Search Results - (Author, Cooperation:W. D. Tilley)

Showing 1 - 5 results of 5, query time: 0.15s Refine Results
  1. 1
    Staff View
    Publication Date:
    2015-08-08
    Publisher:
    Nature Publishing Group (NPG)
    Print ISSN:
    0028-0836
    Electronic ISSN:
    1476-4687
    Topics:
    Biology
    Chemistry and Pharmacology
    Medicine
    Natural Sciences in General
    Physics
    Published by:
    http://www.nature.com/

    Latest Papers from Table of Contents or Articles in Press
  2. 2
    Staff View
    Publication Date:
    2015-07-15
    Publisher:
    Nature Publishing Group (NPG)
    Print ISSN:
    0028-0836
    Electronic ISSN:
    1476-4687
    Topics:
    Biology
    Chemistry and Pharmacology
    Medicine
    Natural Sciences in General
    Physics
    Keywords:
    Animals ; Breast Neoplasms/drug therapy/*genetics/*metabolism/pathology ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Chromatin/drug effects/genetics/metabolism ; DNA Copy Number Variations/genetics ; Disease Progression ; Estrogen Receptor alpha/antagonists & inhibitors/*metabolism ; Estrogens/metabolism/pharmacology ; Female ; *Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Ligands ; Mice ; Progesterone/metabolism/pharmacology ; Protein Binding/drug effects ; Receptors, Progesterone/genetics/*metabolism ; Transcription, Genetic/drug effects ; Xenograft Model Antitumor Assays
    Published by:
    http://www.nature.com/

    Latest Papers from Table of Contents or Articles in Press
  3. 3
    Staff View
    Publication Date:
    2018-05-16
    Publisher:
    The American Association for Cancer Research (AACR)
    Print ISSN:
    1078-0432
    Electronic ISSN:
    1557-3265
    Topics:
    Medicine
    Published by:
    http://www.aacr.org/

    Latest Papers from Table of Contents or Articles in Press
  4. 4
    Staff View
    ISSN:
    1573-7217
    Keywords:
    breast cancer ; cell ; EGF ; estrogen ; growth ; insulin ; mitogens ; progestin
    Source:
    Springer Online Journal Archives 1860-2000
    Topics:
    Medicine
    Notes:
    Summary The mechanism of the antiproliferative effects of progestins on human breast cancer cells is not known. In view of the ability of estrogen to stimulate human breast cancer cell production of peptide growth factors, and since previous studies have suggested that the inhibitory action of progestins is dependent on estrogen-stimulated growth, the present study examined the interaction of growth factors and the synthetic progestin R5020 on the proliferation of T47D human breast cancer cells. In this study, the concentrations of estradiol, insulin, and EGF for optimal stimulation of T47D cell growth in 3% dextran-charcoal treated fetal bovine serum (DCC-FBS) were determined to be 1 nM, 100 nM, and 1 nM, respectively. Furthermore, incubation with these optimal concentrations of estradiol, insulin, and EGF in various combinations produced additive effects on T47D cell proliferation, suggesting that these agents act, at least in part, by different mechanisms. In contrast, in a chemically defined medium (DM), both estradiol and EGF were unable to stimulate T47D cell proliferation. In the case of estradiol, the inability to demonstrate stimulation of T47D cell growth in DM was not due to down-regulation of the estrogen receptor. R5020 inhibited the growth of T47D cells, although its effect was more marked in the presence of 3% DCC-FBS than in DM. Stimulation of T47D cell growth by either estradiol or insulin in 3% DCC-FBS was effectively inhibited by R5020. In contrast, growth of T47D cells stimulated by EGF in the absence of estradiol was not markedly inhibited by R5020, the growth being comparable to that of untreated control cells. These findings suggest that the inhibitory effect of R5020 on T47D cell proliferation is dominant over the action of some, but not all, breast cancer mitogens.
    Type of Medium:
    Electronic Resource
    URL:
    http://dx.doi.org/10.1007/BF01833357

    Articles: DFG German National Licenses
  5. 5
    Birrell, S. N. ; Hall, R. E. ; Tilley, W. D.
    Springer
    Published 1998
    Staff View
    ISSN:
    1573-7039
    Keywords:
    ANDROGENS ; ANDROGEN RECEPTOR ; MEDROXYPROGESTERONE ACETATE ; RECEPTOR VARIANTS
    Source:
    Springer Online Journal Archives 1860-2000
    Topics:
    Medicine
    Notes:
    Abstract Although the androgen receptor (AR)3is often co-expressed with the estrogen receptor (ER)and progesterone receptor (PR) in human breast tumors,its role in breast cancer is poorly understood. Specific growth stimulatory and inhibitory actions ofandrogens have been described in human breast cancercell lines. The mechanisms by which androgens exertthese contrasting growth effects are unknown. A commonly utilized second line therapy for the treatmentof advanced breast cancer is high dosemedroxyprogesterone acetate (MPA). Although MPA, asynthetic progestin, was thought to act exclusivelythrough the PR, the androgenic side-effects observed in womentaking MPA suggest that its action may also be mediatedin part by the AR. In support of this hypothesis, thelevel of AR measured by radioligand binding in primary breast tumors was correlated with theduration of response to MPA treatment following failureof tamoxifen therapy. Recent data suggest that thepresence of structurally altered AR in breast cancers may account for unresponsiveness to MPA in someof these cases. Further studies are warranted todetermine the role of AR mediated pathways in regulatingbreast tumor growth. In particular, identification of androgen-regulated genes may lead to newpossibilities for the hormonal treatment of breastcancer.
    Type of Medium:
    Electronic Resource
    URL:
    http://dx.doi.org/10.1023/A:1018730519839

    Articles: DFG German National Licenses