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  • 1
    Electronic Resource
    Electronic Resource
    Strongly reduced expression of the cell cycle inhibitor p27 in endometrial neoplasia (1999)
    Springer
    Virchows Archiv 434 (1999), S. 423-428 
    Details
    ISSN: 1432-2307
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  In the present study we investigated the expression of the cell cycle inhibitor p27 in endometrial neoplasia using immunohistochemistry with a p27-specific antibody. Expression of p27 in endometrial carcinomas was compared with expression in the normal endometrium throughout the cycle. Normal endometrial cells showed strong nuclear expression of p27. Expression was present throughout the cycle and was stronger during the secretory phase. We found strongly reduced or abolished expression of p27 in endometrial carcinoma (85.3% of cases). The 41 tumours analysed were classified according to p27 staining intensity and percentage of positive cells into the following categories of p27 expression: negative/very low (56.0%); low (29.3%); moderate (14.7%) and high (0.0%). All the p27-positive tumours were well-differentiated endometrioid carcinomas of malignancy grade G1. Comparison with the p53 status showed that all tumours with strong p53 expression had low/negative p27 staining, while those that were positive for p27 had negative/low p53 staining. Reduced or absent p27 levels were also observed by Western blot analysis both in tumour samples and in HEC-1B endometrial adenocarcinoma cells. It thus seems that p27 expression is essential for the control of normal endometrial proliferation, and reduced or absent p27 expression may be an important step in endometrial carcinogenesis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004280050361
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  • 2
    Electronic Resource
    Electronic Resource
    Differential regulation of the human 'leukemia inhibitory factor' (LIF) promoter in T47D and MDA-MB 231 breast cancer cells (1998)
    Springer
    Breast cancer research and treatment 47 (1998), S. 153-161 
    Details
    ISSN: 1573-7217
    Keywords: cytokines ; leukemia inhibitory factor ; estrogen regulation ; progestin regulation ; promoter ; MDA-MB-231 cells ; T47D cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Leukemia inhibitory factor (LIF) is a pleiotropic inflammatory cytokine. A potential role for LIF in the pathogenesis of human breast cancer was recently indicated by the finding that LIF is produced by MDA-MB 231 breast cancer cells and that it stimulates proliferation of the T47D and MCF-7 breast cancer cell lines. Despite its role as a possible therapeutic target in breast cancer, the transcriptional regulation of the LIF gene in breast cancer cells has not been investigated so far. In this context, we investigated the regulation of the human LIF promoter (human LIF666-luciferase) by ovarian steroids in transient transfection assays in MDA-MB 231 and T47D cells. Since the MDA-MB 231 cells are devoid of both estrogen (ER) and progesterone (PR) receptors, these cells were co-transfected with the respective receptor expression vector. Estradiol induced no stimulation in either T47D or ER-transfected MDA-MB 231 cells. Treatment with the progesterone agonist MPA (medroxy-progesterone acetate) resulted in induction of LIF transcription in PR-transfectant MDA-MB 231 cells, while it had no effect in T47D cells. Both PR isoforms (PR-B and PR-A) were effective in inducing the LIF promoter in MDA-MB 231 cells, and this effect was inhibited by the progestin antagonist RU 486. The stimulatory effect of MPA was maintained on deletion constructs (h274LIF-Luc, h148LIF-Luc and h82LIF-Luc), indicating that 82 bp are sufficient to mediate this effect. Our results indicate that the LIF promoter is transcriptionally active in human breast cancer cells and its activity can be modulated by progestins and anti-progestins in cells expressing the LIF protein, which might have therapeutic implications.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1005961403898
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  • 3
    Electronic Resource
    Electronic Resource
    Biphasic effect of medroxyprogesterone-acetate (MPA) treatment on proliferation and cyclin D1 gene transcription in T47D breast cancer cells (2000)
    Springer
    Breast cancer research and treatment 63 (2000), S. 243-248 
    Details
    ISSN: 1573-7217
    Keywords: breast cancer ; cyclin D1 ; MPA ; proliferation ; T47D cell line
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract While progesterone is a known differentiation-inducing factor in the human endometrium, for the breast epithelium both proliferation-inducing and -inhibiting effects have been described. Cyclin D1, which is required for cell cycle progression in G1 and has been shown to play an important role in the pathogenesis of breast cancer has been implicated as a possible mediator of such effects. In the present study we thus investigated the effects of the progestin agonist MPA (medroxy-progesterone acetate) on proliferation of T47D breast cancer cells. In parallel experiments, the regulation of the human cyclin D1 promoter as well as cyclin D1 protein levels under the influence of MPA were studied. Our results show an increase of proliferative activity in T47D cells after 24 and 48 h of MPA treatment follwed by inhibition of proliferation after 72 h. In Western blot analysis an increased expression level of cyclin D1 protein can be observed after 24 h of MPA stimulation, while at 72 h the protein levels are barely detectable. Transient transfection experiments with a luciferase reporter plasmid containing the human cyclin D1 promoter showed an induction of the promoter after 24 and 36 h of MPA treatment followed by a reduction in promoter activity. In conclusion, our results confirm the existence of a biphasic response of T47D cell proliferation in response to MPA treatment, consisting of stimulation of proliferation followed by inhibition, and further implicate cyclin D1 as a mediator of these effects, since the cyclin D1 promoter shows a similar biphasic response in this context.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006432600478
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    Paper (German National Licenses)
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