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Supraphysiologic Testosterone Solutions for Enzalutamide-resistant Prostate Cancer
To view the full text, please login as a subscribed user or purchase a subscription. Click here to view the full text on ScienceDirect. In this issue of European Urology, Lam et al [1] report on their investigation of supraphysiologic testosterone (SPT) in castration-resistant prostate cancer (CRPC) patient-derived xenografts (PDXs). The authors identified PDXs that demonstrate slow or suppressed growth when treated with SPT.
Distinct Activation Mechanisms of NF-κB Regulator Inhibitor of NF-κB Kinase (IKK) by Isoforms of the Cell Death Regulator Cellular FLICE-like Inhibitory Protein (cFLIP)
The viral FLICE-like inhibitory protein (FLIP) protein from Kaposi sarcoma-associated herpesvirus activates the NF-κB pathway by forming a stable complex with a central region (amino acids 150–272) of the inhibitor of NF-κB kinase (IKK) γ subunits, thereby activating IKK. Cellular FLIP (cFLIP) forms are also known to activate the NF-κB pathway via IKK activation.
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