Overview of Treatment for Metastatic HSPC

EP: 1.Overview of Improvements in Prostate Cancer Management

EP: 2.Optimizing Use of PSMA PET Imaging and PSADT in Prostate Cancer

EP: 3.Evolving Treatment Landscape of Nonmetastatic CRPC

EP: 4.Factors in Selecting Novel AR-Targeted Therapy for Nonmetastatic CRPC

EP: 5.Nonmetastatic Castration-Resistant Prostate Cancer: Quality of Life Measures

EP: 6.Monitoring Strategies in Nonmetastatic CRPC

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EP: 7.Overview of Treatment for Metastatic HSPC

EP: 8.Role of Micronized Abiraterone in Metastatic HSPC

EP: 9.Selecting Optimal Therapy for mHSPC: Design of the ARASENS Trial

EP: 10.Interpreting Data From the ARASENS Trial in Metastatic HSPC

EP: 11.Overview of Therapy for mCRPC: PARP Inhibitors

EP: 12.DNA Alterations and Selection of PARP Inhibitors in mCRPC

EP: 13.Metastatic CRPC: Utility of Imaging as a Biomarker

EP: 14.Selecting Among Novel Imaging Options in Metastatic CRPC

EP: 15.Role of 177Lu-PSMA-617 in mCRPC and Bone Metastases

EP: 16.Addressing Bone and Visceral Metastases in Metastatic CRPC

EP: 17.Results of the VISION Trial and Real-World Use of 177Lu-PSMA-617 in mCRPC

EP: 18.Prostate Cancer Management: Future Directions in Care

Transcript:

Alicia Morgans, MD, MPH: Let’s move on to our next module. We’ll talk about metastatic hormone-sensitive prostate cancer. Scott, let’s start with you. Can you review the landscape of treatment as we know it?

Scott T. Tagawa, MD, MS, FACP: Sure. There are some discussions, and it’s likely the terminology will change. Officially, by working group and ASCO [American Society of Clinical Oncology] definitions, we’re talking about metastatic noncastrate. When they start therapy, their serum level of testosterone is normal, or at least not very low. But castration-sensitive and hormone-sensitive are more or less synonyms, just to put that out there. There are 2 main flavors of patients walking in the door: those with that first diagnosis and those who have recurrence. I’ll mention that first.

For some patients who have an entry primarily, that’s a consideration. I’ll leave it at that, because I’m giving an overview. The nice thing about this disease state is that we have a lot of treatment options. These treatment options don’t improve things by just a little—“a little” is my scientific term—by hazard ratio for weeks or months. These are significant improvements in risk reduction for death that translate into years of survival, even when the same drugs are used later. More specifically, ADT [androgen deprivation therapy] has been in the backbone. As a general rule, that can be a surgical bilateral orchiectomy; otherwise, we use LHRH antagonists or agonists.

Unless there’s an exception, which is rare, they should be getting something else, such as an AR [androgen receptor] pathway inhibitor or chemotherapy. We’ll go over some recent data for the triplets. ADT and docetaxel, at least in some of the subsets that present with metastatic disease and have higher-volume disease, do better when we add in a potent AR pathway inhibitor, as well as data for AR pathway inhibitors having a significant overall survival vs ADT alone. I’ll emphasize that it’s a rare-patient population that should be getting only 1 drug.

Alicia Morgans, MD, MPH: Thank you. That’s going to be a key message as we go through this entire section, that the standard of care is ADT plus a partner, whether that’s an AR-targeted agent, ADT plus docetaxel, or even a triplet as you mentioned. Thank you so much for mentioning that.

Transcript edited for clarity.