Key Takeaways From ASCO GU 2025: TALAPRO-2, PSMA PET, and Emerging Treatments

At the 2025 American Society of Clinical Oncology Genitourinary Cancers Symposium, an expert panel convened to discuss the latest research and clinical advancements in prostate cancer diagnosis and treatment. Moderated by Dr. Alan Bryce, City of Hope, Arizona, the roundtable consisted of Dr. Alan Tan, Vanderbilt; Dr. Evan Yu, Fred Hutch/University of Washington; Dr. Priyanka Chablani, UPMC; Dr. Jack Andrews, Mayo Clinic Arizona; and Dr. Chad Tang, MD Anderson Cancer Center.

In the final segment, the panel reflects on the most exciting data from ASCO GU 2025, highlighting key advancements in biomarker-driven treatment, PSMA PET applications, and emerging therapies. Discussions cover the PORTOS score for refining radiation therapy, the TALAPRO-2 trial’s impact on PARP inhibitor use, and the promising role of EZH2 inhibition with mevrometostat.

View the rest of the videos in the series.

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Dr. Bryce: I’ll ask everyone and kind of open here, go down the line. What’s the most exciting piece of data you saw today at GU ASCO 25? And then we’ll wrap up, kind of last word.

Dr. Tang: So as a radiation oncologist, I think I can make a plug for some of the radiation oncology studies here. So I think one of the really interesting studies is a study out of Wisconsin by George Zhao who is looking at the PORTOS score, which is a different set of genes that make the Decipher score. And the idea of that is, they’re trying to find out in patients with high PORTOS score, maybe they don’t, or they can, or they need dose escalator radiation therapy. So this is one of the things that may bridge us towards actually de-escalating the radiation therapy, which might help men with localized prostate or metastatic prostate cancer maintain sexual function and other, and urinary function.

Dr. Andrews: I don’t want to highlight any one particular trial. What I would say is, if you go around the poster section, you’ll see a lot of very interesting data using PSMA PET for the endpoint. And I think that gives us a lot of insight into what’s happening now. And so that was what I found really exciting today.

Dr. Bryce: Yeah, fair enough. Dr. Chablani?

Dr. Chablani: I’m going to go with TALAPRO-2. I think it is a little bit of a vanishing population. We’re not seeing people on ADT alone that are progressing to getting this combination, but it’s good to know that synergy is there. And I think it just makes us remember always to check our NGS, check our germline, and ctDNA or liquid biopsies if we don’t have access to NGS. And I think it’s exciting that the field is moving towards more personalized approaches, not just looking at the efficacy of PARP and ARSI and BRCA1, BRCA2, but also important mutations such as PALB2, CDK12, and the differential responses that we’re seeing in these other DNA damage repair mutations.

Dr. Yu: I’m going to go with mevrometostat, the EZH2 inhibitor. EZH2 has been around for a long time. I remember Chenayan’s paper, it was earth-shattering, exciting to me. What was that, 20 years ago or so? And I’ve been waiting, waiting, waiting, waiting. We’ve seen efficacy in other cancers. We haven’t seen it in prostate cancer, and we haven’t had great successes with EZH2 inhibitors. But this one looked good today. I mean, just a few minutes ago we saw Mike Schweitzer’s presentation that looks like a significant, at least in a randomized phase two setting, rPFS benefit, resist 1.1 response rate and PSA response rate. So, I think that’s pretty impressive. And I’m really excited to see the results of the two randomized phase IIIs that are ongoing.

Dr. Bryce: Yeah. Fair enough. Dr. Tan?

Dr. Tan: I’ll go twofold here. I agree with Priyanka, I think TALAPRO-2 was the big data set phase III study here. But in an unselected population, it was also positive for overall survival. But it has us still scratching our heads. Is it the right answer still on an unselected population? Or do we still look at HR positive only? Or is BRCA2 doing all the heavy lifting? So I think it’s still up to the regulatory agencies to talk about that. But also, this isn’t new data, but just a reiteration of all the novel therapies that are coming, the T cell engagers, the BiTEs, taluridimade. This is a cancer that has traditionally not been immune responsive. It’s been an immune co kind of tumor, but we’re finding ways to have durable responses with some of these T cell engagers.