CAR T-Cell Therapy in Metastatic CRPC and Future Directions in Care

EP: 1.Overview of Metastatic HSPC: Diagnosis and Risk Stratification

EP: 2.Systemic Treatment Armamentarium in Metastatic HSPC

EP: 3.What is the Role of Locoregional Therapy in Metastatic HSPC?

EP: 4.Informing Systemic Therapy Selection With Negative Data in HSPC

EP: 5.Evolving Treatment Landscape of Nonmetastatic Castration-Resistant Prostate Cancer

EP: 6.Advent of PARP Inhibitors in Metastatic CRPC

EP: 7.Combination PARPi Strategies in Metastatic CRPC: Interpreting Data From Clinical Trials

EP: 8.Radioligands in the Treatment of Metastatic CRPC: Lutetium-177–PSMA-617

EP: 9.Radioligands in the Treatment of Metastatic CRPC: Radium-223

EP: 10.Metastatic CRPC: Novel Treatment Strategies With Radioligand Therapy

EP: 11.Novel Therapeutic Targets in Metastatic CRPC

EP: 12.Potential for CDK4/6 Inhibitors in Metastatic CRPC

EP: 13.Ongoing Clinical Trials in the Metastatic CRPC Setting

Now Viewing

EP: 14.CAR T-Cell Therapy in Metastatic CRPC and Future Directions in Care

Transcript:

Rana McKay, MD:That’s a perfect segue into CAR [chimeric antigen receptor] T cells. Where are we there? Tanya [Dorff] presented data on PSCA [prostate stem cell antigen]. The final analysis is that it continues to see toxicity. Regarding efficacy, I don’t think there was even a single PR [partial response] reported from the trial. Are we there yet or not with CAR T therapy? There’s a lot of excitement. Sumit, what do you think about CAR T?

Sumit K. Subudhi, MD, PhD:I don’t think it’s ready for solid tumors. It’s a great option for liquid tumors. That’s because we’re talking about the microenvironment, which is so important. Carl Jones’s group published that PSMA [prostate-specific membrane antigen] CAR T with the TGFB-dominant negative, which also saw a couple of responders. When they looked at the tumor microenvironment, they saw that a lot of the CAR Ts were getting stuck in the stroma area and not making it to the center of the tumor. The microenvironment continues to be a problem. If the issue is with toxicities, you can’t combine them with anything to help the microenvironment, like cabozantinib. We’ve got a ways to go.

Rana McKay, MD:It’s been so exciting seeing all the new data presented at ASCO [American Society of Clinical Oncology Annual Meeting]. The field has been changing rapidly. We’re redefining what all these states are. Repositioning our targeted therapies, our chemotherapies, looking at novel targets. It’s an exciting time for prostate cancer, with new imaging and genomics. Thank you all for joining us on the panel. Any final thoughts from the group?

Sumit K. Subudhi, MD, PhD:I’m excited about T-cell bispecifics.

Rana McKay, MD:Arash, any final thoughts from you?

Arash Rezazadeh Kalebasty, MD:It’s been a great discussion. I don’t have much to add, but I enjoyed the discussion.

Rana McKay, MD:Scott?

Scott Tagawa, MD, MS, FACP:I’m all for more confusion—having many more diagnostics and therapeutics. It gives us more options. I’ll live with that confusion.

Rana McKay, MD:Ulka?

Ulka Vaishampayan MD:No matter what, clinical trials are what help advance things. It’s important to keep considering patients for clinical trials.

Rana McKay, MD:Thank you all for a wonderful discussion. Thank you to our audience. We hope you found this OncLive® Peer Exchange® discussion to be useful and informative. I appreciate your time.

Transcript edited for clarity.