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  • estrogen  (1)
  • mitogenic signal transduction  (1)
  • p53 transformation  (1)
  • 1
    Electronic Resource
    Electronic Resource
    p53Val135 temperature sensitive mutant suppresses growth of human breast cancer cells (1994)
    Springer
    Breast cancer research and treatment 30 (1994), S. 167-177 
    Details
    ISSN: 1573-7217
    Keywords: breast cancer ; oncogenes ; p53 transformation ; temperature sensitive mutant ; tumor suppressors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary One common step in the malignant progression of a wide variety of human cancers seems to be inactivation of the p53 gene, via point mutation or deletion or both; or overexpression of mutated protein with dominant transforming activity. This study shows a suppressive effect of wild type p53 on the growth of human breast cancer cells. Introduction of wild type p53 versus mutant into five human breast cancer cell lines containing mutant p53 resulted in a marked reduction in colony formation. Two of these were transfected with human wt p53 expression vectors and the other three were infected with retroviruses packaging human wt p53, both showing similar reduction in the number of surviving colonies, suggesting a role for wt p53 in suppression of breast cancer cell growth. Direct evidence for growth suppression was obtained by introduction of the temperature sensitive p53Val135 into Hs578T human breast cancer cells containing a mutant p53. This murine mutant allele p53Val135 functions as an oncogene at 37° C and as a tumor suppressor at 32° C. The cell line generated was strongly growth inhibited at the restrictive temperature (31.5° C), at which temperature the suppressor form is expressed. This inhibition of proliferation was reversible upon a temperature upshift. Analysis of the cell cycle distribution shows these growth suppressed cells to be inhibited in the G1 phase of the cell cycle. Thus wt p53 may have an important role in breast cancer tumorigenesis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00666061
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Farnesyltransferase inhibitors and anti-Ras therapy (1996)
    Springer
    Breast cancer research and treatment 38 (1996), S. 75-83 
    Details
    ISSN: 1573-7217
    Keywords: oncogenes ; mitogenic signal transduction ; cancer chemotherapy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The oncoprotein encoded by mutantras genes is initially synthesized as a cytoplasmic precursor which requires posttranslational processing to attain biological activity; farnesylation of the cysteine residue present in the CaaX motif located at the carboxy-terminus of all Ras proteins is the critical modification. Once farnesylated and further modified, the mature Ras protein is inserted into the cell's plasma membrane where it participates in the signal transduction pathways that control cell growth and differentiation. The farnesylation reaction that modifies Ras and other cellular proteins having an appropriate CaaX motif is catalyzed by a housekeeping enzyme termed farnesyl-protein transferase (FPTase). Inhibitors of this enzyme have been prepared by several laboratories in an effort to identify compounds that would block Ras-induced cell transformation and thereby function as Ras-specific anticancer agents. A variety of natural products and synthetic organic compounds were found to block farnesylation of Ras proteinsin vitro. Some of these compounds exhibit antiproliferative activity in cell culture, block the morphological alterations associated with Ras-transformation, and can block the growth of Ras-transformed cell lines in tumor colony-forming assays. By contrast, these compounds do not affect the growth or morphology of cells transformed by the Raf or Mos oncoproteins, which do not require farnesylation to achieve biological activity. The efficacy and lack of toxicity observed with FPTase inhibitors in an animal tumor model suggest that specific FPTase inhibitors may be useful for the treatment of some types of cancer.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01803786
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Growth regulation of human breast carcinoma occurs through regulated growth factor secretion (1987)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 35 (1987), S. 1-16 
    Details
    ISSN: 0730-2312
    Keywords: breast cancer ; growth factors ; estrogen ; IGF-I ; TGF ; PDGF ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: We describe studies on human breast cancer in which it is shown that specific growth factors (IGF-I, TGFα, PDGF) are secreted by human breast cancer cells and likely to be involved in tumor growth and progression. These activities are regulated by estradiol in hormone-dependent breast cancer and secreted constitutively by hormone-independent cells. These growth factor activities can induce the growth of hormone-dependent cells in vivo in athymic nude mice. Hormone-dependent breast cancer cells also secrete TGFβ, a growth-inhibitory substance, when treated with antiestrogens. TGFβ functions as a negative autocrine growth regulator and is responsible for some of the growth-inhibitory effects of antiestrogens.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240350102
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    Paper (German National Licenses)
    Fulltext
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