📬 GU Oncology Intelligence Digest — Week 2026-W34
PSMAddition and LITESPARK-011 published in the Lancet, FDA expands perioperative EV-pembrolizumab to all cystectomy-eligible MIBC, and GU clinicians debate PSMA PET endpoints, EV neuropathy and de-escalation.
⚡ TL;DR
📄 Publications
- [177Lu]Lu-PSMA-617 in patients with PSMA-positive metastatic androgen pathway modulator-naive/sensitive prostate cancer (PSMAddition): a phase 3 randomised, controlled trial. — 1144 patients randomised 1:1 (n=572 per arm), 779 (68%) with high-volume disease
- Belzutifan plus lenvatinib versus cabozantinib in patients with previously treated advanced renal cell carcinoma (LITESPARK-011): an open-label, randomised, controlled, phase 3 trial. — 747 participants randomly assigned to belzutifan-lenvatinib (n=371) or cabozantinib (n=376)
🐦 Twitter / 🦋 Bluesky
- Second-line urothelial cancer is the harder question once EV plus pembrolizumab is used up front — Clinicians describe the first-line question in metastatic urothelial cancer as easier and the second-line question as harder after EV plus pembrolizumab changed the algorithm
- Hereditary RCC algorithm circulates as a one-figure guide to genotype-driven surveillance and surgery — The algorithm advises VHL imaging from age 15 with intervention around 3 cm and nephron-sparing surgery, and annual imaging from age 8–10 with prompt aggressive surgery for FH-deficient RCC/HLRCC
- LITESPARK-011 in the Lancet: belzutifan plus lenvatinib beats cabozantinib on PFS but not overall survival — Median PFS 14.8 vs 10.7 months (HR 0.70) with OS not significantly different at interim (HR 0.85) in 747 patients
- HER1–HER4 co-expression in urothelial carcinoma opens ADC targets beyond HER2 — More than 90% of bladder cancer patients express HER1 and HER3, usually concurrently, motivating the HER1/3 dual-target ADC trial IZABRIGHT R3
- Duke manuscript on extraordinary versus poor responders to ADT/ARPI lands alongside new approvals — The manuscript reports clinical and genetic predictors of extraordinary and poor responses to ADT/ARPI therapy in mAPMS prostate cancer
Full details below ↓
📄 What's Being Published
Systemic Therapy in Patients with Metastatic Castration-Resistant Prostate Cancer: ASCO Living Guideline, Version 2026.1.4. — Taplin Mary-Ellen et al., J Clin Oncol
This living guideline is updated on a regular schedule by a standing expert panel that systematically reviews the health literature on a continuous basis. The guideline explicitly states it is not intended to substitute for independent professional judgment of the treating clinician and does not account for individual variation among patients.
Clinical bottom line: The mCRPC living guideline continues on its rolling update cycle, and clinicians are reading the newest version as clarifying that PSMA PET positivity gates 177Lu-PSMA-617 eligibility rather than excluding PSMA-independent options.
[177Lu]Lu-PSMA-617 in patients with PSMA-positive metastatic androgen pathway modulator-naive/sensitive prostate cancer (PSMAddition): a phase 3 randomised, controlled trial. — Tagawa Scott T et al., Lancet
PSMAddition randomly assigned 1144 patients 1:1 (n=572 per arm), with 779 (68%) having high-volume disease; radiographic progression-free survival was significantly improved in the 177Lu-PSMA-617 arm, representing a 28% reduction in the relative risk of radiographic progression or death (HR 0·72, 95% CI 0·58–0·90; p=0·0021), with median rPFS not reached in either arm. Grade 3 or worse adverse events occurred in 51% of patients in the 177Lu-PSMA-617 arm versus 43% in the control arm, with dry mouth reported in 46% versus 4%.
Clinical bottom line: The full PSMAddition publication in the Lancet now provides the randomised evidence behind the FDA approval, and the conversation has shifted from whether radioligand therapy works earlier to which PSMA-positive patients actually need the added toxicity.
Impact of PSA Nadir on Outcomes in Metastatic Hormone-Sensitive Prostate Cancer: A Systematic Review and Reconstructed Individual Patient Data Meta-analysis. — Di Civita Mattia Alberto et al., Target Oncol
This meta-analysis pooled 8 studies comprising 1638 patients for the OS analysis and 1104 for the PFS analysis. Patients achieving a PSA nadir ≤0.2 had a median OS of 92.8 months versus 34 months (HR 0.27, 95% CI 0.22–0.33, p<0.0001) and a median PFS not reached versus 12.1 months (HR 0.19, 95% CI 0.16–0.23, p<0.0001).
Clinical bottom line: The PSA nadir meta-analysis is now being circulated by European GU oncologists as a practical early prognostic checkpoint at ≤0.2 ng/mL for men on ARPI or docetaxel.
FDA Approval Summary: Erdafitinib for FGFR3-Altered Locally Advanced or Metastatic Urothelial Carcinoma. — Maguire William F et al., Clin Cancer Res
THOR (BLC3001) Cohort 1 randomised 266 patients with FGFR3-altered locally advanced or metastatic urothelial carcinoma 1:1 to erdafitinib versus chemotherapy; median OS was 12.1 months in the erdafitinib arm versus 7.8 months in the chemotherapy arm (HR 0.64; p=0.0050). Cohort 2 showed no OS benefit of erdafitinib versus pembrolizumab (HR 1.18, 95% CI 0.92–1.51), which drove a limitation of use in the approval: erdafitinib is not recommended for patients eligible for and who have not received prior PD-(L)1 inhibitor therapy.
Clinical bottom line: Erdafitinib belongs after PD-(L)1 exposure in FGFR3-altered urothelial carcinoma, and the regulatory record makes clear it should not displace checkpoint inhibition in the front line.
Belzutifan plus lenvatinib versus cabozantinib in patients with previously treated advanced renal cell carcinoma (LITESPARK-011): an open-label, randomised, controlled, phase 3 trial. — Motzer Robert J et al., Lancet
LITESPARK-011 randomly assigned 747 participants to belzutifan plus lenvatinib (n=371) or cabozantinib (n=376); progression-free survival was significantly longer in the belzutifan-lenvatinib group (median 14·8 months vs 10·7 months; HR 0·70, 95% CI 0·59–0·84; one-sided p<0·0001). Overall survival was not significantly different between groups (median 34·9 months vs 27·6 months; HR 0·85, 95% CI 0·68–1·05; one-sided p=0·061), and grade 3 or worse treatment-emergent adverse events occurred in 84% versus 83% of participants, most commonly hypertension.
Clinical bottom line: Belzutifan plus lenvatinib buys four months of progression-free survival over cabozantinib after checkpoint inhibition without a survival signal, so the second-line choice now turns on toxicity and patient priorities rather than efficacy alone.
The pan-tumor landscape, allelic status, and genomic complexity of SMARCA4 alterations. — Repetto Matteo et al., Clin Cancer Res
Analysis of 68,920 tumor-normal paired samples sequenced with MSK-IMPACT between 2015 and 2023 found SMARCA4 alterations in 5.6% of bladder cancers; class 1 and class 2 alterations occurred in 2.9% and 0.7% of tumors, respectively. In a phase I trial of the BRM degrader PRT3789, patients with monoallelic class 2 SMARCA4 alterations and preserved BRG1 expression saw clinical benefit, including one complete response.
Clinical bottom line: SMARCA4 alteration class and allelic status should be reported, not just the gene name, because they define which bladder and other tumors are candidates for BRM-directed degraders.
🗣️ What People Were Discussing This Week
How these are chosen: filtered for clinical relevance, grouped by the new development discussed, then ordered by engagement (bookmarks and reposts).
Second-line urothelial cancer is the harder question once EV plus pembrolizumab is used up front
Oncologists describe the first-line question in metastatic urothelial cancer as becoming easier while the second-line question grows harder now that EV plus pembrolizumab has changed the algorithm. A Nectin-4 PET case illustrated that new metastases remained strongly Nectin-4-avid despite progression on EV plus pembrolizumab, raising the possibility that EV resistance does not necessarily equal Nectin-4 loss. The central debate is whether the next choice after EV plus pembrolizumab should be driven by target imaging, a different payload, or a different receptor family altogether.
Discussed by: @EladSharonMD, @OncoAlert
Hereditary RCC algorithm circulates as a one-figure guide to genotype-driven surveillance and surgery
A widely shared algorithm advises imaging VHL patients from age 15, with intervention around 3 cm and nephron-sparing surgery, and annual imaging from age 8–10 with prompt aggressive surgery for FH-deficient RCC/HLRCC. Twenty-five-year prospective NCI data support the 3 cm rule in bilateral multifocal papillary RCC, with excellent oncologic outcomes. The broader debate is whether surveillance intervals and surgical thresholds in hereditary renal cancer should be set by genotype rather than by tumor size alone.
Discussed by: @OncoAlert, @drphil_urology
LITESPARK-011 in the Lancet: belzutifan plus lenvatinib beats cabozantinib on PFS but not overall survival
LITESPARK-011, published in the Lancet, compared belzutifan plus lenvatinib against cabozantinib in 747 patients with advanced clear cell RCC after anti-PD-(L)1 therapy; median PFS was 14.8 versus 10.7 months (HR 0.70), while overall survival did not significantly differ at 34.9 versus 27.6 months (HR 0.85), with grade ≥3 adverse events similarly frequent across arms. Clinicians are framing the combination as another second-line option for advanced clear cell RCC, with the question centred on what should carry the most weight when choosing belzutifan-lenvatinib over cabozantinib given a PFS benefit without a survival signal.
Discussed by: @drenriquegrande, @jgong15, @OncoAlert, @g_procopio_
HER1–HER4 co-expression in urothelial carcinoma opens ADC targets beyond HER2
Data circulating this week show that more than 90% of bladder cancer patients express HER1 and HER3, usually concurrently, providing the biological rationale for the IZABRIGHT R3 trial, which is enrolling and tests the HER1/3 dual-target ADC IzaBren in urothelial carcinoma. HER1–HER4 receptors were detected in most tumours and co-expressed in 61%, with HER3 expression particularly frequent. Specialists describe this co-expression data as a strong biological rationale for HER-targeted ADC strategies beyond HER2, and the open question is which receptor should be hit first and whether that choice requires an assay.
Discussed by: @stolaney1, @OncoAlert, @OncoAlert
Duke manuscript on extraordinary versus poor responders to ADT/ARPI lands alongside new approvals
A Duke manuscript reports clinical and genetic predictors of extraordinary and poor responses to ADT/ARPI therapy in mAPMS prostate cancer. In a real-world cohort, favorable features such as low-volume disease, better performance status, and normal laboratory markers predicted improved outcomes, while alterations in genes including TP53 and MYC were linked to poorer survival. Authors tie the work to recent FDA approvals and frame the key question as who needs intensification and which strategy best fits the biology.
Discussed by: @neerajaiims, @OncoAlert, @OncoAlert
Nature Reviews Urology review of oligometastatic prostate cancer sharpens who should get metastasis-directed therapy
PSMA PET-CT is improving identification of patients with limited metastatic burden; phase II trials support metastasis-directed therapy in metachronous disease, while evidence in de novo oligometastatic prostate cancer remains preliminary. Specialists advise against omitting systemic therapy in patients with PSA doubling time under three months or high-risk mutations including BRCA and TP53, with metachronous oligorecurrent hormone-sensitive prostate cancer identified as the population where metastasis-directed therapy alone is most supported. The core debate is which oligometastatic patients can be treated with metastasis-directed therapy alone versus those who need systemic therapy from the start.
Discussed by: @diegoadiazg, @urotoday
🔥 Top Ranked Tweets
UroToday.com @urotoday
RT @ggebraelmd: PSMAaddition out @TheLancet 👉addition of Lu-177 to ADT/ARPI ⬆️ rPFS (HR 0.72) in pts w/ mAPMS #prostatecancer Congrats @DrScottTagawa et al. Check our editorial published @TheLancet discussing the role of Lu in mAPMS 👉https://t.co/xuCXeNnZT0 @neerajaiims @urotoday @OncoAlert https://t.co/iYybrERS3M
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Neeraj Agarwal, MD, FASCO @neerajaiims
RT @ggebraelmd: PSMAaddition out @TheLancet 👉addition of Lu-177 to ADT/ARPI ⬆️ rPFS (HR 0.72) in pts w/ mAPMS #prostatecancer Congrats @DrScottTagawa et al. Check our editorial published @TheLancet discussing the role of Lu in mAPMS 👉https://t.co/xuCXeNnZT0 @neerajaiims @urotoday @OncoAlert https://t.co/iYybrERS3M
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OncoAlert @OncoAlert
RT @ggebraelmd: PSMAaddition out @TheLancet 👉addition of Lu-177 to ADT/ARPI ⬆️ rPFS (HR 0.72) in pts w/ mAPMS #prostatecancer Congrats @DrScottTagawa et al. Check our editorial published @TheLancet discussing the role of Lu in mAPMS 👉https://t.co/xuCXeNnZT0 @neerajaiims @urotoday @OncoAlert https://t.co/iYybrERS3M
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OncoAlert @OncoAlert
RT @OncoAlert: 79.4% vs 66.2%: Could enfortumab vedotin plus pembrolizumab redefine perioperative treatment for bladder cancer?
Enfortumab Vedotin and Pembrolizumab in Cisplatin-Eligible Bladder Cancer
The phase 3 🗝️ KEYNOTE-B15/EV-304 trial found that perioperative enfortumab vedotin plus pembrolizumab 🧪 significantly improved outcomes versus neoadjuvant cisplatin–gemcitabine in cisplatin-eligible muscle-invasive #BladderCancer . Two-year event-free survival was 79.4% versus 66.2%, while overall survival was 86.9% versus 81.3%. Pathologic complete response was also higher (55.8% vs 32.5%), but grade ≥3 adverse events were more frequent, highlighting improved efficacy alongside increased toxicity.
@marcodoc
@DrChrisHoimes
@docjavip
@ZakhariaYousef
@y_loriot
@tompowles1
@AndreaNecchi
@TomFlaigMD
@Uro_Oncologist
Ping OncoAlert Faculty
@DrChoueiri
@apolo_andrea
@neerajaiims
@montypal
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👉 Article Link in first Comment
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OncoAlert @OncoAlert
RT @APCCC_Lugano: 🚨 Could radioligand therapy be moving into the frontline setting for metastatic hormone-sensitive prostate cancer?
Article 📰
https://t.co/pZPz7qdYKX
[177Lu]Lu-PSMA-617 in patients with PSMA-positive metastatic androgen pathway modulator-naive/sensitive prostate cancer (PSMAddition): a phase 3 randomised, controlled trial
The phase 3 PSMAddition trial showed that adding ^177Lu-PSMA-617 to standard androgen deprivation therapy (ADT) 💊 plus an androgen receptor pathway inhibitor (ARPI) significantly 📈 improved radiographic progression-free survival in patients with PSMA-positive metastatic hormone-sensitive #ProstateCancer , reducing the risk of progression or death by 28%.
✅ Although adverse events, particularly dry mouth, cytopenias, and gastrointestinal effects, were more frequent, no unexpected safety concerns emerged, supporting this combination as a potential new frontline treatment.
@DrScottTagawa
@OJSartor
@mishabeltran
@shilpaonc
@cdanicas
@adapthyun
@DrNordquist
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OncoAlert @OncoAlert
RT @niklas_kluemper: Full phase 3 PSMAddition data are now published in @TheLancet!
Last week this data already led to @FDA approval!
In 1,144 patients with PSMA+ mHSPC, adding ^177Lu-PSMA-617 to ADT + ARPI improved rPFS:
HR 0.72 (95% CI 0.58–0.90)
Important proof that PSMA-directed therapy can work much earlier in the disease course.
But the precision-oncology question remains: which PSMA+ patients actually require this additional treatment intensity?
OS remains immature but heads to improvement, and toxicity was increased.
Biomarker and imaging correlatives from PSMAddition will therefore be particularly important.
https://t.co/btwXU2ysOx
@urotoday @OncoAlert @weoncologists @ProfKHerrmann @DrChoueiri @ChrisSweens1 @Markuseckstein3 @DrYukselUrun @drenriquegrande
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OncoAlert @OncoAlert
RT @Markuseckstein3: 🚨 New IBCG Consensus Statement in Nature Reviews Urology: biomarkers across the bladder cancer spectrum. Hensley, Kamat and 30+ colleagues. Essential reading - absolutely fantastic summary! 🔬
The headline recommendations:
🧬 FGFR3 testing in all locally advanced/metastatic disease.
🎯 HER2 IHC in every patient at advanced-stage diagnosis, scored by gastric-adapted ASCO/CAP criteria.
💧 ctDNA as a predictive biomarker for adjuvant immunotherapy after cystectomy, first level 1 evidence via IMvigor 011 (though its practical utility against perioperative EV+P is questionable).
🚫 PD-L1 and TMB: not sufficient to guide ICI use.
🚫 Nectin-4 profiling: currently not recommended to guide enfortumab vedotin.
On that last one I largely agree with the panel, and I want to be precise about why, because the reasoning matters more than the verdict. 🧠
The recommendation is right for today. For most patients with mUC there is simply no better alternative to EV+P. A biomarker only earns its place when a negative result changes what you do. Broad, unselected Nectin-4 testing today would generate numbers without decisions. That is not a good use of tissue, time, or a patient's therapeutic window.
Two points deserve to stay on the table for future trial considerations. 🔬
1️⃣ The membranous Nectin-4 expression evidence keeps growing, independently. Membranous Nectin-4 IHC and NECTIN4 amplification associate with EV outcome across separate groups, including excellent work from MSKCC (@Dr_Aggen @DrRosenbergMSK @h_alahmadie). The EV-301 EPAR contains something the discussion often skips (because it is not easily accessible): patients with low Nectin-4 did not appear to benefit from EV over monochemotherapy, from a randomised phase 3 dataset. That does not mandate routine testing, but it is not hypothesis-generating noise either.
The EPAR report is here - check out pages 117-~130 and specifically the forest plots. https://t.co/9h6fELkYXL
2️⃣ EV-302 was not designed to answer this question, and it has a histological blind spot. Post hoc data at ASCO show the trials recruited almost exclusively conventional mUC, which reliably expresses high Nectin-4 (Chou et al, 2021; Bahlinger et al, 2024). mUC with divergent squamous differentiation, roughly 20 to 25% of the disease spectrum and typically Nectin-4 low (but not always!), is underrepresented across EV-302, EV-303 and EV-304. "Benefit consistent across subgroups (compared to platin)" and "who benefits most" are different questions, and the panel itself notes the highest response rates in high-Nectin-4 tumours. With ORR around two thirds, roughly a third of patients receive a highly toxic ADC without objective response. That is a strong argument for investing in stratification, even while we treat everyone, because there is no better choice for most patients right now (EV plus P is a great regimen).
This highlights - and IBCG concludes that as well: heterogeneity is real, and it argues for spatially aware, standardised membranous scoring, and especially prospective validation before Nectin-4 can enter the clinic - probably Nectin-4 wont be the target we test for in the future but rather other targets that could be a fallback for patients not benefiting well from EV (e.g., EGFR, HER3, HER2, TROP2 and many others).
The methodological point either way: score the membrane, and only the membrane. The binding site is the cell surface, and pooling cytoplasmic with membranous signal measures something the drug or better the antibody cannot reach. H-score is legitimate applied membranously, but a tiered 0 to 3+ system is far more reproducible across observers and labs, which is what a guideline-grade assay requires. Lets see if we can get that set up and harmonized for Nectin-4 and other targets of major relevance in the future.
Where this is heading. The paper says it too: novel target profiling should be prospectively built into trial end points for personalised approaches with competing ADCs. That is the crux. The moment we have two or more viable ADCs for the same patient, "does the target matter?" becomes "which target should we hit first?" That is when Nectin-4 status, read membranously and interpreted together with histology, conventional versus divergent squamous, moves from academic to decisive. 🔬
We should be building and validating these insights in the future, so it is ready when the therapeutic landscape catches up.
🔗 https://t.co/N7fFIWhOTQ
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UroToday.com @urotoday
FDA approval of capivasertib with abiraterone and prednisone in PTEN-deficient androgen pathway modulation-naïve or -sensitive #ProstateCancer. @neerajaiims @huntsmancancer hosts an expert panel discussion with @EHeath4100 @MayoClinic, @hoperugo @cityofhope, and @Daniel_J_George @DukeCancer on the CAPItello-281 trial. #WatchNow > https://t.co/vb4Rek0EMj @AstraZeneca
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The ASCO Post @ASCOPost
🚨 #FDAApproval: The @US_FDA has granted approval for lutetium Lu-177 vipivotide tetraxetan (LuPSMA-617; Pluvicto) + ARPI therapy for adults with PSMA+ metastatic hormone-sensitive #ProstateCancer.
Approval based on the phase III PSMAddition trial.
🔗 https://t.co/ssYWu8CzVk https://t.co/0oV8aCqrr3
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UroToday.com @urotoday
🧬 Capivasertib + abiraterone offers a precision-medicine alternative to chemotherapy-based triplet therapy in PTEN-deficient metastatic APMN/S prostate cancer.
At #USPCC26, Dr. Russell Szmulewitz @UChicagoMed highlighted CAPItello-281: in 1,012 patients with PTEN-deficient de novo metastatic disease, capivasertib improved median rPFS from 25.7 to 33.2 months, with the largest apparent benefit in complete PTEN loss. OS is still immature, while toxicity—including diarrhea, hyperglycemia, rash, and anemia—was manageable but led to discontinuation in ~18%.
Bottom line: For high-volume, de novo PTEN-deficient disease, capivasertib + abiraterone targets a poor-prognosis biology at the earliest opportunity—without requiring docetaxel.
Written coverage by @zklaassen_md on UroToday > https://t.co/LEiVlqqq17
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UroToday.com @urotoday
The CAPItello-281 trial and FDA approval of capivasertib in PTEN-loss #mHSPC. @EHeath4100 @MayoClinic joins @zklaassen_md @GACancerCenter to discuss the FDA approval of capivasertib for PTEN-deficient metastatic hormone-sensitive prostate cancer, reviewing CAPItello-281 data in de novo patients randomized to capivasertib plus abiraterone versus abiraterone alone, both with ADT. #WatchNow on UroToday > https://t.co/MCsogP1R6R
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UroToday.com @urotoday
Pluvicto® Approved for PSMA-Positive mHSPC: Bringing Radioligand Therapy Earlier in the Disease Course. @sartor_oliver @EJHospital joins @PhillipKooMD @PCFnews to discuss the @FDA approval of Pluvicto™ (lutetium-177 PSMA-617) in metastatic hormone-sensitive prostate cancer based on PSMAddition. #WatchNow on UroToday > https://t.co/cZB9TKP6x5 @DrScottTagawa @Novartis
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Kate Sears @MedwatchKate
Hi friends, it's #ProstateCancer Friday! Here are Top Posts of the Week 🧵
1/ @neerajaiims on FDA approval of Lutetium-177 for PSMA+ mAPMS/mHSPC:
https://t.co/w3i2i5MR4a
[Quoting @neerajaiims: Just in👉today @US_FDA approved Pluvicto (Lutetium-177)for PSMA+ metastatic androgen pathway modulation-sensitive #prostatecancer (mAPMS/mHSPC), based on the results of ph3 PSMAddition trial👇 @PCF_Science @urotoday @OncoAlert Congrats @DrScottTagawa & team https://t.co/SKFn9bnTNG]
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ClinicalOncologyNews @ClinOncNews
🚨 Tecentriq (atezolizumab) approved for adjuvant treatment of MIBC with ctDNA MRD after cystectomy.
IMvigor011 showed improved DFS + OS in MRD-positive patients: https://t.co/ae0x2s8NdA
#BladderCancer #Oncology #FDA https://t.co/SftDymwbSQ
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Velindre Library @vcclibrary.bsky.social
Systemic Therapy in Patients with Metastatic Castration-Resistant #ProstateCancer: ASCO Living Guideline, Version 2026.1.4 ascopubs.org/doi/10.1200/...
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