Overview on Androgen Deprivation Therapy in Prostate Cancer

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EP: 1.Overview on Androgen Deprivation Therapy in Prostate Cancer

EP: 2.ADT Therapy in Prostate Cancer: Agonists vs Antagonists

EP: 3.Patient Scenario 1: nmCRPC Identification and Work-up

EP: 4.AR Inhibitor Selection in Nonmetastatic Castration-Resistant Prostate Cancer

EP: 5.PSMA-Targeted Therapy for nmCRPC

EP: 6.Patient Scenario 2: Selecting Therapy for mHSPC

EP: 7.Novel Approaches to Optimizing Management of mHSPC

EP: 8.Genomic Testing Practices in Prostate Cancer

EP: 9.Triplet Combination Strategies to Manage Metastatic HSPC

EP: 10.Recap: Updates of Androgen Deprivation Therapy in Prostate Cancer

Transcript:

Robert Dreicer, MD, MS, MACP, FASCO: Welcome to this CancerNetwork® [Around the Practice] presentation [titled], “Prostate Cancer: Androgen Deprivation Therapy Updates.” I’m your host, Dr Robert Dreicer. I’m head of the section [of] medical oncology and deputy director of the University of Virginia Cancer Center. I’m fortunate to be joined for this program by 2 outstanding urologic oncologists: Dr Saby George, [MD, FACP], who runs the oncology program at the Roswell Park Comprehensive Cancer Center; and Dr Mark Scholz, [MD], from Cedars-Sinai Marina del Rey Hospital. [Scholz is] also the medical director of the Prostate Oncology Specialty Group in Marina del Rey.

Today, we’re going to discuss the use of androgen deprivation therapy as a backdrop to the use of the newer antiandrogens in the treatment of prostate cancer across a couple of disease spectrums. We’ll review a couple cases and try to bring into play recent data [and] existing data in terms of informing treatment decisions. Let’s get started.

Dr George, give us a bit of [high-level] background about the role of [androgen] deprivation therapy in prostate cancer. It was 1941 [when] the famous [Charles] Huggins, [MD], and [Clarence] Hodges, [MD], paper about the introduction of testosterone suppression was first published, leading to the Nobel Prize, which was awarded in the mid-1960s. Why do we do T-cell suppression in prostate cancer?

Saby George, MD, FACP: That’s an important question in the management of prostate cancer. Prostate cancer thrives, multiplies, propagates, and metastasizes, [depending] on antigen receptor signaling, by testosterone binding to the [antigen receptor]. That allows for the cancer cells to multiply and spread. This seminal discovery by the Nobel Prize–winning doctors in 1941 led to the implementation of antigen suppression as a mainstay of treatment. We have seen many new developments in terms of adding more to the androgen suppression, [and] yet androgen suppression is the mainstay.

There are different ways this can be achieved. No. 1, [by] bilateral orchiectomy. That’s [probably] one of the fastest ways to achieve castrate-range testosterone levels. As soon as you clip the artery feeding to the testicles, they’re almost castrated. The most common way is to suppress via the pituitary testicular access by using LHRH [luteinizing hormone–releasing hormone] agonist and LHRH antagonist. LHRH agonist, [such as] leuprolide, takes 3 to 4 weeks for castrate-range testosterone levels to be achieved, [whereas] newer agents—LHRH antagonists, [such as] degarelix—can achieve that. 5% of patients become castrated within 3 days of LHRH antagonist use. There are other ways to suppress the T-cell signaling, by targeting the androgen receptor blockers and novel agents that can block the signaling, like enzalutamide, apalutamide, and bicalutamide. Those are the newer agents. We have a whole host of different ways of blocking testosterone signaling, binding, and internalization into the nucleus and preventing the propagation and multiplication of prostate cancer cells. This is crucial in managing the disease.

Transcript edited for clarity.