Relevant bibliographies by topics / Human Mammary Glands

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Human Mammary Glands'

Author: Grafiati
Published: 4 June 2021
Last updated: 24 February 2023

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Journal articles on the topic "Human Mammary Glands"

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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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Dissertations / Theses on the topic "Human Mammary Glands"

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Chang, Cheng. "Function and Regulation of the α6 Integrins in Mammary Epithelial Biology and Breast Cancer: A Dissertation." eScholarship@UMMS, 2015. http://escholarship.umassmed.edu/gsbs_diss/734.

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Integrins have the ability to impact major aspects of epithelial biology including adhesion, migration, invasion, signaling and differentiation, as well as the formation and progression of cancer (Hynes 2002; Srichai and Zent 2010; Anderson et al. 2014). This thesis focuses on how integrins are regulated and function in the context of mammary epithelial biology and breast cancer with a specific focus on the α6 integrin heterodimers (α6β1 and α6β4). These integrins function primarily as receptors for the laminin family of extracellular matrix (ECM) proteins and they have been implicated in mammary gland biology and breast cancer (Friedrichs et al. 1995; Wewer et al. 1997; Mercurio et al. 2001; Margadant and Sonnenberg 2010; Muschler and Streuli 2010; Nistico et al. 2014). The first project investigates how alternative splicing of the α6 subunit impacts the genesis and function of breast cancer stem cells (CSCs). This work revealed that the α6Bβ1 splice variant, but not α6Aβ1, is necessary for the function of breast CSCs because it activates the Hippo transducer TAZ (Zhao et al. 2008a), which is known to be essential for breast CSCs (Cordenonsi et al. 2011). My work also led to the discovery that laminin (LM) 511 is the specific ligand for α6Bβ1 and that autocrine LM511, which is mediated by TAZ, is needed to sustain breast CSCs by functioning as a ‘ECM niche’. An important aspect of this study is the finding that surface-bound LM511 characterizes a small population of cells in human breast tumors with CSC properties. The second project of my thesis concentrated on identifying transcription factors that regulate expression of the β4 subunit. The expression of the α6β4 integrin is repressed during the epithelial-mesenchymal transition (EMT) (Yang et al. 2009) but the contribution of specific transcription factors to this repression is poorly understood. This study revealed that Snai1 is a transcriptional repressor of β4, which is responsible for establishing the PRC2 (Polycomb complex 2)- associated repressive histone mark H3K27Me3. However, I also found that the ability of Snai1 to repress transcription is abrogated by its interaction with Id2. Specifically, I identified the biochemical mechanism for how Id2 regulates Snai1. Id2 binds the SNAG domain of Snai1 that is the docking site for several corepressors (Peinado et al. 2004; Lin et al. 2010b; Dong et al. 2012a). One important consequence of Id2 interacting with Snai1 on the β4 promoter is that it prevents repressive epigenetic modifications. This finding may explain why some epithelial cells express Snai1 and β4 because they also express Id2 (Vincent et al. 2009; Bastea et al. 2012). The repression of the α6β4 integrin during the EMT is consistent with data indicating that this integrin is not expressed in CSCs (Mani et al. 2008; Goel et al. 2012; Goel et al. 2013; Goel et al. 2014). An important question going forward is to understand how the α6β4 integrin contributes to tumor formation. In summary, my thesis provides novel insights into the biology of the α6 integrins that has important implications for the function of these integrins in mammary gland biology and breast cancer, especially our understanding of breast CSCs.
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Ogba, Ndiya. "Transcriptional Regulation Of Estrogen Receptor Alpha Target Genes By Hexamethylene Bisacetamide-Inducible Gene 1 (HEXIM1) And Its Role In Mammary Gland Development And Breast Cancer." Cleveland, Ohio : Case Western Reserve University, 2010. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1258406511.

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Tunzi, Christina R. "Defensins, endogenous antibiotic peptides in the human mammary gland." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape9/PQDD_0005/MQ46148.pdf.

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Kwok, Bruce Chia-Wah. "Characterization on OCTN1 and OCTN2 in the human mammary gland." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/MQ63172.pdf.

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Wang, Qian. "Regulation of sodium transport across epithelia derived from human mammary gland." Diss., Kansas State University, 2014. http://hdl.handle.net/2097/17600.

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Doctor of Philosophy
Department of Anatomy and Physiology
Bruce D. Schultz
The first aim of this project is to define the cellular mechanisms that account for the low Na[superscript]+ concentration in human milk. MCF10A cells, which were derived from human mammary epithelium and grown on permeable supports, exhibit amiloride- and benzamil-sensitive short circuit current (I[subscript]sc), suggesting activity of the epithelial Na[superscript]+ channel, ENaC. When cultured in the presence of cholera toxin (Ctx), MCF10A cells exhibit greater amiloride sensitive I[subscript]sc at all time points tested, an effect that is not reduced with Ctx washout for 12 hours or by cytosolic pathways inhibitors. Ctx increases the abundance of both beta and gamma-ENaC in the apical membrane and increases its monoubiquitination but without changing total protein and mRNA levels. Additionally, Ctx increases the levels of both the phosphorylated and the nonphosphorylated forms of Nedd4-2, a ubiquitin-protein ligase that regulates ENaC degradation. The results reveal a novel mechanism in human mammary gland epithelia by which Ctx regulates ENaC-mediated Na[superscript]+ transport. The second project aim is to develop a protocol to isolate mammary gland epithelia for subsequent in vitro culture. Caprine (1[superscript]0CME) and bovine mammary epithelia (1[superscript]0BME) were isolated and cultured on permeable supports to study hormone- and neurotransmitter-sensitive ion transport. Both 1[superscript]0CME and 1[superscript]0BME cells were passed for multiple subcultures and all passages formed electrically tight barriers. 1[superscript]0CME were cultured in the presence of hydrocortisone and exhibited high electrical resistance and amiloride-sensitive I[subscript]sc, suggesting the presence of ENaC-mediated Na[superscript]+ transport. 1[superscript]0BME were grown in a complex media in the presence or absence of dexamethasone. In contrast to 1[superscript]0CME, 1[superscript]0BME exhibited no detectable amiloride-sensitive I[subscript]sc in either culture condition. However, 1[superscript]0BME monolayers responded to an adrenergic agonist, norepinephrine, and a cholinergic agonist, carbamylcholine, with rapid increases in I[subscript]sc. Thus, this protocol for isolation and primary cell culture can be used for future studies that focus on mammary epithelial cell regulation and functions. In conclusion, the results from these projects demonstrate that mammary epithelial cells form electrically tight monolayers and can exhibit neurotransmitter- and/or hormone-induced net ion transport. The mechanisms that regulate Na[superscript]+ transport across mammary gland may provide clues to prevent or treat mastitis.
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Clément, Flora. "Regulating human mammary epithelial stem cells transformation : an interplay between extrinsic and intrinsic signals." Thesis, Lyon, 2017. http://www.theses.fr/2017LYSE1078.

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L'incidence, le coût et l'issue fatale dans un nombre encore trop élevé de cas font du cancer un problème majeur en santé publique. Malgré les progrès réalisés dans le développement de thérapies ciblées, la plupart des cancers rechutent, vraisemblablement à cause de l'échappement des cellules souches cancéreuses (CSC) qui survivent et régénèrent la tumeur. L'enjeu clinique en cancérologie aujourd'hui est d'éliminer les cellules souches cancéreuses en épargnant les cellules souches normales. Pour atteindre cet objectif, il est primordial de comprendre leurs mécanismes spécifiques de transformation. Nous évaluons dans mon équipe de recherche l'implication du microenvironnement dans la transformation et la résistance des CSC épithéliales, à travers les effets de facteurs solubles et de contacts cellulaires : l'enzyme CD10, et la voie des BMPs (Bone Morphogenetic Proteins).Notre équipe étudie le rôle du dialogue permanent entre la CS normale et son microenvironnement qui régule la prolifération, et la survie des CS. Nous utilisons la glande mammaire et la prostate comme systèmes modèles car ces deux types d'épithélium présentent des similitudes, ce qui nous permet d'aborder la question de l'apparition et la résistance des CSC dans deux modèles tumoraux correspondants. Des dérégulations de la voie des BMPs, comme de l'enzyme CD10 sont observées dans ces tumeurs. Enfin, nous cherchons à comprendre comment les dérégulations de la voie des BMPs apparaissent, en s'intéressant principalement aux facteurs pouvant modifier directement le microenvironnement, tels que les polluants présents dans l'environnement (bisphénols, benzoapyrène)
It has been shown for a number of cancers that a cell population characterized by stem cell (SC) properties and therapeutic resistance is likely responsible for relapse several years after treatment. Current therapies kill most of the tumor cells, but fail to eradicate the so-called cancer stem cells (CSC). Therefore a complete cure of the disease will require the eradication of the tumor-sustaining CSC. We propose to study these CSC in the context of breast cancer as the existence of CSC as already been highlighted in this epithelia.CD10 is a membrane enzyme able to cleave several peptide of the microenvironment (such as oxytocin, bombesin, enkephalin.. ) that can also interact with intracellular signalling pathway through its direct interaction with PTEN. Our results, and those of the literature, indicate that CD10 enzyme controls the fate of SC and is deregulated in normal breast and cancerous tissues. We showed that CD10 membrane expression allows the maintenance of immature cells partly through its enzymatic function that inhibits mammary stem cells differentiation. As CD10 has been described in breast cancer initiation, progression and resistance, we then decided to test the role of CD10 in tumor context. Our strategy consists in flow cytometry cell sorting for CD10+/CD10- cells to compare the functional properties of both sub-population. Only CD10+ cells are able to regenerate both CD10+ and CD10- subpopulations, and CD10+ cells exhibit higher expression of immature genes. Interestingly, modulating CD10 using stable expression of CD10 in our models and Sh strategies do not mimick the normal functions of CD10, indicating that CD10 could be more a marker of a certain population with immature properties prone to transformation rather than a driver. To better characterize the role of CD10 in luminal breast transformation, we developed a new human mammary model, initiated from immature cells to obtain transformed luminal epithelial cells and their resistant counterpart. We observed a higher level of CD10 expression during mammary epithelial cell transformation process. We then performed a microarray on CD10+ and CD10- subpopulations. Preliminary analysis seems to confirm that CD10 is a potential marker for a stem cell population prone to transformation rather than a direct driver of the cell transformation
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Chiche, Aurélie. "Etude des cellules souches et progénitrices mammaires et de leur contribution à la tumorigenèse : rôle des facteurs de transcription Myc et p53." Phd thesis, Université Paris Sud - Paris XI, 2012. http://tel.archives-ouvertes.fr/tel-00924981.

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L'épithélium mammaire est organisé en bicouche : une couche de cellules luminales sécrétrices et une couche de cellules basales myoépithéliales. Des cellules souches multipotentes capables de régénérer l'épithélium mammaire après transplantation résident dans le compartiment basal tandis que les deux couches épithéliales mammaires contiennent des cellules souches/progénitrices à propriétés clonogéniques. De nombreuses études suggèrent que les cellules souches et progénitrices de la glande mammaire pourraient être les cibles d'une transformation oncogénique menant à des cancers du sein, justifiant l'attention particulière portée à ces populations cellulaires mineures.Pour étudier les rôles du proto-oncogène Myc, ou du suppresseur de tumeurs Trp53, dans le contrôle des fonctions des cellules souches et progénitrices, nous avons généré des souris transgéniques présentant une invalidation de Myc ou Trp53 dans la couche basale de l'épithélium mammaire. Les souris déficientes en Myc présentent des glandes hypoplasiques et les cellules basales dépourvues de Myc perdent complètement leur capacité régénérative. En revanche, la perte de p53 induit une augmentation des populations de cellules souches et progénitrices avec un potentiel d'autorenouvellement accru, suggérant que p53 restreint la propagation des cellules souches/progénitrices dans l'épithélium mammaire. Ces résultats montrent que Myc et p53 jouent un rôle essentiel dans le contrôle des fonctions des cellules souches et progénitrices mammaires.Les souris transgéniques K5Ncat générées précédemment dans notre laboratoire, développent des carcinomes mammaires de type basal avec des composants métaplastiques, induits par l'expression d'une forme activée de la -caténine dans la couche basale mammaire. Nous avons trouvé que la population de cellules souches fonctionnelles est augmentée dans l'épithélium pré-néoplasique des souris K5Ncat. Pour étudier les mécanismes cellulaires et moléculaires du développement de ces tumeurs, les souris déficientes en Myc ou Trp53 ont été croisées avec des souris K5Ncat. Nous avons constaté une inhibition complète de la tumorigenèse induite par la -caténine en absence de Myc et une accélération de celle-ci en absence de p53. Nos résultats suggèrent que les cellules souches/progénitrices basales pourraient être à l'origine des tumeurs mammaires de type basal avec des caractéristiques métaplastiques et que les rôles joués par Myc et p53 dans la tumorigenèse sont liés à leurs fonctions régulatrices des cellules souches mammaires.
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Butler, Stephen P. "Production and Secretion of Recombinant Human Fibrinogen by the Transgenic Murine Mammary Gland." Thesis, Virginia Tech, 1997. http://hdl.handle.net/10919/36776.

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The mammary gland of lactating transgenic animals has several advantages for production of heterologous proteins including a high cell density that results in high concentrations of secreted protein and the ability to perform several types of post-translational modifications. Transgenes were constructed from the 4.1 kbp murine Whey Acidic Protein promoter (mWAP) and the three cDNAs coding for the Aα, Bβ and γ fibrinogen chains to evaluate the requirements of the transgenic murine mammary gland for high level secretion of fully assembled human fibrinogen. After introducing the constructs into the murine zygotes by microinjection, secretion of fully assembled fibrinogen into milk was measured at concentrations between 10 ug/ml to 200 ug/ml. In one line of mice the total secretion of fibrinogen and unassembled subunits approached 700 ug/ml in milk. The level of assembled fibrinogen was proportional to the lowest amount of subunit produced where both the Bβ and γ chains were rate limiting. Also, the subunit complexes γ₂, Aαγ₂ and the individual subunits Aα, Bβ and γ were found as secretion products. This is the first time that secretion of individual Bβ-subunits by any cell type has been reported and suggests the organization of the secretion pathway in mammary epithelia is different from that in liver. Glycosylated forms of individual Bβ-chain contained a complex saccharide with low mannose. Glycosylation of the γ-chain was also observed. These results suggest the 4.1 mWAP promoter can drive expression of fibrinogen cDNAs to high levels and that the amount of fully assembled fibrinogen secreted is equal to the level of the lowest expressing chain.
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Dhillon, Upinder. "The function and expression of the human organic cation transporters, hOCT1 and hOTC2, in mammary gland." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape9/PQDD_0005/MQ46140.pdf.

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Burchell, J. M. "Use of monoclonal antibodies in the study of differentiation and malignancy of the human mammary gland." Thesis, Institute of Cancer Research (University Of London), 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.370166.

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Books on the topic "Human Mammary Glands"

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Tavassoli, Fattaneh A. Tumors of the mammary gland. Washington, D.C: American Registry of Pathology in collaboration with the Armed Forces Institute of Pathology, 2009.

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Kwok, Bruce Chia-Wah. Characterization of OCTN1 and OCTN2 in the human mammary gland. Ottawa: National Library of Canada, 2001.

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Clarke, Robert Bryan. The control of proliferation in the normal and neoplastic human mammary gland. Manchester: University of Manchester, 1995.

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Dhillon, Upinder. The function and expression of the human organic cation transporters, HOCT1 and hOTC2, in mammary gland. Ottawa: National Library of Canada, 1999.

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L, Larson Bruce. Mammary Gland / Human Lactation / Milk Synthesis. Elsevier Science & Technology Books, 2013.

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Defensins: Endogenous antibiotic peptides in the human mammary gland. Ottawa: National Library of Canada, 1999.

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Kraemer, Jennifer Marie. Glyburide transport in the human mammary gland and the placenta: Implications for developmental toxicology. 2005.

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Kraemer, Jennifer Marie. Glyburide transport in the human mammary gland and the placenta: Implications for developmental toxicology. 2005.

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Book chapters on the topic "Human Mammary Glands"

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Alekseev, Nikolai Petrovitch. "Origin and Development of the Mammary Glands." In Physiology of Human Female Lactation, 11–66. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-66364-3_2.

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Kim, Sun Jung, Dae-Yeul Yu, Yong-Mahn Han, Chul-Sang Lee, and Kyung-Kwang Lee. "Cloning of Human Genomic Lactoferrin Sequence and Expression in the Mammary Glands of Transgenic Animals." In Advances in Lactoferrin Research, 79–83. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4757-9068-9_9.

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Huff, Dale S. "Mammary Gland." In Color Atlas of Human Fetal and Neonatal Histology, 385–95. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-11425-1_35.

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Russo, Jose, and Irma H. Russo. "Development of the Human Mammary Gland." In The Mammary Gland, 67–93. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4899-5043-7_3.

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Neifert, Marianne R., and Joy M. Seacat. "Mammary Gland Anomalies and Lactation Failure." In Human Lactation 2, 293–99. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4615-7207-7_26.

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Castro, Fidel Ovidio, Alina Rodríguez, José Limonta, Alina Aguirre, and José de la Fuente. "Selection of Genes for Expression in Milk: The Case of the Human Erythropoietin Gene." In Mammary Gland Transgenesis, 91–106. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-662-03372-2_6.

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Forsman, C. L., and K. L. Schwertfeger. "Mammary gland development and structure: an overview." In Handbook of dietary and nutritional aspects of human breast milk, 15–34. The Netherlands: Wageningen Academic Publishers, 2013. http://dx.doi.org/10.3920/978-90-8686-764-6_1.

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Clarke, Catherine, Paul Monaghan, and Michael J. O’Hare. "High Density Culture of Immuno-Magnetically Separated Human Mammary Luminal Cells." In Intercellular Signalling in the Mammary Gland, 75–76. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1973-7_11.

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Loomes, Kerry M. "Human Bile Salt-Activated Lipase: Structural Organisation at the C-Terminus." In Intercellular Signalling in the Mammary Gland, 179–80. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1973-7_36.

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Alekseev, Nikolai Petrovitch. "The Structure of the Lactating Mammary Gland of a Woman." In Physiology of Human Female Lactation, 67–105. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-66364-3_3.

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Conference papers on the topic "Human Mammary Glands"

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Sau, A., A. Arnaout, and C. Pratt. "Abstract PD09-01: BRCA1 inactivation induces NF-κB in human breast cancer cells and in murine and human mammary glands." In Abstracts: Thirty-Fifth Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 4‐8, 2012; San Antonio, TX. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/0008-5472.sabcs12-pd09-01.

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Running, During. "Biomechanical Model of Bare-Breasts." In Applied Human Factors and Ergonomics Conference. AHFE International, 2020. http://dx.doi.org/10.54941/ahfe100423.

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Sports bras are designed to reduce mammary glands or breast movement during exercises, but there is no standardized, valid and reliable method to evaluate relative three-dimensional (3D) breast movement; and there is no literature to predict the 3D force acting on the breasts during activities. A reliable method is essential to evaluate 3D breast movement and to determine the effective design features of supportive sports bras. This study derived and validated a new Breast Coordinate System (BCS) for investigating 3D breast movement, so as to identify the most effective bra features and to analyze the effects of breast volume and bra strap properties on breast movement, then to develop theoretical models of breast force generated during bare-breasted running. In the light of this, 3D mechanical models have been developed based on a system comprising a mass, springs and dampers. The orthogonal force exerted on the breasts during running was derived. The predicted results of maximum breast force were verified with previous literature. The new methods will contribute to future research on human locomotion and the design of close-fitting garments.
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Rosenbluth, Jennifer M., Ronald Schackmann, Carman Li, Norman Sachs, Deborah Dillon, Andrea Richardson, Jane Brock, et al. "Abstract 989: Organoid cultures from normal and cancer-prone human breast tissues preserve complex epithelial lineages and can form chimeric mammary glands in vivo." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-989.

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Carter, Matthew, Melissa Troester, Melissa Johnson, D. Joseph Jerry, and Sallie Schneider. "Abstract B115: Parity alters responses to ionizing radiation in the human mammary gland." In Abstracts: Frontiers in Cancer Prevention Research 2008. American Association for Cancer Research, 2008. http://dx.doi.org/10.1158/1940-6207.prev-08-b115.

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Elliott, Gloria D., and John J. McGrath. "Freezing Response of Mammary Tissue: A Mathematical Study." In ASME 1999 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1999. http://dx.doi.org/10.1115/imece1999-0584.

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Abstract Cryosurgery, the use of low temperatures to devitalize neoplastic tissue, has become an accepted treatment modality for many cancers such as those of the liver and prostate. Recently, the application of cryosurgery to human breast malignancies has been explored (Staren et. al, 1997, Pham and Rubinsky, 1998). Breast cancer will affect 1 in 9 women over the course of their lifetime (American Cancer Society, 1997). Although there are a wide variety of therapies available to treat this disease, the broad pathological spectrum of patients with breast cancer necessitates newer and better treatments before these numbers will decline. The composition of human mammary tissue is highly varied (age, body mass, and hormone dependent) making the application of cryosurgery to this tissue complex. Although the preponderance of breast cancer lesions occur in post-menopausal patients, women of all ages are affected by this disease. More importantly, lesions persist in all types of breast tissue. If cryosurgery is to become a viable therapy for breast cancer, it is important to understand the range of responses expected from the different tissue compositions, and, if relevant, identify the tissue types most suited to cryo-based therapies. To this end, an understanding of the response of these various classes of breast tissue to freezing can be accomplished using accurate heat and mass transfer models. Based on a review of basic human breast histology during all stages of mammary gland development, several different categories of human breast tissue were chosen for constitutional analysis. The volumetric dominance of each of the different tissue constituents was determined and then using this information, the volume-averaged thermal properties for each category calculated. A preliminary analysis, utilizing basic heat conduction equations and effective heat transfer properties, was performed to understand if, in a pure conduction sense, the various categories of breast tissue would respond differently to the same applied freezing protocol, and if so, which components were thermally most relevant. This analysis, although not completely descriptive of the physical situation occurring during an actual cryosurgery protocol, represents the first steps in determining the morphological features of mammary tissue which must be taken into consideration in future modeling efforts.
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Virador, VM, G. Casagrange, A. Raafat, R. Callahan, and E. Kohn. "Abstract P2-04-08: Targeted Expression of the Human Chaperone BAG3 to the Murine Mammary Gland Dysregulates Mammary Gland Development and Differentiation By Unrestricted Expansion of Luminal Cells." In Abstracts: Thirty-Fifth Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 4‐8, 2012; San Antonio, TX. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/0008-5472.sabcs12-p2-04-08.

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Castillo, Lilian F., Rocio S. Tascon, Elisa Bal de Kier Joffé, and Maria G. Peters. "Abstract 133: Role of Glypican-3 (GPC3) on tumor progression of the human mammary gland." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-133.

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Junkin, Michael, and Pak Kin Wong. "Plasma Lithography for Probing Cell Mechanoregulation." In ASME 2009 Second International Conference on Micro/Nanoscale Heat and Mass Transfer. ASMEDC, 2009. http://dx.doi.org/10.1115/mnhmt2009-18206.

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Mechanical and physical cues in the cellular microenvironment are important factors in the regulation of cellular activities, such as proliferation, apoptosis, differentiation, migration and adhesion. For instance, cells are known to respond dynamically to different topographical cues and biophysical structures, such as surface roughness, fiber diameters, and micro/nano scale patterns. Nevertheless, little is known about the fundamental physical mechanisms that govern the cell-substrate interactions and their roles in the regulation of physiological processes. This presents a major hurdle toward the realization of nanoengineered medicine. Herein, we report a plasma lithography technique to elucidate the influences of biophysical cues on different cellular activities. The plasma lithography technique selectively functionalizes polymeric and other biologically relevant surfaces, such as PDMS, glass and polystyrene, at scales ranging from millimeters to hundreds of nanometers. We applied this method to cellular patterning and examined the response of human mammary gland epithelial cells and mouse embryo fibroblasts to patterns of hydrophobic and hydrophilic areas towards the elucidation of the mechanoregulation of cellular processes. The technique enables us to systematically investigate the essential role of physical cues on cell migration, proliferation, and morphology. Collectively, these activities are not only fundamental in cell biology but also essential to the creation of novel tissue engineering constructs and medical implants. This study will shed light on how cells interact with their microenvironment as well as demonstrate a means to exercise control over cellular processes for future nanoengineered medical applications.
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Gupta, Akash, Rajeshwari R. Mehta, Ronald Wiehle, Michael Hawthorne, and Rajendra G. Mehta. "Abstract 3275: Development of a newex-vivoorthotopic model-Human breast cancer cells in mouse mammary gland organ culture." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3275.

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Bouamar, Hakim, Larry Broome, Xiang Gu, Alia Nazarullah, Andrew Brenner, Virginia Kaklamani, Ismail Jatoi, and Lu-Zhe Sun. "Abstract PS14-17: Rapamycin inhibits stem cell function and diminishes inflammation and senescence markers in human mammary gland." In Abstracts: 2020 San Antonio Breast Cancer Virtual Symposium; December 8-11, 2020; San Antonio, Texas. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.sabcs20-ps14-17.

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Reports on the topic "Human Mammary Glands"

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Barash, Itamar, J. Mina Bissell, Alexander Faerman, and Moshe Shani. Modification of Milk Composition via Transgenesis: The Role of the Extracellular Matrix in Regulating Transgene Expression. United States Department of Agriculture, July 1995. http://dx.doi.org/10.32747/1995.7570558.bard.

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Altering milk composition via transgenesis depends on three main factors. (1) The availability of an efficient regulatory sequences for targeting transgene(s) to the mammary gland; (2) a reliable in vitro model to test the expression of transgenes prior to their introduction to the animal genome; and (3) better understanding of the major factors which determine the rate of gene expression and protein synthesis. The current studies provide the necessary means and knowledge to alter milk protein composition via transgenesis. The following specific goals were achieved: a: Identifying regulatory regions in the b-lactoglobulin (BLG) gene and the cross-talk between elements which enabled us to construct an efficient vector for the expression of desirable cDNA's in the mammary gland. b: The establishment of a sheep mammary cell line that serves as a model for the analysis of endogenous and exogenous milk protein synthesis in the mammary gland of livestock. c: An accurate comparison of the potency of the 5' regulatory sequences from the BLG and whey acidic protein (WAP) promoters in directing the expression of human serum albumin (HSA) to the mammary gland in vitro and in vivo. In this study we have also shown that sequences within the coding region may determine a specific pattern of expression for the transgene, distinct from that of the native milk protein genes. d: Characterizing the dominant role of ECM in transgene expression in mammary epithelial cells. e: Further characterization of the BCE-1 enhancer element in the promoter of the b-casein gene as a binding site for the c/EBP-b and Stat5. Identifying its interaction with chromatin and its up regulation by inhibitors of histone deacetylation. f: Identifying a mechanism of translational control as a mediator for the synergistic effect of insulin and prolactin on protein synthesis in the mammary gland.
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Masckauchan, T. N. Activation of Alternative Wnt Signaling Pathways in Human Mammary Gland and Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, June 2004. http://dx.doi.org/10.21236/ada429686.

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Masckauchan, T. N. Activation of Alternative Wnt Signaling Pathways in Human Mammary Gland and Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, June 2006. http://dx.doi.org/10.21236/ada459280.

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Barash, Itamar, and Robert E. Rhoads. Translational Mechanisms that Govern Milk Protein Levels and Composition. United States Department of Agriculture, November 2004. http://dx.doi.org/10.32747/2004.7586474.bard.

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Original objectives: The long term objective of the project is to achieve higher content of protein in the milk of ruminants by modulating the translational machinery in the mammary gland. The first specific aim of the BARD proposal was to characterize responsiveness of various experimental systems to combination of lactogenic hormones and amino acids with particular emphasis on discrimination between the control of total protein synthesis and milk protein synthesis. Based on the results, we planned to proceed by characterizing the stage of protein synthesis in which the stimulation by lactogenic hormones and amino acid occur and finally we proposed to identify which components of the translation machinery are modified. Background to the topic: Milk protein is the most valuable component in milk, both for direct human consumption and for manufacturing cheese and other protein-based products. Attempts to augment protein content by the traditional methods of genetic selection and improved nutritional regimes have failed. The proposal was based on recent results suggesting that the limiting factor for augmenting protein synthesis in the bovine mammary gland is the efficiency of converting amino acids to milk proteins. Major conclusions, solutions, achievements: Insulin and prolactin synergistically stimulate â-casein mRNA translation by cytoplasmatic polyadenylation. The interaction between insulin and prolactin was demonstrated two decades ago as crucial for milk-protein synthesis, but the molecular mechanisms involved were not elucidated. We found in differentiated CID 9 mouse mammary epithelial cells line that insulin and prolactin synergistically increases the rate of milk protein mRNA translation. We focused on â-casein, the major milk protein, and found that the increase in â-casein mRNA translation was reflected in a shift to larger polysomes, indicating an effect on translational initiation. Inhibitors of the PI3K, mTOR, and MAPK pathways blocked insulin-stimulated total protein and â-casein synthesis but not the synergistic stimulation. Conversely, cordycepin, a polyadenylation inhibitor, abolished synergistic stimulation of protein synthesis without affecting insulin-stimulated translation. The poly(A) tract of â-casein mRNA progressively increased over 30 min of treatment with insulin plus prolactin. The 3’-untranslated region of â-casein mRNA was found to contain a cytoplasmic polyadenylation element (CPE), and in reporter constructs, this was sufficient for the translational enhancement and mRNA-specific polyadenylation. Furthermore, insulin and prolactin stimulated phosphorylation of cytoplasmic polyadenylation element binding protein (CPEB) but did not increase cytoplasmic polyadenylation.
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Weller, Joel I., Harris A. Lewin, and Micha Ron. Determination of Allele Frequencies for Quantitative Trait Loci in Commercial Animal Populations. United States Department of Agriculture, February 2005. http://dx.doi.org/10.32747/2005.7586473.bard.

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Individual loci affecting economic traits in dairy cattle (ETL) have been detected via linkage to genetic markers by application of the granddaughter design in the US population and the daughter design in the Israeli population. From these analyses it is not possible to determine allelic frequencies in the population at large, or whether the same alleles are segregating in different families. We proposed to answer this question by application of the "modified granddaughter design", in which granddaughters with a common maternal grandsire are both genotyped and analyzed for the economic traits. The objectives of the proposal were: 1) to fine map three segregating ETL previously detected by a daughter design analysis of the Israeli dairy cattle population; 2) to determine the effects of ETL alleles in different families relative to the population mean; 3) for each ETL, to determine the number of alleles and allele frequencies. The ETL on Bostaurusautosome (BT A) 6 chiefly affecting protein concentration was localized to a 4 cM chromosomal segment centered on the microsatellite BM143 by the daughter design. The modified granddaughter design was applied to a single family. The frequency of the allele increasing protein percent was estimated at 0.63+0.06. The hypothesis of equal allelic frequencies was rejected at p<0.05. Segregation of this ETL in the Israeli population was confirmed. The genes IBSP, SPP1, and LAP3 located adjacent to BM143 in the whole genome cattle- human comparative map were used as anchors for the human genome sequence and bovine BAC clones. Fifteen genes within 2 cM upstream of BM143 were located in the orthologous syntenic groups on HSA4q22 and HSA4p15. Only a single gene, SLIT2, was located within 2 cM downstream of BM143 in the orthologous HSA4p15 region. The order of these genes, as derived from physical mapping of BAC end sequences, was identical to the order within the orthologous syntenic groups on HSA4: FAM13A1, HERC3. CEB1, FLJ20637, PP2C-like, ABCG2, PKD2. SPP, MEP, IBSP, LAP3, EG1. KIAA1276, HCAPG, MLR1, BM143, and SLIT2. Four hundred and twenty AI bulls with genetic evaluations were genotyped for 12 SNPs identified in 10 of these genes, and for BM143. Seven SNPs displayed highly significant linkage disequilibrium effects on protein percentage (P<0.000l) with the greatest effect for SPP1. None of SNP genotypes for two sires heterozygous for the ETL, and six sires homozygous for the ETL completely corresponded to the causative mutation. The expression of SPP 1 and ABCG2 in the mammary gland corresponded to the lactation curve, as determined by microarray and QPCR assays, but not in the liver. Anti-sense SPP1 transgenic mice displayed abnormal mammary gland differentiation and milk secretion. Thus SPP 1 is a prime candidate gene for this ETL. We confirmed that DGAT1 is the ETL segregating on BTA 14 that chiefly effects fat concentration, and that the polymorphism is due to a missense mutation in an exon. Four hundred Israeli Holstein bulls were genotyped for this polymorphism, and the change in allelic frequency over the last 20 years was monitored.
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