Loss of bone mineral density with androgen deprivation therapy (ADT) for prostate cancer is well recognised, with significant loss of bone mineral density (BMD) occurring within 12 months of starting therapy. With ADT, annual loss of BMD is about 2%-8% per year at the lumbar spine and 1.8%-6.5% at the hip; the loss appears to continue indefinitely while treatment continues, and there is no recovery after therapy is ceased. 19.4% of men surviving at least 5 years after diagnosis of prostate cancer have a fracture if treated with ADT compared with 12.6% of men not receiving ADT; this is equivalent to one additional fracture for every 28 men treated with ADT. Vitamin D deficiency exacerbates the development of osteoporosis, so vitamin D status should be evaluated before commencing ADT in men with prostate cancer. Treatment with bisphosphonates (zoledronate, pamidronate and alendronate) in men treated with ADT have been shown to prevent bone loss in prospective studies and to increase BMD in one randomised controlled trial; bisphosphonates have not been shown to prevent fractures in men with prostate cancer. Further prospective trials are required to assess the efficacy and cost-effectiveness of bisphosphonates in men with prostate cancer who require treatment with ADT. All doctors need to take an active role in monitoring bone health in patients with prostate cancer requiring ADT.
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http://dx.doi.org/10.5694/j.1326-5377.2006.tb00180.x | DOI Listing |
Biomarkers
January 2025
Department of Pathology, Anhui Medical University, Hefei, Anhui, China.
Objective: To examine the role and diagnostic potential of miR-421 in prostate cancer (PCa).
Methods: Expression data and clinical information for miR-421 were obtained from the TCGA and Genotype-Tissue Expression (GTEx) databases. Experimental validation was performed at the cellular, blood, and tissue levels to confirm miR-421 expression and its association with clinicopathological features.
Am J Cancer Res
December 2024
Department of Biomedical Sciences, Discipline of Pharmacology, Edward Via College of Osteopathic Medicine (VCOM) Monroe, LA 71203, USA.
Prostate cancer (PCa) is the second leading cause of cancer-related deaths among American men. The development of metastatic castration resistant PCa (mCRPC) is the current clinical challenge. Antiandrogens such as Enzalutamide (ENZ) are commonly used for CRPC treatment.
View Article and Find Full Text PDFAm J Cancer Res
December 2024
Laboratory of Translational Oncology and Experimental Cancer Therapeutics, The Warren Alpert Medical School, Brown University Providence, RI 02903, USA.
Androgen receptor (AR) signaling is a target in prostate cancer therapy and can be treated with non-steroidal anti-androgens (NSAA) including enzalutamide, and apalutamide for patients with advanced disease. Metastatic castration-resistant prostate cancer (mCPRC) develop resistance becomes refractory to therapy limiting patient overall survival. Darolutamide is a novel next-generation androgen receptor-signaling inhibitor that is FDA approved for non-metastatic castration resistant prostate cancer (nmCRPC).
View Article and Find Full Text PDFBio Protoc
January 2025
Department of Structural and Cellular Biology, Tulane University, New Orleans, LA, USA.
The initiation and progression of prostate cancer (PCa) are associated with aging. In the history of age-related PCa research, mice have become a more popular animal model option than any other species due to their short lifespan and rapid reproduction. However, PCa in mice is usually induced at a relatively young age, while it spontaneously develops in humans at an older age.
View Article and Find Full Text PDFAnal Cell Pathol (Amst)
January 2025
Department of Urology, The First Hospital of Jilin University, Changchun, China.
This study aims to study how gold nanoparticles (AuNPs) function in the recruitment and polarization of tumor-associated macrophages (TAMs) in hormone-sensitive prostate cancer (HSPC) and castration-resistant prostate cancer (CRPC). Phorbol ester (PMA)-treated THP-1 cells were cocultured with LNCaP or PC3 cells to simulate TAMs. Macrophage M2 polarization levels were detected using flow cytometry and M2 marker determination.
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