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  • 1
    Electronic Resource
    Electronic Resource
    Hypermethylation of the Wilms' tumor suppressor gene CpG island in human breast carcinomas (1999)
    Springer
    Breast cancer research and treatment 56 (1999), S. 35-43 
    Details
    ISSN: 1573-7217
    Keywords: breast cancer ; CpG island ; DNA hypermethylation ; Wilms' tumor suppressor gene
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract CpG island hypermethylation is known to be associated with transcriptional silencing of tumor suppressor genes in neoplasia. We have previously detected aberrantly methylated sites in the first intron of the Wilms' tumor suppressor (WT1) gene in breast cancer. In the present study, we extended the investigation to a CpG island located in the promoter and first exon regions of WT1. Methylation of this CpG island was found to be extensive in MCF‐7 and MDA‐MB‐231 breast cancer cells, as well as in 25% (five of 20 patients) of primary breast tumors. While levels of the known 3.0‐kb WT1 mRNAs were decreased or not detected in these cell lines, the expression could be partially restored following treatment with a demethylation agent, 5‐aza‐2′‐deoxycytidine. Surprisingly, a novel 2.5‐kb WT1 transcript was expressed at high levels in both untreated and treated MDA‐MB‐231 cells. This novel transcript was likely a WT1 variant missing the first exon, and therefore escaped the methylation control present in the normal transcript. Our study implicates the future need to investigate the significance of this aberrant transcript as well as the role of WT1 CpG island hypermethylation in breast neoplasia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006222803788
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  • 2
    Electronic Resource
    Electronic Resource
    Morphology and glycoprotein synthesis of uterine glandular epithelium in human basal plate at term: An ultrastructural and autoradiographic study (1986)
    New York, NY [u.a.] : Wiley-Blackwell
    The @Anatomical Record 216 (1986), S. 146-153 
    Details
    ISSN: 0003-276X
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: This study describes the morphologic features of uterine glandular epithelium in human basal plate at term and identifies this epithelium as an active site of glycoprotein synthesis. Wedge biopsies were obtained from the basal plate at the time of repeat cesarean section from 11 normal pregnant patients at term. Biopsy specimens were either processed immediately for microscopic examination or incubated in vitro with 25μCi/cc of 3H-galactose or 3H-leucine. Tissues incubated with tritiated compounds (2-hour pulse ± 3-hour chase in nonradioactive medium) were either processed for light microscopic autoradiographic analysis or extracted for determination of trichloroacetic-acid-precipitable tritiated macromolecules in tissues and medium. Profiles of cuboidal-columnar glandular epithelium were identified in the decidual component of the basal plate region adjacent to spiral arterioles and perpendicular to the inner layers of myometrial muscle. Autoradiographic and biochemical studies identified the glandular epithelium, as well as large decidual cells, to be major sites of incorporation of both 3H-galactose and 3H-leucine and to be prime sources for secretion of tritiated macromolecules that appeared in the medium during in vitro incubation of basal plate tissue. Ultrastructurally, the glandular epithelium was noted to rest on a basal lamina, to have lateral cell membranes with numerous desmosomes, and to exhibit an apical surface with microvilli projecting into a luminal space. Cytologic features of the cells included abundant profiles of rough endoplasmic reticulum, multiple mitochondria with lamellar cristae, a well-developed perinuclear but nonpolarized Golgi apparatus, and nuclei containing predominantly euchromatin. Lipid droplets and glycogen deposits were present in some cells. This study indicates that uterine glands persist throughout human gestation in the basal plate and that these glands continue to be active in glycoprotein synthesis and secretion.
    Additional Material: 12 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/ar.1092160206
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  • 3
    Electronic Resource
    Electronic Resource
    Lithium-stimulated proliferation and alteration of phosphoinositide metabolites in MCF-7 human breast cancer cells (1995)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 165 (1995), S. 134-144 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Lithium, which is used to treat bipolar psychiatric disorders, can stimulate proliferation of a number of cells in tissue culture. Proliferation of MCF-7 human breast cancer cells, which also respond to EGF and estrogens, was stimulated by LiCl (1-5 mM) within the concentration range that is encountered during human therapy with lithium. Stimulation of growth was specific for lithium; rubidium, potassium, and sodium showed no such effect. In the presence of antiestrogen, lithium stimulated the growth of hormone-dependent breast cancer cells MCF-7, ZR-75-1, and T47D but not hormone-independent MDA-MB-231 cells or an estrogen-independent clone of MCF-7 cells. Lithium-stimulated proliferation was limited by cytotoxicity which could be moderated by added potassium chloride (5-20 mM) in the medium. Each of the mitogens lithium, 17β-estradiol, and EGF increased the rate of uptake of myo-inositol into MCF-7 cells. Whether normalized to inositol lipids, to protein, or to DNA, steady-state levels of inositol phosphates were elevated by each of the mitogens including lithium, which inhibits the breakdown of inositol phosphates in the phosphoinositide signaling pathway. These data indicate that therapeutic concentrations of lithium can stimulate the proliferation of human breast cancer cells by a mechanism that may involve the phosphoinositide pathway. © 1995 Wiley-Liss Inc.
    Additional Material: 8 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041650116
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