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  • 1
    Electronic Resource
    Electronic Resource
    The ER-positive / PgR-negative breast cancer phenotype is not associated with mutations within the DNA binding domain (1993)
    Springer
    Breast cancer research and treatment 26 (1993), S. 191-202 
    Details
    ISSN: 1573-7217
    Keywords: estrogen receptor ; breast cancer ; DNA binding domain ; gel-retardation analysis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We have used in vitro DNA binding assays as a measure of estrogen receptor (ER) function in human breast tumors. We found that the majority of ER+ (25 ER+/progesterone receptor [PgR]+, and 25 ER+/PgR−) tumors we examined were capable of binding consensus estrogen response element (ERE) oligonucleotides in this assay system. We found significant proteolytic activity in many of the tumors such that protease inhibitors were found to be essential during the preparation of tumor extracts. We next applied direct sequence analysis of the ER DNA binding domain of several of these tumors, and determined that the ER+/PgR− breast tumors did not contain mutations within the DNA binding domain which might explain their apparent discordant receptor phenotype. We did identify an alternatively spliced ER variant missing exon 3 of the DNA binding domain. This variant was unable to function as a transcriptional inducer of an estrogen-responsive reporter in a yeast assay system. Furthermore, the exon 3 ER deletion variant was expressed at equivalent levels in all of the ER+ breast tumors, so that it does not appear to be involved in the evolution of the ER+/PgR− breast cancer phenotype.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00689692
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Constitutive overexpression of the 27,000 dalton heat shock protein in late passage human breast cancer cells (1994)
    Springer
    Breast cancer research and treatment 32 (1994), S. 177-186 
    Details
    ISSN: 1573-7217
    Keywords: hsp27 ; gene regulation ; breast cancer ; heat shock transcription factors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We present evidence that the mechanisms controlling induction of heat shock transcription factors (HSFs) and mRNA expression of the 27,000 molecular weight heat shock protein, hsp27, are diverse in human breast cancer cells. Heat shock accumulation of hsp27 RNA is associated with the activation of HSF in MDA-MB-231 cells. We have later passage MCF-7 breast cancer cell lines with elevated, constitutive expression of hsp27 mRNA, perhaps due to hsp 27 gene amplification. Estradiol and heat shock treatment no longer affect the level of hsp27 mRNA in these cells. Heat induction of HSF is inhibited in cells overexpressing hsp27, although metal ions and amino acid analogs are still capable of activating HSF. These cells will provide a useful system for characterizing alternative pathways in HSF inhibition and activation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00665768
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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