogenesis in nulliparous animals and the nosological diversity that mastitis may present should be considered, once the etiological agent and host were the same, and different inflammatory responses were observed in the two halves.
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Kinoshita, Yuichi, Katsuhiko Yoshizawa, Yuko Emoto, Michiko Yuki, Takashi Yuri, Nobuaki Shikata, and Airo Tsubura. "Similarity of GATA-3 Expression between Rat and Human Mammary Glands." Journal of Toxicologic Pathology 27, no. 2 (2014): 159–62. http://dx.doi.org/10.1293/tox.2014-0008.
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