π¬ GU Oncology Intelligence Digest β Week 2026-W39
GUARD Symposium 2026 dominated GU discussion with ADC sequencing after enfortumab vedotin, PARP inhibitor selection in mHSPC and adjuvant RCC debate, alongside a Nature rapid-autopsy map of metastatic bladder cancer, a Nature analysis of 959 prostate cancer genomes, an ASTRO bladder radiotherapy guideline, a CHMP positive opinion in resectable MIBC, and new testosterone-monitoring data during ADT.
β‘ TL;DR
π¦ Twitter / π¦ Bluesky
- Testosterone monitoring during ADT plus radiotherapy: systematic review argues the threshold that matters is below 20 ng/dL, not 50 β A systematic review of 29 studies found that on-treatment suppression below 20 ng/dL, rather than the standard 50 ng/dL cutoff, tracked with better outcomes
- Sequencing ADCs after EV plus pembrolizumab: payload switching, not target switching, frames the next trials β Switching payload appears more important than switching target, with iZABREN (HER1/3 Topo1) versus platinum chemotherapy and SACTMT (TROP2/TOPO1 versus taxane) enrolling in EVP-resistant disease
- ctDNA moves from prognosis to decision-making in bladder cancer, with IMvigor011 and NIAGARA anchoring the argument β Adjuvant atezolizumab improved survival outcomes in muscle-invasive bladder cancer patients with no radiographic disease but detectable circulating tumor DNA in IMvigor011
- Small cell carcinoma of the bladder shows NECTIN4 amplification without membranous protein, pointing toward DLL3 and SLFN11 instead β In 88 SmCCB cases with 79 fully profiled, membranous Nectin-4 was completely negative in 75% (60/80) while NECTIN4 amplification occurred in 16/73 (21.9%), and DLL3 was positive in 35/43 evaluable High-NE cases (81%)
- Rapid-autopsy Nature study maps metastatic bladder cancer as a self-seeding network rather than a one-way cascade β In 13 of 16 evaluable patients metastases seeded other metastases, and in 9 a single early metastatic lesion appeared to seed all the others; the cohort comprised 20 rapid-autopsy patients
Full details below β
π What's Being Published
No new manuscripts cleared the relevance bar this week.
π Every paper considered this week, including the ones that didnβt make it β
π£οΈ 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).
Testosterone monitoring during ADT plus radiotherapy: systematic review argues the threshold that matters is below 20 ng/dL, not 50
A systematic review of 29 studies (PRISMA 2020) examined testosterone monitoring and recovery after curative ADT and radiotherapy in intermediate/high-risk prostate cancer. On-treatment suppression below 20 ng/dL, rather than the standard 50 ng/dL cutoff, tracked with better outcomes, while baseline testosterone predicted post-treatment recovery rather than oncologic endpoints. Recovery can take years, and evidence for testosterone replacement after treatment remains limited β raising the practical question of whether 50 ng/dL remains a defensible target in routine practice.
Discussed by: @OncoAlert, @weoncologists
Sources cited: ScienceDirect
Sequencing ADCs after EV plus pembrolizumab: payload switching, not target switching, frames the next trials
Discussion at GUARD Symposium 2026 centered on whether payload class rather than target antigen should drive ADC selection after enfortumab vedotin plus pembrolizumab (EVP) failure. MRG002 (trastuzumab vedotin) delivered an ORR of 53.4% in HER2 2+/3+ disease in patients with at least 1 prior therapy and no prior ADC exposure, while EGFRxHER3 izalontamab brengitecan showed an ORR of 80% with 1 prior line (n=15) versus 26.3% with more than 1 prior line (n=19). LY4101174, evaluated in a heavily pretreated population in which approximately 93% had prior EV, showed an ORR around 36% at the 4 mg/kg dose, with hematologic toxicity becoming an important dose-limiting issue. Trials enrolling in EVP-resistant disease include iZABREN (HER1/3 Topo1 versus platinum chemotherapy) and SACTMT (TROP2/TOPO1 versus taxane); post-EV resistance data further complicate planning because loss of Nectin-4 does not uniformly explain cross-resistance.
Discussed by: @tompowles1, @nataliagandur, @nataliagandur, @OncoAlert, @nataliagandur
ctDNA moves from prognosis to decision-making in bladder cancer, with IMvigor011 and NIAGARA anchoring the argument
IMvigor011 demonstrated that adjuvant atezolizumab improved survival outcomes in muscle-invasive bladder cancer patients with no radiographic disease but detectable circulating tumor DNA, establishing a case that ctDNA is clinically actionable β not merely prognostic β in the adjuvant setting. Clinicians also noted that ctDNA can be measured as a continuous variable rather than only a binary positive/negative readout. Data from NIAGARA added nuance: ctDNA-positive status showed low correlation with pathologic complete response, whereas utDNA-negative status showed high correlation with pCR, suggesting these modalities capture different biology. The broader trajectory was framed alongside five years of MRD progress, including less chemotherapy in stage II colon cancer with DYNAMIC and longer survival in ctDNA-positive bladder cancer with IMvigor011.
Discussed by: @OncoAlert, @OncoAlert, @ozdogan_md, @OncoAlert, @NatureMedicine
Sources cited: Liquid biopsy-guided adjuvant therapy in bladder cancer (Nature Medicine, 2025)
Small cell carcinoma of the bladder shows NECTIN4 amplification without membranous protein, pointing toward DLL3 and SLFN11 instead
In 88 small cell carcinoma of the bladder (SmCCB) cases with 79 fully profiled, membranous Nectin-4 was completely negative in 75% (60/80), with a median H-score of 0 and mean of 11.6. NECTIN4 amplification by FISH occurred in 16/73 cases (21.9%), a frequency comparable to conventional urothelial carcinoma, yet without corresponding protein expression at the membrane. DLL3 was positive in 35 of 43 evaluable high-NE cases (81%), and the striking divergence between genomic amplification and target expression argues against extrapolating conventional urothelial carcinoma biology to SmCCB β with DLL3 and SLFN11 identified as potentially more biologically rational targets.
Discussed by: @brookmans76, @Markuseckstein3
Sources cited: Immunohistochemical stratification of bladder small cell carcinoma reveals two major phen⦠(Histopathology, 2026)
Rapid-autopsy Nature study maps metastatic bladder cancer as a self-seeding network rather than a one-way cascade
A Fred Hutch rapid autopsy program study published in Nature, conducted with patient and family consent, characterized metastatic bladder cancer spread across 20 patients. In 13 of 16 evaluable patients, metastases seeded other metastases; in 9, a single early metastatic lesion appeared to seed all the others. More complex, polyclonal spread tracked with poorer survival β a finding that shifts the conceptual frame from a linear primary-to-distant cascade toward a network model of self-seeding.
Discussed by: @PGrivasMDPhD, @AponiaAnalytics, @EladSharonMD
Sources cited: Evolution and heterogeneity of lethal metastatic bladder cancer subtypes (Nature, 2026)
Perioperative MIBC de-escalation: EMA approvals set the standard while surgery-sparing after EV plus pembrolizumab remains investigational
Perioperative durvalumab-GC and EVP are now EMA-approved for muscle-invasive bladder cancer, and pathologic complete response remains the strongest surrogate of outcome, achieved in approximately 35β60% of patients on neoadjuvant therapy. Merck announced a positive CHMP opinion for a combination treatment regimen for adults with resectable MIBC in the European Union. Despite these advances, clinicians debated the safety of surgery-sparing approaches: 52% of patients with endoscopic clinical complete response still harbor residual tumor at cystectomy, and ctDNA misses up to 1 in 5 cases of residual disease. Questions persist about local relapses when pursuing surgery-sparing with EVP and without radiotherapy in the context of trials EV209 and EV309, and whether local therapies such as TAR200 or BCG could reduce that risk.
Discussed by: @tompowles1, @OncoAlert, @Merck, @MedwatchHQ, @OncoAlert
Sources cited: Merck press release
T-cell effector signatures track with worse BCG outcomes, splitting biomarker logic between checkpoint inhibitors and intravesical immunotherapy
T-cell effector signatures that correlate with checkpoint inhibitor response in urothelial carcinoma were associated with poor rather than good outcomes with BCG β a finding presented at GUARD Symposium 2026. CD8 T cells are associated with response to checkpoint inhibitors but not with BCG, illustrating that different immunotherapies require different biomarkers rather than a single immune-infiltration framework. The divergence in biomarker directionality between these two forms of immunotherapy directly shapes how cancer vaccine trials in bladder cancer should approach patient selection.
Discussed by: @weoncologists, @OncoAlert, @OncoAlert
EBMT registry of 2,204 men shows salvage high-dose chemotherapy works in relapsed germ cell tumors and that delay costs outcomes
An analysis from the cellular therapy and immunobiology working party of the EBMT examined 2,204 men with relapsed germ cell tumors receiving salvage high-dose chemotherapy with carboplatinβetoposide, reporting a median overall survival of 36.4 months and median progression-free survival of 9.9 months. Longer time to high-dose chemotherapy was associated with increased risks of progression and death, though the relationship varied by IPFSG risk, particularly for overall survival in nonβhigh-risk patients. The real-world scale of the registry lends weight to the argument that access to and timing of high-dose chemotherapy are clinically consequential.
Discussed by: @OncoAlert, @weoncologists
Sources cited: ESMO Open
ASTRO issues its first standalone bladder cancer radiotherapy guideline and endorses trimodality therapy as a curative alternative to cystectomy
ASTRO released its first standalone clinical practice guideline on radiation therapy for bladder cancer, covering bladder preservation with trimodality therapy, adjuvant radiotherapy after cystectomy, and evidence-based approaches for advanced disease. The American Society for Radiation Oncology's position is that radiation therapy combined with limited surgery and chemotherapy can cure muscle-invasive bladder cancer. Whether a formal standalone guideline carrying this endorsement will shift referral patterns away from radical cystectomy for eligible patients with cT2-4aN0M0 MIBC is an open question for multidisciplinary teams.
Discussed by: @CancerNetwrk, @igzalina, @AuntMinnie, @OncoAlert, @tumayipekci
Sources cited: Cancer Network
π₯ Top Ranked Tweets
UroToday.com @urotoday
Lutetium-177-PSMA-617 radiographic PFS benefit in the #PSMAddition trial for metastatic hormone-sensitive #ProstateCancer. @DrScottTagawa @WeillCornell joins @CaPsurvivorship @DanaFarber to discuss the PSMAddition FDA approval. The study enrolled patients with PSMA-positive #mHSPC on an ADT plus ARPI doublet and randomized them to addition of up to six cycles of lutetium-177 PSMA-617; any ARPI was permitted. #WatchNow on UroToday > https://t.co/9sts1AdWrF
π 1 β€οΈ 6 π 2 π 522
Nature Medicine @NatureMedicine
βResearch highlight: #Adjuvant #atezolizumab improved survival outcomes in patients with muscle-invasive #bladdercancer who had no radiographic disease but had detectable circulating tumor DNA in their blood. #IMvigor011 #liquidbiopsy #ESMO @NEJM
https://t.co/C0vkL8FqZN
π 1 β€οΈ 6 π 5 π 5,006
Giuseppe Procopio @g_procopio_
Published in @NEJM: Phase 3 LITESPARK-022 shows improved disease-free survival with adjuvant pembrolizumab + belzutifan in #ccRCC after surgery. @elena_verzoni is among the authors, with @IstTumori Β at the forefront of advancing #adjuvant treatment.
https://t.co/Yt6VOcLrgF https://t.co/oZNgXtTHXb
π 0 β€οΈ 16 π 3 π 641
Oncology Brothers @OncBrothers
Belzutifan + Pembro now @US_FDA β based off LITESPARK-022: PhIII (vs. Pembro) in adj RCC:
- 2.5yrs DFS: 75.8% vs. 68.6% (HR: 0.72)
- mOS NR
- 2.5yrs OS: 95.6% vs. 93.8% (HR: 0.78)
- AEs: 42.2% vs. 17.9% w/ Gr β₯ 3
#MedTwitter #gusm #KidneyCancer @OncoAlert https://t.co/esYsGSHX3s
π 14 β€οΈ 74 π 39 π 6,255
Oncology Brothers @OncBrothers
Lu 177/Pluvicto now β @US_FDA for mCSPC based off PSMAddition!
#OncTwitter #gusm https://t.co/eco3POc8fg
[Quoting @DrKarineTawagi: π£ FDA approval of Pluvicto triplet vs ADT/ARPI for mCSPC (APMS) #PSMAddition
βοΈ rPFS: HR 0.72
βοΈ time to mCRPC: HR 0.70
βοΈ similar QoL
βOS data immature
βοΈ wide eligibility criteria for β PSMA
βvs chemo or other triplets (PARP/AKT)
Exciting year for GU onc! https://t.co/WgkF00r97z]
π 4 β€οΈ 33 π 9 π 4,656
Oncology Brothers @OncBrothers
Durvalumab now @US_FDA β for Non-Muscle Invasive Bladder cancer based off #POTOMAC: PhIII, BCG + Durvalumab vs. BCG alone in BCG naive HR-NMIBC:
- DFS waiting maturity (HR: 0.68)
- 3yr mDFS 82% vs 77%
- MedOncs will now see HR-NMIBC
#gusm #OncTwitter https://t.co/OESE7Xy4Hn
π 17 β€οΈ 72 π 35 π 18,907
Journal of Clinical Oncology @JCO_ASCO
Systemic Therapy in Patients with Metastatic Castration-Resistant Prostate Cancer: ASCO Living Guideline, Version 2026.1.4.
Read the full article. https://t.co/pNWluRmLKQ
#ProstateCancer #pcsm
π 3 β€οΈ 6 π 3 π 2,007
OncoAlert @OncoAlert
RT @Markuseckstein3: Our NECTIN4 scoring system for predicting enfortumab vedotin response in urothelial carcinoma is just published. π¬
The short version: NECTIN4 is not a failed biomarker. It has been measured in the wrong compartment.
π 179 EV-treated mUC patients, multicenter, FISH plus IHC, benchmarked against EV-301 EPAR data.
Why the field thought NECTIN4 was ubiquitous π§
In EV-301 the median H-score was 250, with 82.6% β₯150. That near-universal expression underpinned the biomarker-unselected label.
In our cohort, membranous H-score alone was 160. Cytoplasmic was 200. Combined, 260, with 78.2% β₯150, almost exactly mirroring EV-301.
So the trial numbers most likely reflect membranous plus cytoplasmic staining. That single methodological choice is why NECTIN4 looked like it was everywhere. π―
And it matters, because only one compartment predicts anything:
β Membranous 2+/3+ vs 0/1+: ORR 55.1% vs 25.5% (p<0.001), mPFS 7.1 vs 2.9 months (HR 0.45), mOS 12.3 vs 6.9 months (HR 0.57).
β Cytoplasmic: ORR 49.6% vs 39.5% (p=0.4). No PFS or OS signal.
β Bulk NECTIN4 mRNA, which cannot resolve localisation: no association either.
Adding cytoplasmic staining inflates positivity and dilutes prediction. Negativity rate drops from 12% to 3.4%. More positives, less information. π
The scoring system π¬
Four tiers (0, 1+, 2+, 3+) adapted from the ASCO/CAP HER2 gastric algorithm, chosen deliberately because it accounts for incomplete membranous staining, the same framework that carried T-DXd to tumour-agnostic approval.
Blinded interobserver testing, 44 cases, three raters, two with no prior NECTIN4 experience:
π Fleiss' ΞΊ 0.749 across all four tiers.
π Fleiss' ΞΊ 0.874 for the clinically relevant 0/1+ vs 2+/3+ cutoff. Almost perfect agreement.
Reproducible, teachable in a short training session, deployable in routine practice.
Genomics on top π§¬
NECTIN4 amplification in 25.1% (45/179). ORR 76.2% vs 36.6%. mPFS 12.2 vs 3.9 months (HR 0.40). mOS 30.1 vs 8.5 months (HR 0.33). At 24 months, 58.8% of amplified patients were alive versus 19.0%.
And IHC prescreens for it: 80% of amplified tumours are 3+, under 5% of 0/1+ tumours carry an amplification. Restricting FISH to 2+/3+ captures 97.8% of amplified cases while sparing 29.1% of patients any molecular testing. β‘
The integrated three-tier model:
1οΈβ£ Amplified: ORR 76.2%, mOS 30.1 mo
2οΈβ£ Non-amplified, membranous high: ORR 42.9%, mOS 8.8 mo
3οΈβ£ Non-amplified, membranous low: ORR 26.1%, mOS 6.9 mo
Both remained independent in multivariable models. C-index for OS improves from 0.557 to 0.621 when amplification and membranous expression are combined. Neither marker alone does what the two do together.
Where I think this lands π―
I do not (!) read this as an argument for testing every patient . With EV+P as first-line standard and few alternatives, a negative result rarely changes what you do today and shouldn't change it right now given the high EVP efficacy.
But that is an argument about the therapeutic landscape, not about the biology. And the landscape is changing fast: HER2 ADCs, TROP2, HER3/EGFR, NECTIN4 radioligands and T-cell engagers. The moment two viable options compete for the same patient, the question stops being "does the target matter" and becomes "which target first."
Notably, unlike the HER2-low paradigm, EV-301 showed an attenuated treatment effect in NECTIN4-low disease, PFS HR around 0.9 with confidence intervals crossing 1 (check out Figure 1 of the paper).
β οΈProspective validation is running: EVOKE (DRKS00034745).
Immense thanks to @niklas_kluemper and Jonas Saal, to Thomas BΓΌttner, Sebastian Rauch and Fabienne Lange, and to every centre and biobank that contributed. This was a genuinely collaborative effort within the fantastic GUARDIANS and BRIDGE Consortium. π
π https://t.co/CuQR9LJe6k
@Uroweb @AmerUrological @ASCO @PathSoc @OncoAlert @Histo_Journal @andreanecchi @emanuele_crupi @danieleraggi83 @raffcolo @Dr_Aggen @DrRosenbergMSK @h_alahmadie @PGrivasMDPhD @shilpaonc @drenriquegrande @amerseburger @brookmans76 @DrYukselUrun @onkowissen @imedverse @UroDocAsh @urotoday @EUplatinum @JCO_ASCO @CCR_AACR @niklas_kluemper @DrRosenbergMSK @Dr_Aggen @Uromigos @tompowles1 @shilpaonc @PGrivasMDPhD
#Uropathology #urothelial #BladderCancer #NECTIN4 #pathtwitter
π 32 β€οΈ 78 π 27 π 14,308
Gil Morgan, MD @weoncologists
RT @APCCC_Lugano: Is 50 ng/dL the wrong number to be chasing during ADT? Data suggest the threshold that actually tracks with better outcomes is less than half that π§¬
Articleπ°
https://t.co/zipBClUmeS
Testosterone monitoring and supplementation in patients with intermediate or high risk prostate cancer treated with 6-26 months of androgen deprivation therapy and radiotherapy
A new systematic review of 29 studies (PRISMA 2020) examined testosterone monitoring and TRT safety after curative ADT and radiotherapy β’οΈ for intermediate/high-risk #ProstateCancer .
β‘οΈ Baseline testosterone didn't predict oncologic outcomes but strongly predicted post-treatment recovery.
β‘οΈOn-treatment suppression below 20 ng/dL, not the standard 50 ng/dL cutoff, tracked with better outcomes.
β‘οΈ Recovery was slow, often incomplete, and shaped by age, baseline T, and ADT type. Limited data suggest TRT is safe.
@Achard_Verane, @AmarUKishan, @PBlanchardMD, @lisahorvath73, @BarbaraJereczek, @BertrandTOMBAL
@OncoAlert π¨ #LPCCC27
@Silke_Gillessen
@AOmlin
@ProfKHerrmann
@weoncologists
π 18 β€οΈ 39 π 19 π 2,215
OncoAlert @OncoAlert
RT @APCCC_Lugano: Is 50 ng/dL the wrong number to be chasing during ADT? Data suggest the threshold that actually tracks with better outcomes is less than half that π§¬
Articleπ°
https://t.co/zipBClUmeS
Testosterone monitoring and supplementation in patients with intermediate or high risk prostate cancer treated with 6-26 months of androgen deprivation therapy and radiotherapy
A new systematic review of 29 studies (PRISMA 2020) examined testosterone monitoring and TRT safety after curative ADT and radiotherapy β’οΈ for intermediate/high-risk #ProstateCancer .
β‘οΈ Baseline testosterone didn't predict oncologic outcomes but strongly predicted post-treatment recovery.
β‘οΈOn-treatment suppression below 20 ng/dL, not the standard 50 ng/dL cutoff, tracked with better outcomes.
β‘οΈ Recovery was slow, often incomplete, and shaped by age, baseline T, and ADT type. Limited data suggest TRT is safe.
@Achard_Verane, @AmarUKishan, @PBlanchardMD, @lisahorvath73, @BarbaraJereczek, @BertrandTOMBAL
@OncoAlert π¨ #LPCCC27
@Silke_Gillessen
@AOmlin
@ProfKHerrmann
@weoncologists
π 18 β€οΈ 39 π 19 π 2,215
Gil Morgan, MD @weoncologists
RT @niklas_kluemper: The NECTIN4 biomarker signal was already there.
We were quite surprised when revisiting the pivotal EV-301 data: higher NECTIN4 expression was already significantly associated with response to enfortumab vedotin β ORR 45.8% vs 20.0%.
At the time, this was not the prevailing view: EV was considered effective largely irrespective of NECTIN4 expression.
One possible explanation is how NECTIN4 was measured. The unusually high expression levels in EV-301 suggest that overall/combined staining may have captured both membranous and cytoplasmic NECTIN4, potentially diluting the biologically relevant signal.
Our new data show clearly:
π― Membranous NECTIN4 predicts EV response and survival. Cytoplasmic NECTIN4 does not.
This makes sense mechanistically: an ADC needs an accessible cell-surface target to bind and deliver its payload
-> well established eg for HER2 (Tumor agnostic approval in HER2 3+)
Since EV-301, the evidence supporting membranous NECTIN4 as a biomarker has continued to grow β including independent EV+pembrolizumab data and now other NECTIN4-targeting ADCs such as SHR-A2102.
The next step is prospective validation. Our EVOKE trial is fully enrolled β stay tuned.
And perhaps the most important question: Can we improve outcomes for NECTIN4-low tumors by selecting a different target, payload or therapeutic strategy?
This is where ADCs should be heading: from target expression to true precision oncology
@Markuseckstein3 @DrRosenbergMSK @Dr_Aggen
#DGU26 @amerseburger @dgukongress @DGUrologie
@OncoAlert @weoncologists @urotoday @DrChoueiri @PTarantinoMD @raffcolo @tompowles1 @UroDocAsh @Uromigos @imedverse @CCR_AACR @Uroweb @PGrivasMDPhD @montypal @apolo_andrea @AndreaNecchi @DrYukselUrun
π 7 β€οΈ 40 π 16 π 2,088
OncoAlert @OncoAlert
RT @niklas_kluemper: The NECTIN4 biomarker signal was already there.
We were quite surprised when revisiting the pivotal EV-301 data: higher NECTIN4 expression was already significantly associated with response to enfortumab vedotin β ORR 45.8% vs 20.0%.
At the time, this was not the prevailing view: EV was considered effective largely irrespective of NECTIN4 expression.
One possible explanation is how NECTIN4 was measured. The unusually high expression levels in EV-301 suggest that overall/combined staining may have captured both membranous and cytoplasmic NECTIN4, potentially diluting the biologically relevant signal.
Our new data show clearly:
π― Membranous NECTIN4 predicts EV response and survival. Cytoplasmic NECTIN4 does not.
This makes sense mechanistically: an ADC needs an accessible cell-surface target to bind and deliver its payload
-> well established eg for HER2 (Tumor agnostic approval in HER2 3+)
Since EV-301, the evidence supporting membranous NECTIN4 as a biomarker has continued to grow β including independent EV+pembrolizumab data and now other NECTIN4-targeting ADCs such as SHR-A2102.
The next step is prospective validation. Our EVOKE trial is fully enrolled β stay tuned.
And perhaps the most important question: Can we improve outcomes for NECTIN4-low tumors by selecting a different target, payload or therapeutic strategy?
This is where ADCs should be heading: from target expression to true precision oncology
@Markuseckstein3 @DrRosenbergMSK @Dr_Aggen
#DGU26 @amerseburger @dgukongress @DGUrologie
@OncoAlert @weoncologists @urotoday @DrChoueiri @PTarantinoMD @raffcolo @tompowles1 @UroDocAsh @Uromigos @imedverse @CCR_AACR @Uroweb @PGrivasMDPhD @montypal @apolo_andrea @AndreaNecchi @DrYukselUrun
π 7 β€οΈ 40 π 16 π 2,088
UroToday.com @urotoday
PSMA PET interpretation in biochemical recurrence after #ProstateCancer treatment. Steve Cho, MD joins @tranpt21 highlighting that detection is most reliable at PSA 0.2β0.5 ng/mLβbelow this, a negative scan does not exclude disease.
β Small PSMA-avid lymph nodes can be highly specific even when CT/MRI is negative
β οΈ Common pitfalls: sympathetic ganglia and low-level rib uptake
π― Bone mets should show focal, high uptake plus supportive CT findings before being called positive
π Many conventionally imaging-negative EMBARK patients would likely be PSMA PET+
#WatchNow on UroToday > https://t.co/Z8LjOo7bUD @UTMDAnderson
π 6 β€οΈ 4 π 1 π 1,059
Petros Grivas @PGrivasMDPhD
Thrilled to see our work over years in #bladdercancer published in @Nature THANKS to patients/families consenting to our research autopsy program wanting to support others! Kudos to @HsiehLab @GavinHa #OmarMian #MingLam et al. @fredhutch @HutchPresident
https://t.co/7KrL0tviL1
[Quoting @fredhutch: Published today in @Nature: A new Fred Hutch study using a first-in-kind rapid autopsy program shows details of metastatic bladder cancer subtypes; could improve diagnosis and future treatment. https://t.co/mQIo8YjE9r
@pushpa_itagi @HsiehLab @GavinHa @DrOmarMian]
π 5 β€οΈ 80 π 13 π 6,589
Tom Powles @tompowles1
How do we sequence ADCs after EVP in advanced bladder cancer. @DrRosenbergMSK Switching payload appears more important than switching target. iZABREN (HER1/3 Topo1) vs platinum chemo and SACTMT (TROP2/TOPO1 vs taxane) in EVP resistant disease are enrolling #GuardSymposium2026 https://t.co/SytOnqXIlx
π 5 β€οΈ 59 π 24 π 9,748
π§ͺ Newly Recruiting Trials
3 trials (2 phase II, 1 phase I) opened this week, testing Lutetium Lu 177 Vipivotide Tetraxetan, quemliclustat and JANX013 plus JANX007
Phase 2 Β· Mayo Clinic Β· Lutetium Lu 177 Vipivotide Tetraxetan Β· Minnesota Β· CT.gov β
Phase 1/2 Β· Fred Hutchinson Cancer Center Β· quemliclustat Β· Washington Β· CT.gov β
Phase 1 Β· Janux Therapeutics Β· JANX013 plus JANX007 Β· Tennessee Β· CT.gov β
Open all 3 on the trials page β
Agent descriptions from the NCI Thesaurus.
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