High Progesterone Receptor Expression in Prostate Cancer Is Associated with Clinical Fa... - 0 views
www.ncbi.nlm.nih.gov/...PMC4344236
prostate cancer progesterone progesterone receptor hormones cancer prostate
shared by Nathan Goodyear on 03 Jun 18
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Currently, there is a general agreement of PGR presence in the stromal cells of PCa
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Our large-sized study demonstrates a wide distribution of PGR in stromal and epithelial cells of both benign and malignant prostate tissue
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In line with our findings, several have also reported a high PGR expression in TE of PCa [9,10,23,25]. In contrast, others have demonstrated a total lack of PGR expression in TE
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In our work univariate analysis demonstrated a high PGR expression in TS to be associated with clinical failure in PCa patients. So far we have not yet demonstrated the mechanism underlying this association
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Several non-genomic proliferative actions of progesterone have been proposed in tumor cells of other organs, including breast [35–37], astrocytoma [38] and osteosarcoma [39] cell lines. However, such results are contradicted by suggestions of anti-proliferative actions of progesterone in endometrial cancer
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Latil and co-workers found a decreased PGR expression in clinically localized tumors and increased PGR expression in hormone-refractory tumors, when compared with normal prostate tissue
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Our findings provide further support to these findings, indicating that PGR plays a role in the pathogenesis of PCa
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Ki67 and PGR in TE were correlated with CF (S3 Text), indicating an association between PGR and proliferative activity
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The PGR is, like the glucocorticoid receptor, similar to androgen receptor with 88% sequence homology in the ligand-binding domain
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progesterone induced expression of androgen receptor-regulated genes could be a potential mechanism contributing to the development of castrate resistant PCa
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A possibility of different roles by the two PGR isoforms in normal prostate tissue and PCa, as is suggested for the estrogen receptors [13], must also be taken into account
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STudy finds that increased Progesterone receptor expression on epithelial and stromal cells is associated with increased clinical failure of therapy. Several proposed mechanisms: 88% homologous with androgen receptor suggesting cross-stimulation and via progesterone induced increased androgen receptor gene stimulation i.e. epigenetics.