Browsing by Subject "castration-resistant prostate cancer"

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    Alkaline phosphatase in metastatic castration-resistant prostate cancer: reassessment of an older biomarker
    (Future Medicine, 2018-06-21) Heinrich, Daniel; Bruland, Øyvind; Guise, Theresa A; Suzuki, Hiroyoshi; Sartor, Oliver; Medicine, School of Medicine
    Since most patients with metastatic castration-resistant prostate cancer (mCRPC) have bone metastases, it is important to understand the potential impact of therapies on prognostic biomarkers, such as ALP. Clinical studies involving mCRPC life-prolonging agents (i.e., sipuleucel-T, abiraterone, enzalutamide, docetaxel, cabazitaxel, and radium-223) have shown that baseline ALP level is prognostic for overall survival, and may be a better prognostic marker for overall survival than prostate-specific antigen in patients with bone-dominant mCRPC. Mechanism of action differences between therapies may partly explain ALP dynamics during treatment. ALP changes can be interpreted within the context of other parameters while monitoring disease activity to better understand the underlying pathology. This review evaluates the current role of ALP in mCRPC.
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    Epigenetic Modulations and Lineage Plasticity in Advanced Prostate Cancer
    (Elsevier, 2020-04) Ge, R.; Wang, Z.; Montironi, R.; Jiang, Z.; Cheng, M.; Santoni, M.; Huang, K.; Massari, F.; Lu, X.; Cimadamore, A.; Lopez-Beltran, A.; Cheng, L.; Pathology and Laboratory Medicine, School of Medicine
    Prostate cancer is the most common cancer and second leading cause of cancer-related death in American men. Antiandrogen therapies are part of the standard of therapeutic regimen for advanced or metastatic prostate cancers; however, patients who receive these treatments are more likely to develop castration-resistant prostate cancer (CRPC) or neuroendocrine prostate cancer (NEPC). In the development of CRPC or NEPC, numerous genetic signaling pathways have been under preclinical investigations and in clinical trials. Accumulated evidence shows that DNA methylation, chromatin integrity, and accessibility for transcriptional regulation still play key roles in prostate cancer initiation and progression. Better understanding of how epigenetic change regulates the progression of prostate cancer and the interaction between epigenetic and genetic modulators driving NEPC may help develop a better risk stratification and more effective treatment regimens for prostate cancer patients.