https://www.onclive.com/peer-exchange-archive/gu-clinical-challenges/treatment-of-bone-metastases-in-prostate-cancer
Treatment of Bone Metastases in Prostate Cancer

Panelists:Raoul S. Concepcion, MD, FACS, Urology Associates; Michael S. Cookson, MD, MMHC, University of Oklahoma Health Sciences Center; Daniel P. Petrylak, MD, Yale School of Medicine; Daniel I. Quinn, MBBS, PhD, FRACP, FACP, University of Southern California; Neal D. Shore, MD, FACS, Carolina Urologic Research Center; Charles J. Ryan, MD, UCSF Helen Diller Family Comprehensive Cancer Center



Transcript:

Raoul S. Concepcion, MD:
Hello, and, thank you, for joining us today for this OncLive Peer Exchange panel discussion on the topic of “Clinical Challenges in Genitourinary Cancers.” An increased understanding of the underlying biology of prostate and bladder cancers, coupled with recent clinical trial findings, are improving treatment options in these tumors. However, there are still many clinical scenarios for which there are no clear-cut answers. This OncLive Peer Exchange will focus on some of the more challenging scenarios facing oncologists and urologists in the genitourinary field, using a case-based approach to bring about important discussion points.

My name is Raoul Concepcion, and I’m the director of the Advanced Therapeutic Centers at the Urology Associates, in Nashville, Tennessee. Participating today on our distinguished panel is: Dr. Michael Cookson, professor and the Donald D. Albers chair in Urology at The Stephenson Cancer Center of The University of Oklahoma Sciences Center; Dr. Daniel Petrylak, director of the Genitourinary Oncology Research Program, and co-director of the Signal Transduction Program at Yale Comprehensive Cancer Center, Yale School of Medicine; Dr. David Quinn, medical director, at Norris Cancer Hospital and Clinics, head of the Genitourinary Section, Division of Oncology, and associate professor of medicine, at the Kenneth J. Norris Jr. Comprehensive Cancer Center, a part of the Keck School of Medicine at the University of Southern California; and Dr. Neal Shore, a medical director and certified physician investigator, at Carolina Urologic Research Center, in Myrtle Beach, South Carolina.

Thanks so much for joining us. Let’s begin.

So, the first case that we are going to discuss today is a 63-year-old white male who, in 2007, was diagnosed with high-grade prostate cancer, and on biopsy was found to have multiple cores of Gleason 4+5. He was evaluated, worked up by urology in October of 2007, opted to undergo radical retropubic prostatectomy, and at the time was noted to have pathologic T3c disease, N0, M0. This was subsequently followed up—because of the high risk of recurrence—with external beam radiotherapy to the pelvis. He was followed again by his urologist, and in November of 2010, he started having a rise of his PSA (prostate-specific antigen) biochemically, and was started on continuous androgen deprivation therapy for a PSA rise to 5.4 ng/ml and a very rapid doubling time of 7 months. With the institution of androgen deprivation therapy, he did have a PSA drop to less than 1 ng/ml, and was being followed very closely by his urologist. But, in February of 2013, he developed castration resistant prostate cancer with a PSA of 4.3 ng/ml and a testosterone level of less than 10. He had a staging workup—including technetium bone scan and CT (computed tomography)—which showed iliac nodal disease, but no evidence of osseous of bone metastases on the bone scan.

The options were discussed with him, and in April of 2013, the patient underwent three cycles of sipuleucel-T. He was then followed very closely again by urology. October of 2013, approximately 6 months after his initiation of sipuleucel-T, his PSA was 7.5 ng/ml, alkaline-phosphatase was 95. January of 2014, his PSA had a rise to 10.7, testosterone less than 10. And, in July of 2014, he had now a more significant rise of his PSA to 19.8 ng/ml. He was still in the castration range of testosterone of less than 10, but a bump in his alkaline-phosphatase at this time went to 145. The urologist, at this point, opted to restage him, and he was found to have a 1 cm left-common iliac node, multiple bone lesions to T12, L2, sacrum—the right 10th rib, left scapula—but was asymptomatic at this timeframe.

So, we have this gentleman who has progressed despite aggressive definitive therapy, and has now received sipuleucel-T—which is an immunotherapy that was approved in 2010. Mike, you are the head of the AUA (American Urological Association) Guidelines committee for metastatic castration resistant prostate cancer. Give us your insight where he stands now, what the guidelines say about this particular patient and what the urologists and medical oncologists ought to be looking at for this patent.

Michael S. Cookson, MD, MMHC: This is an interesting patient, and there is a little more that I would need to know to enable him to fit into the AUA Guidelines. As you know, the AUA Guidelines not only took the FDA-approved agents and classified them based on patient profiles, but they needed certain other information. And that included performance status, which we would assume is pretty good in a 63-year-old man, whether or not he had symptoms. That’s not really been discussed yet. If he had minimal symptoms or was asymptomatic—which I assume he was when he received his sipuleucel-T—then you have certain options. If he is symptomatic, with these bone lesions in the absence of visceral metastases, that opens up another avenue. So, a little bit about that is needed to be able to more clearly define him in the index patients of the AUA. But, in minimally symptomatic or asymptomatic patients, certainly we have active agents that have improved the survival. Those include enzalutamide, abiraterone, and docetaxel. We’ve already mentioned the use of sipuleucel-T. If he moved into a more symptomatic stage, those agents would also be included. But because of the bone lesions, and the absence of visceral metastases, radium-223 would be an excellent option as well.

Transcript Edited for Clarity
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