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Dr. Tagawa:
This is CE on ReachMD, and I'm Dr. Scott Tagawa. I'm glad to have Dr. Mary-Ellen Taplin with me today to discuss a patient case. Let's consider a patient with metastatic hormone-sensitive prostate cancer.

Dr. Taplin:
Thank you, Scott. I have this case, a renowned scientist who came to me. He was a vigorous 78 years old, despite having some underlying medical issues. Namely, he had compensated heart failure, treated hypertension, but otherwise was vigorous. I mean exercising, doing calisthenics and weights, and mentally, while 78, he perceived himself as being like 30.

And he had not had regular PSA screening. He moves all around the world and came into the practice with a very high PSA of 150, metastatic disease by conventional imaging, and about 3 bone metastases: 1 in the spine, 1 in the pelvis, and 1 in a rib that was clearly a metastasis based on imaging criteria. He had a prostate biopsy and had Gleason 8 cancer, had both germline and somatic testing done. Very important point to the audience: please consider early both germline and somatic sequencing of our metastatic patients.

This patient had a normal germline, and he had an SPOP mutation in his tumor. The significance of the SPOP mutation, for me, means that those patients typically respond quite well to androgen deprivation therapy. I would say better than the median.

So this patient wanted to be as aggressive as possible. He was like, “You know I'm 78, but I plan to live to be 108. I want to keep being active, keep being intellectually stimulated in my science and entrepreneurship.” So the treatment plan that I put forward for him was multifactorial and included androgen deprivation therapy. I recommended an ARPI, and it was earlier days, so my choice was basically between abiraterone and enzalutamide.

[I was] cautious about the abiraterone because of his compensated heart failure. He didn't live his life like a heart failure patient, and his EF actually was corrected on all his imaging, but I was nervous and cautious about his underlying cardiovascular risk for abiraterone.

I was also concerned about his risk for fatigue with double ADT, ADT and an ARPI such as enzalutamide, but that was the choice. So I treated him with leuprolide and enzalutamide. I decided with him, because of the burden of his tumor, to just start with full-dose enzalutamide, rather than an attenuated dose and work up. I started with full dose and figured I would work down if needed.

And then I sent him to one of my colleagues in radiation oncology for consideration of prostate radiation and stereotactic radiation to his 3-bone metastases. Patient was happy with this recommendation, felt that he was being given aggressive therapy.

I briefly did consider triplet therapy. And I'll be honest with you, if he was younger, in his 50s, say, early 60s, I might have also considered triplet therapy with the addition of docetaxel, even despite his low-volume disease. But I felt that the data at the time didn't warrant the additional possible toxicity of triplet therapy with docetaxel. And with the SPOP mutation, I felt like he had a really good shot at a better-than-average response to doublet therapy. So this is what was started about 5 years ago, and he remains in complete remission on his ADT and ARPI at this time.

Dr. Tagawa:
Yeah, I think that's a great example of a case where both the overall clinical factors in terms of the cancer, genomic factors in terms of cancer, and certainly the patients with both comorbidities and wishes are taken to account.

And, you know, it was mentioned in a prior episode, particularly in lower-volume disease, treating the primary. I wouldn't say we know that 100% in the current era with all these drugs, but there are some data to show survival advantages, especially in the lower-volume setting.

So I think that all makes sense. And obviously, you can't argue with the outcome, which we have doing well at 5 years.

So thank you very much, Dr. Taplin. And for everyone else, please don't miss our next episode, and thanks for listening.

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