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Dr. Joshua K. Sabari and Dr. Daniel V. Araujo provide expert insights into genitourinary cancer updates from ASCO 2025.
Updates from ASCO 2025 explored PARP inhibitors, PSA as a prognostic biomarker and the role of ctDNA in personalizing genitourinary cancer care.
At the 2025 ASCO Annual Meeting, there was a plethora of insights shared across the realm of oncology, including genitourinary (GU) cancers of the prostate and bladder. These updates continue to push the envelope of care that providers may give their patients based on new standard of care and treatment updates.
To fully understand the practice-changing updates to have come out of the meeting, Dr. Joshua K. Sabari sat down with Dr. Daniel V. Araujo to further delve into these insights.
Sabari is the editor in chief of CURE, as well as an assistant professor in the Department of Medicine at NYU Grossman School of Medicine and director of High Reliability Organization Initiatives at Perlmutter Cancer Center. Araujo serves as a medical oncologist at the University of Florida Health (UF) Health.
Read on to learn more from their conversation and meeting insights from ASCO 2025 on genitourinary cancers below!
Sabari: Hello and welcome. My name is Dr. Joshua Sabari. I'm a thoracic medical oncologist at NYU Langone Health Perlmutter Cancer Center, in New York, and I'm excited to be joined by my colleague, Dr. Daniel Araujo. So, Dr. Araujo, please introduce yourself.
Araujo: Thank you so much, Dr. Sabari. My name is Dr. Daniel Araujo. I'm a genitourinary medical oncologist at the University of Florida Gainesville. It's a pleasure to be here.
Sabari: Daniel, welcome. I'm also the editor in chief for CURE, and we're excited for you to give us some of the ASCO updates in the genitourinary, of GU, space. Walk us through what some of the exciting takeaways from this ASCO 2025.
Araujo: Thanks a lot. ASCO, as you know, is always a great meeting to attend, where numerous abstracts are presented, and data is consolidated. This year, particularly in genitourinary cancers, we saw some interesting developments. Perhaps the most practice-changing abstract would be the AMPLITUDE trial.
AMPLITUDE was a randomized controlled trial investigating the role of Zejula (niraparib), which is a PARP inhibitor, in patients with metastatic hormone-sensitive prostate cancer. PARP inhibitors already have an established role in patients with castration-resistant prostate cancer, and now, for the first time, they are being tested in the hormone-sensitive setting.
Essentially, patients with homologous recombination repair (HRR) gene defects were randomized to receive Akeega (niraparib plus abiraterone acetate [Zytiga]) versus abiraterone [alone.] This population represents about 30% of all patients with prostate cancer, so it's a minority, but this group is known for having more aggressive disease with worse outcomes. Essentially, the addition of Zejula to Zytiga was able to extend progression-free survival, especially for patients with BRCA mutations.
This data will likely be assessed by the FDA and other regulators. Other trials with different molecules besides Zejula are being tested in the same space to see if this is a class effect, and it's probably akin to what we see in the castration-resistant setting.
Sabari: Daniel, [PARP inhibitors] are an exciting [area of interest]. We have seen approvals [of these agents across cancer types]. What are some of the side effects that patients should know about that are associated with PARP inhibitors?
Araujo: That's a great question. PARP inhibitors have some class effects, which primarily involve toxicity to the bone marrow, leading to conditions like anemia, neutropenia, and thrombocytopenia. Therefore, before each cycle, we usually repeat blood work to ensure that patients' blood counts are within the reference range. Sometimes, we have to implement dose reductions to manage these effects. Other potential side effects include fatigue and sometimes diarrhea. For some patients, we need to adjust the dose accordingly.
Sabari: Very exciting update, I completely agree with you. Well, what else is exciting in the genitourinary space at ASCO 2025 this year?
Araujo: We saw some interesting prognostic data, which, while perhaps not immediately treatment-changing, provides some important insights. For example, in a large database of prostate cancers treated with ARPIs (androgen receptor pathway inhibitors) and ADT (androgen deprivation therapy) — which is essentially the standard of care for patients with hormone-sensitive prostate cancer — we observed that patients who achieved a PSA of less than 0.2 at six months since treatment initiation have a very good prognosis.
This is interesting because it presents a scenario where you could potentially test de-escalation strategies for patients who achieve that PSA less than 0.2. Conversely, you could also test escalation strategies for patients who did not achieve that target, perhaps intensifying treatment to try and achieve that. It's a very clear outcome-based biomarker of prognosis. There are already some trials investigating, for example, the role of adding chemotherapy to the treatment regimen for patients who have not achieved a PSA less than 0.2.
Sabari: We know how important biomarkers are across all solid tumors, and I agree with you, this could become a critical biomarker to allow us to escalate or potentially deescalate therapy into the future. Any other exciting insights from ASCO before wrapping up?
Araujo: Another technology that is becoming widespread in virtually all cancers is circulating tumor DNA (ctDNA). This was also presented at ASCO, demonstrating its prognostic effect in patients with muscle-invasive bladder cancer. We know that patients with positive ctDNA before chemotherapy in the neoadjuvant setting have a worse prognosis and a lower chance of achieving a pathologic complete response to treatment. This essentially helps identify a group of patients with a poorer prognosis. This is important because it can help us target these specific groups to intensify treatment, perhaps with more aggressive approaches, and try to get the disease under control.
The opposite is also true: we can eventually de-escalate treatment for patients with negative ctDNA upfront. So, the more we know about the behavior and biology of the disease, the more accurately we can employ the correct treatment for the correct patient.
Sabari: Yeah, I couldn't agree more. Here, we're seeing in bladder cancer, utilization of ctDNA, as you mentioned, as a molecular biomarker to help potentially guide therapy. So very exciting updates. Dr Araujo, it's a pleasure to meet you. A pleasure to have this discussion with you, and thank you to the CURE readership and listeners for your attention. Daniel, I look forward to talking again soon.
Araujo: Thank you so much. It was a pleasure to be here.
Transcript has been edited for clarity and conciseness.
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