Published Date: December 2019
Bone health is a critical area of unmet need among men with advanced prostate cancer. Age increases the risk for fragility fractures among both men and women, and older men with fragility fractures are at higher risk of subsequent death than are women.1-3 Systemic anti-androgen therapies for prostate cancer, while life-prolonging, accelerate bone loss by tipping the balance of bone homeostasis toward bone resorption, which further increases patients’ risk of fragility fractures.4
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The Latest Research on mCRPC Treatment
In the summary slide of one of my 'go-to' talks I pose the question “Have we reached the limits of androgen receptor (AR) targeting?”. Of course, I don’t know the answer, which is precisely why it is framed in the form of a question on a summary slide. But I think about it a lot. So, let’s ponder this question a little.
Charles J. Ryan, MD is the B.J. Kennedy Chair in Clinical Medical Oncology at the University of Minnesota and Director of the Division of Hematology, Oncology and Transplantation. He previously held the position of Professor of Clinical Medicine and Urology and the Clinical Program Leader for Genitourinary Medical Oncology at the UCSF Helen Diller Family Comprehensive Cancer Center
Published Date: December 2019
During much of the past 30 years, genetic tests for heritable disorders have assessed limited numbers of genes and have often employed serial testing algorithms in which the next test was determined by the results of the prior test.¹ The advent of next-generation (also known as massively parallel high-throughput) sequencing has transformed this picture by making it possible to sequence the entire human genome for less than $1,000.1,2
Protecting and improving bone health is critical when managing all stages of prostate cancer. Androgen deprivation therapy (ADT) accelerates bone resorption, which compromises bone mass and integrity starting early in treatment.1 Metastatic prostate cancer is associated with a marked increase in risk of skeletal events (fracture, spinal cord compression, and bone surgery or radiotherapy) associated with both bone metastases and treatment-induced bone loss.
The European Association of Urology defines castration-resistant prostate cancer (CRPC) as serum testosterone < 50 ng/dL or < 1.7 nmol/L plus either biochemical progression (three consecutive rises in prostate-specific antigen [PSA] one week apart, resulting in two 50% increases over the nadir, and PSA > 2 ng/mL) or radiologic progression
Until 2010, our treatment armamentarium for prostate cancer (PC) was fairly limited. Patients received local therapy for non-metastatic disease, androgen deprivation therapy (ADT) for hormone-naïve metastatic disease, denosumab and zoledronic acid for metastatic castration-resistant prostate cancer (mCRPC), and bisphosphonates or docetaxel for symptomatic mCRPC.
There are a growing number of treatment options for patients with metastatic castrate-resistant prostate cancer including those targeting the androgen axis (abiraterone acetate plus prednisone and enzalutamide), cytotoxic chemotherapy (docetaxel and cabazitaxel), radiopharmaceuticals (radium-223), and immunotherapeutic approaches (sipuleucel-T).Read More
Several trials have recently focused on delineating the optimal radiotherapy fractionation schedule for the primary treatment of prostate cancer. In 2016, efficacy results of the Dutch HYPRO trial were published, assessing hypofractionated radiotherapy compared with conventionally fractionated radiotherapy among patients with intermediate-risk to high-risk T1b-T4NX-N0MX-M0 localized prostate cancer.1Read More