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Query: UNIPROT:P04155 (pS2)
 1,234 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

pS2 expression in normal breast tissue removed for cosmetic reasons was significantly lower than in uninvolved breast tissues from mastectomies for breast carcinomas. It is speculated that the presence of the carcinoma, or factors related to its development, could be the reason for this difference.
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PMID:Expression of the pS2 gene in normal breast tissue. 801 58

pS2 protein is a cysteine-rich polypeptide, of unknown function, the expression of which is induced in the human cancer cell line MCF-7 by oestrogen. The availability of a murine monoclonal antibody to human pS2 protein has prompted us to evaluate its expression in 47 cases of primary breast carcinoma. Using a double indirect immunoperoxidase technique, we compared the expression of pS2 protein in fine needle aspiration (FNA) cytology smears with that in formalin-fixed, paraffin-embedded sections from subsequently excised tumours from the same patients. We also compared the expression of pS2 protein and oestrogen receptor (ER) status using immunocytochemical assay (ER-ICA) in formalin-fixed, paraffin-embedded sections from 22 primary breast carcinomas. We found the application of immunocytochemistry in the assessment of pS2 protein expression in FNA cytology to be a reliable and cost-effective technique, having a sensitivity of 84% and a specificity of 100%. There was also a good correlation between the expression of pS2 protein and ER status.
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PMID:Immunocytochemistry in the assessment of pS2 protein expression in fine needle aspiration cytology from breast carcinoma. 811 Sep 71

Most breast tumors show estrogen-dependent growth and are thus susceptible to antiestrogenic therapy. MCF-7 cells, obtained from a human estrogen-dependent breast carcinoma, are widely used for studying the modulation of estrogenic responses by different effectors. All-trans-retinoic acid (RA) and 1,25-dihydroxyvitamin D3 (Vit D3) inhibited estrogen-induced growth of MCF-7 cells and their effect was potentiated by the classical antiestrogen, hydroxytamoxifen. In MCF-7 cells, we found that RA and Vit D3 also inhibited estrogen-induced transcription; this was shown both for an endogenous gene (pS2) and for various exogenous transfected genes. Their inhibitory effect could not be reversed by increasing estradiol concentrations, showing that contrary to classical antiestrogens, they did not compete with estradiol to bind the estrogen receptor (ER). Analysis of the inhibitory mechanisms indicates that RA and Vit D3 receptors can directly or indirectly impair the binding of ER to the estrogen responsive element. The antagonist effect of RA would be found especially at DNA level since it seems to essentially involve an estrogen responsive element. The antagonist effect of Vit D3 would be found especially at the ER level since it seems to concern estrogen binding and dimerization domains of ER. We conclude that the antiestrogenic effects of RA and Vit D3 are similar since they can, via their receptors, interfere with estrogenic action at the estrogen responsive element level but that they are not identical since different molecular mechanisms are involved.
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PMID:Antiestrogenic effects of all-trans-retinoic acid and 1,25-dihydroxyvitamin D3 in breast cancer cells occur at the estrogen response element level but through different molecular mechanisms. 813 48

Four oestrogen-regulated proteins of reported prognostic value, oestrogen receptor (ER), progesterone receptor (PR), pS2 and cathepsin D (Cat D), have been quantified by immunoassays, and the latter studied by immunohistochemistry (IHC) in primary tumours from clinically node-negative early breast cancer patients, entered into a trial of breast conservation therapy in which all the patients received adjuvant tamoxifen. ER, PR and pS2 significantly co-correlated but none correlated with Cat D. ER, PR and pS2, but not Cat D, were significantly associated with tumour size and grade, although Cat D tended to show an inverse relationship with the latter. Cat D (radioimmunoassay) in pmol/mg significantly correlated with the IHC score for Cat D in carcinoma cells as well as the number of Cat D-expressing macrophages. At a median follow-up of only 16 months, recurrence was significantly more common in patients with tumours having negative status for ER, PR and pS2 but was not associated with Cat D status.
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PMID:Steroid receptors, pS2 and cathepsin D in early clinically node-negative breast cancer. 814 64

A third of breast cancers are estrogen dependent and respond to endocrine therapy. The estrogen receptor (ER) was the first marker used to predict the responses to treatment, and two-thirds of ER positive tumors show a favourable response. Several estrogen-regulated proteins were further studied in a search to enhance the prediction accuracy of ER status: progesterone receptors, 24-K heat shock protein, cathepsin D, and recently pS2 protein. The pS2 gene, also named BCEI, pNR-2 [4], Md2, was first identified by two groups using differential screening of a complementary DNA library derived from a human breast carcinoma cell line (MCF-7) grown with and without estrogens. Later on two independent English groups and a Japanese group identified a gene similar to pS2. The pS2 mRNA, relatively abundant (0.8%) in the MCF-7 cell line when stimulated by estrogens, encodes a cystein-rich, 84 aminoacids peptide which is secreted by breast cancer cells. The expression of the pS2 gene, pS2 protein assays in tumor cytosols and more recently pS2 detection by immunocytochemistry, have been described in several series of breast cancers.
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PMID:Clinical significance of the estrogen regulated pS2 protein in mammary tumors. 824 Jul 4

We examined the expression of pS2 protein in 48 invasive ductal breast carcinomas with an extensive intraductal component, using immunohistochemical staining of paraffin-embedded sections. The patients selected for this study would have met the criteria for breast-conserving surgery applied at our institute at present. The rate of pS2 expression in the intraductal lesion was significantly higher than that in the main invasive lesion. The incidence of pS2 protein expression in the latter lesions was very similar to that in invasive carcinoma without intraductal lesions. The pS2 positivity of the intraductal lesion was equal to or higher than that of the invasive lesion. Of intraductal lesions, those classified as non-comedo carcinomas frequently contained more pS2 protein than did comedo carcinomas.
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PMID:Immunohistochemical survey of pS2 expression in intraductal lesions associated with invasive ductal carcinoma of the breast. 825 23

The effects of the anti-estrogens 4-hydroxytamoxifen (OHTam), ICI 164,384 and ICI 182,780 were tested on the MCF-7/LCC2 breast-carcinoma cell line, which grows significantly in the presence of OHTam and serves as a model for studying anti-estrogen resistance of estrogen-receptor-positive breast cancer. Cell proliferation and cathepsin-D secretion were strongly inhibited by either ICI 182,780 or ICI 164,384 alone or ICI 164,384 in combination with 17-beta-estradiol (E2) or OHTam. ICI 164,384 alone did not affect the cathepsin-D and pS2 mRNA levels, but antagonized the stimulatory effects of E2 or OHTam on these 2 mRNAs. OHTam was more effective than E2 in increasing cathepsin-D mRNA levels, supporting the idea that anti-estrogen-resistant breast cancer continues to overexpress cathepsin-D. These data show that the steroidal anti-estrogens ICI 164,384 and ICI 182,780 retain their ability to inhibit cell proliferation and the estrogen-responsiveness of cathepsin-D and pS2 genes in the OHTam-resistant MCF-7/LCC2 cell lines. These pure anti-estrogens may thus be efficient second-line treatments of some Tamoxifen-resistant tumors.
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PMID:Anti-proliferative and anti-estrogenic effects of ICI 164,384 and ICI 182,780 in 4-OH-tamoxifen-resistant human breast-cancer cells. 831 14

A new complementary DNA, p27, has been cloned and sequenced from estradiol-treated MCF7 human breast carcinoma cells. It encodes a putative highly hydrophobic protein of 122 amino acids which has a 33% overall sequence similarity to the product of the 6-16 gene (R. L. Friedman, S. P. Manly, M. McMahon, I. M. Kerr, and G. R. Stark, Cell, 38: 745-755, 1984), which is transcriptionally induced by interferons of the alpha/beta type. We demonstrate here that the p27 gene, which is located in band q32 of human chromosome 14, is also induced by interferon-alpha in human cell lines of different origin and that expression is independent of the presence of estradiol receptor in the cells. High levels of p27 RNA were found in vivo in approximately 50% of primary human breast carcinomas (21 were tested by Northern blotting). In situ hybridization to some of the p27-overexpressing tumors showed that the p27 RNA is localized in cancer cells and sometimes also in fibroblastic cells of tumor stroma. p27 RNA levels in the tumors did not correlate with the presence of estrogen receptor or with the expression of the estrogen-induced pS2 gene. Further studies are now necessary to elucidate the cause of p27 gene overexpression in breast carcinoma and in particular to determine whether it corresponds to chromosomal rearrangements in the 14q32 region and/or to induction by interferons of the alpha/beta type.
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PMID:Identification of a new interferon-alpha-inducible gene (p27) on human chromosome 14q32 and its expression in breast carcinoma. 835 38

A novel oestrogen-responsive breast-tumour cell line, EFF-3, has been established from a pleural exudate of a patient with metastatic breast cancer. The cells show morphological and immunohistochemical features consistent with their origin from a metastatic breast carcinoma. The cells aggregate and form sheets in culture, and electron microscopy confirms the presence of cell-surface microvilli and intercellular tight junctions. The epithelial origin of EFF-3 cells was confirmed by their expression of low-molecular-weight cytokeratins and carcinoembryonic antigen. The karyotype of the cells is markedly abnormal and there are large numbers of structurally abnormal chromosomes. EFF-3 cells express oestrogen receptor, oestrogen-receptor mRNA, their growth is oestrogen-responsive, and specific genes are regulated by oestrogens. The pNR-2/pS2 and pNR-25 oestrogen-regulated mRNAs are induced 15- and 13-fold respectively by oestrogen, whereas the oestrogen-receptor and cathepsin D mRNAs are not regulated. This pattern of regulation differs from that reported previously for other cell lines. The EFF-3 cell line should be useful for studying the mechanisms involved in oestrogen-stimulated proliferation and the factors determining the regulation of specific genes by oestrogens.
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PMID:Isolation and characterization of an oestrogen-responsive breast-cancer cell line, EFF-3. 842 92

Expression of pS2 protein (an oestrogen-induced gene discovered in the MCF-7 breast carcinoma cell line) and its homologue human spasmolytic polypeptide (hSP) was analysed, using immunohistochemistry and in situ hybridization to their mRNAs, in the proximal duodenum of 17 partial gastrectomy specimens removed from individuals with chronic peptic ulceration. Eight were found to have gastric-type metaplasia. In gastric metaplasia, mRNAs for pS2 and hSP, and pS2 peptide antibody were co-localized in the cells covering the duodenal villi. pS2 immunostaining was diffusely cytoplasmic in nature. A similar pattern was seen in Brunner's gland ducts. The trefoil peptide localization in gastric metaplasia closely resembles that seen in superficial gastric epithelium and the distal Brunner's gland duct, which in turn shares morphological similarities with gastric epithelium. We therefore conclude that gastric metaplasia may be the result of an expansion of the surface component of the Brunner's gland duct. The function of these trefoil peptides is at present unknown, but their distribution elsewhere suggests an involvement in reparative mechanisms. The similarities between gastric foveolar and Brunner's gland duct epithelium may derive from common restitution-enhancing features pertinent to a locally harsh environment.
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PMID:The expression of the trefoil peptides pS2 and human spasmolytic polypeptide (hSP) in 'gastric metaplasia' of the proximal duodenum: implications for the nature of 'gastric metaplasia'. 849 29


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