A phase II study of mifepristone (RU‐486) in castration‐resistant prostate cancer, with a correlative assessment of androgen‐related hormones

@article{Taplin2008API,
  title={A phase II study of mifepristone (RU‐486) in castration‐resistant prostate cancer, with a correlative assessment of androgen‐related hormones},
  author={Mary-Ellen Taplin and Judith B. Manola and William K. Oh and Philip W. Kantoff and Glenn J. Bubley and Matthew R. Smith and Diana Barb and Christos S. Mantzoros and Edward P. Gelmann and Steven P. Balk},
  journal={BJU International},
  year={2008},
  volume={101}
}
To evaluate mifepristone (RU‐486) in patients with castration‐resistant prostate cancer (CRPC), with a correlative assessment of serum androgens and androgen metabolites 
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Prostate cancer develops first as an androgen-dependent tumor in which androgens promote the growth of the PCa cells, and develops into a castration resistant stage that no longer depends on androgens.
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A treatment pathway for patients with CRPC is proposed and strategies to optimize the use of these agents are considered, including the incorporation of predictive and intermediate end point biomarkers, such as circulating tumor cells.
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Artikkel 3 i avhandlingen er kun i manuskriptformat for oyeblikket. Den er inne til vurdering i et internasjonalt tidsskrift og kan derfor ikke publiseres i Munin pa dette tidspunkt.
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TLDR
This Review highlights emerging mechanisms of acquired resistance to contemporary therapies targeting the AR pathway, which fall into the three broad categories of restored AR signalling, AR bypass signalling and complete AR independence.
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Do We Really Need New Trials on Fulvestrant in Prostate Cancer?
TLDR
In this clinical case, the patient did not have castration-refractory prostate cancer (CRPC), but this case report raises two major concerns: the problem of the hormonal status of the disease and the interest of further studies of fulvestrant in this indication.
Reappraisal of glucocorticoids in castrate-resistant prostate cancer
TLDR
The investigators report a correlation between GR expression in patient-derived prostate cancer specimens and clinical response to enzalutamide, and discuss the possibility that these findings have important clinical relevance.
Antiandrogenic, maspin induction, and antiprostate cancer activities of tanshinone IIA and its novel derivatives with modification in ring A.
TLDR
It is discovered tanshinone IIA (TS-IIA) is a potent antagonist of mutated ARs and induces maspin expression through AR and suppressed AR expression and induced apoptosis in LNCaP cells.
Upregulation of glucocorticoid receptor‐mediated glucose transporter 4 in enzalutamide‐resistant prostate cancer
TLDR
It is reported that chronic Enz treatment induced GR‐mediated glucose transporter 4 (GLUT4) upregulation, and that upregulation was associated with resistance to Enz and other AR signaling inhibitors.
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