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  1. Article ; Online: Stromal effects on mammary gland development and breast cancer.

    Wiseman, Bryony S / Werb, Zena

    Science (New York, N.Y.)

    2002  Volume 296, Issue 5570, Page(s) 1046–1049

    Abstract: Breast cancer manifests itself in the mammary epithelium, yet there is a growing recognition that mammary stromal cells also play an important role in tumorigenesis. During its developmental cycle, the mammary gland displays many of the properties ... ...

    Abstract Breast cancer manifests itself in the mammary epithelium, yet there is a growing recognition that mammary stromal cells also play an important role in tumorigenesis. During its developmental cycle, the mammary gland displays many of the properties associated with breast cancer, and many of the stromal factors necessary for mammary development also promote or protect against breast cancer. Here we review our present knowledge of the specific factors and cell types that contribute to epithelial-stromal crosstalk during mammary development. To find cures for diseases like breast cancer that rely on epithelial-stromal crosstalk, we must understand how these different cell types communicate with each other.
    MeSH term(s) Adipocytes/cytology ; Adipocytes/physiology ; Animals ; Apoptosis ; Breast/cytology ; Breast/embryology ; Breast/growth & development ; Breast/physiology ; Breast Neoplasms/pathology ; Breast Neoplasms/physiopathology ; Cell Communication ; Epithelial Cells/physiology ; Extracellular Matrix/physiology ; Female ; Humans ; Mammary Glands, Animal/cytology ; Mammary Glands, Animal/embryology ; Mammary Glands, Animal/growth & development ; Mammary Glands, Animal/physiology ; Mammary Neoplasms, Animal/pathology ; Mammary Neoplasms, Animal/physiopathology ; Morphogenesis ; Neoplasm Metastasis ; Pregnancy ; Signal Transduction ; Stromal Cells/physiology
    Language English
    Publishing date 2002-05-10
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, U.S. Gov't, P.H.S. ; Review
    ZDB-ID 128410-1
    ISSN 1095-9203 ; 0036-8075
    ISSN (online) 1095-9203
    ISSN 0036-8075
    DOI 10.1126/science.1067431
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  2. Article: Development of the mammary gland requires DGAT1 expression in stromal and epithelial tissues.

    Cases, Sylvaine / Zhou, Ping / Shillingford, Jonathan M / Wiseman, Bryony S / Fish, Jo Dee / Angle, Christina S / Hennighausen, Lothar / Werb, Zena / Farese, Robert V

    Development (Cambridge, England)

    2004  Volume 131, Issue 13, Page(s) 3047–3055

    Abstract: Mammary gland development is a complex process that is dependent on interactions between the developing mammary epithelium and the surrounding stromal tissues. We show that mice lacking the triglyceride synthesis enzyme acyl CoA:diacylglycerol ... ...

    Abstract Mammary gland development is a complex process that is dependent on interactions between the developing mammary epithelium and the surrounding stromal tissues. We show that mice lacking the triglyceride synthesis enzyme acyl CoA:diacylglycerol transferase 1 (DGAT1) have impaired mammary gland development, characterized by decreased epithelial proliferation and alveolar development, and reduced expression of markers of functional differentiation. Transplantation studies demonstrate that the impaired development results from a deficiency of DGAT1 in both the stromal and epithelial tissues. Our findings are the first to link defects in stromal lipid metabolism to impaired mammary gland development.
    MeSH term(s) Acyltransferases/biosynthesis ; Acyltransferases/physiology ; Animals ; Apoptosis ; Cell Differentiation ; Diacylglycerol O-Acyltransferase ; Epithelial Cells/metabolism ; Image Processing, Computer-Assisted ; Immunoblotting ; Immunohistochemistry ; Lactation ; Lipid Metabolism ; Mammary Glands, Animal/embryology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Precipitin Tests ; RNA/metabolism ; Stromal Cells/metabolism ; Time Factors ; Tissue Transplantation
    Chemical Substances RNA (63231-63-0) ; Acyltransferases (EC 2.3.-) ; Dgat1 protein, mouse (EC 2.3.1.20) ; Diacylglycerol O-Acyltransferase (EC 2.3.1.20)
    Language English
    Publishing date 2004-07
    Publishing country England
    Document type Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 90607-4
    ISSN 1477-9129 ; 0950-1991
    ISSN (online) 1477-9129
    ISSN 0950-1991
    DOI 10.1242/dev.01158
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Site-specific inductive and inhibitory activities of MMP-2 and MMP-3 orchestrate mammary gland branching morphogenesis.

    Wiseman, Bryony S / Sternlicht, Mark D / Lund, Leif R / Alexander, Caroline M / Mott, Joni / Bissell, Mina J / Soloway, Paul / Itohara, Shigeyoshi / Werb, Zena

    The Journal of cell biology

    2003  Volume 162, Issue 6, Page(s) 1123–1133

    Abstract: During puberty, mouse mammary epithelial ducts invade the stromal mammary fat pad in a wave of branching morphogenesis to form a complex ductal tree. Using pharmacologic and genetic approaches, we find that mammary gland branching morphogenesis requires ... ...

    Abstract During puberty, mouse mammary epithelial ducts invade the stromal mammary fat pad in a wave of branching morphogenesis to form a complex ductal tree. Using pharmacologic and genetic approaches, we find that mammary gland branching morphogenesis requires transient matrix metalloproteinase (MMP) activity for invasion and branch point selection. MMP-2, but not MMP-9, facilitates terminal end bud invasion by inhibiting epithelial cell apoptosis at the start of puberty. Unexpectedly, MMP-2 also represses precocious lateral branching during mid-puberty. In contrast, MMP-3 induces secondary and tertiary lateral branching of ducts during mid-puberty and early pregnancy. Nevertheless, the mammary gland is able to develop lactational competence in MMP mutant mice. Thus, specific MMPs refine the mammary branching pattern by distinct mechanisms during mammary gland branching morphogenesis.
    MeSH term(s) Animals ; Apoptosis/drug effects ; Apoptosis/genetics ; Cell Differentiation/drug effects ; Cell Differentiation/genetics ; Dipeptides/pharmacology ; Embryonic Induction/drug effects ; Embryonic Induction/genetics ; Enzyme Inhibitors/pharmacology ; Epithelial Cells/cytology ; Epithelial Cells/drug effects ; Epithelial Cells/enzymology ; Female ; Immunohistochemistry ; Lactation/drug effects ; Lactation/genetics ; Mammary Glands, Animal/cytology ; Mammary Glands, Animal/enzymology ; Mammary Glands, Animal/growth & development ; Matrix Metalloproteinase 2/genetics ; Matrix Metalloproteinase 2/metabolism ; Matrix Metalloproteinase 3/genetics ; Matrix Metalloproteinase 3/metabolism ; Matrix Metalloproteinase Inhibitors ; Mice ; Mice, Inbred BALB C ; Mice, Transgenic ; Morphogenesis/drug effects ; Morphogenesis/genetics ; Mutation/drug effects ; Mutation/genetics ; Organ Culture Techniques ; Pregnancy ; Protease Inhibitors/pharmacology ; Sexual Maturation/drug effects ; Sexual Maturation/genetics ; Tissue Inhibitor of Metalloproteinase-1/genetics ; Tissue Inhibitor of Metalloproteinase-1/metabolism
    Chemical Substances Dipeptides ; Enzyme Inhibitors ; Matrix Metalloproteinase Inhibitors ; N-(2(R)-2-(hydroxamidocarbonylmethyl)-4-methylpentanoyl)-L-tryptophan methylamide ; Protease Inhibitors ; Tissue Inhibitor of Metalloproteinase-1 ; Matrix Metalloproteinase 3 (EC 3.4.24.17) ; Matrix Metalloproteinase 2 (EC 3.4.24.24)
    Language English
    Publishing date 2003-09-15
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 218154-x
    ISSN 1540-8140 ; 0021-9525
    ISSN (online) 1540-8140
    ISSN 0021-9525
    DOI 10.1083/jcb.200302090
    Database MEDical Literature Analysis and Retrieval System OnLINE

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