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Expression of glutathione S-transferase B1, B2, Mu and Pi in breast cancers and their relationship to oestrogen receptor status.
The concentrations of glutathione S-transferase (GST) B1 and B2 (Alpha), Pi and Mu have been measured by radioimmunoassay in cytosols from 28 oestrogen receptor (ER) rich an 30 ER-poor breast tumours. GST B1, B2 and Pi was detected in all 58 breast tumour cytosols whilst GST Mu was found in only 28....
Autores principales: | , , , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
1989
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2247272/ https://www.ncbi.nlm.nih.gov/pubmed/2605095 |
Sumario: | The concentrations of glutathione S-transferase (GST) B1 and B2 (Alpha), Pi and Mu have been measured by radioimmunoassay in cytosols from 28 oestrogen receptor (ER) rich an 30 ER-poor breast tumours. GST B1, B2 and Pi was detected in all 58 breast tumour cytosols whilst GST Mu was found in only 28. Of the GSTs, Pi was expressed most strongly in all cytosols and the concentration was significantly higher in ER-poor tumour cytosols than in ER-rich tumours (P less than 0.01). As with GST Pi, the highest levels of GST B1 and GST B2 were found in ER-poor tumour cytosols; the levels of GST B1 and GST B2 were positively correlated (r = 0.66, P less than 0.001). No quantitative or qualitative association was found between ER status and GST Mu which was expressed in 46% of ER-rich and 50% of ER-poor tumour cytosols. No relationship could be found between GST expression and age, menopausal status, lymph node involvement or tumour T stage in the subgroup of patients in whom this information was available. These data suggest that a common mechanism is responsible for GST induction in ER-poor tumours and that the nulled Mu phenotype has no increased susceptibility to developing breast cancer. |
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