ASCO Annual Meeting 2026
MROQC ADT Practice Patterns
ForHigh-risk M0/N0-1 prostate on definitive RT, GG4-5 predominant
TL;DRGuideline-concordant ADT (≥18mo) recommended in 67.0% of high-risk pts on definitive RT; ARPI intensification just 23.2% of STAMPEDE-eligible.
The RT prescriber's read is the adoption gap, not a treatment effect: even in a quality consortium, only 67.0% of high-risk pts on definitive RT are recommended ≥18mo ADT, and just 23.2% of STAMPEDE-eligible get ARPI intensification. Facility-level variability persists on multivariable analysis (P<.0001), so where a man is treated, not only his risk, sets his ADT. Prompts an audit of your own duration and intensification practice.
8 details
Prospective practice-pattern study within the Michigan Radiation Oncology Quality Consortium (MROQC), a statewide RT registry. 553 pts across 26 centers, Jun 2020–Nov 2024. Facility modeled as a random intercept (mixed-effects).
Intact, high-risk M0/N0-1 prostate cancer on definitive RT. GG4-5 75.0%, PSA ≥20 40.0%, cN1 19.9%, cT3/4 13.3%. 27.9% met STAMPEDE M0 intensification criteria.
Primary: intended guideline-concordant ADT (≥18mo). Also assessed: ARPI adoption before vs after STAMPEDE M0 publication, facility-level variability, and multivariable predictors of concordance.
91.3% recommended any ADT, 67.0% guideline-concordant. ARPI intensification among STAMPEDE-eligible rose 0% → 23.2% post-publication. Facility variability persisted on MVA (P<.0001).
| Factor | OR (GC-ADT) | 95% CI |
|---|---|---|
| cN1 | 2.94 | 1.44-5.99 |
| GG4 | 6.23 | 2.85-13.62 |
| GG5 | 9.45 | 4.46-20.06 |
| PSA ≥40 | 3.64 | 1.22-10.87 |
Benchmarks real practice against the 2022 AUA/ASTRO guideline (18-36mo ADT) and STAMPEDE M0 (ARPI for high-burden high-risk). Documents a persistent adoption gap, not a treatment effect.
Captures intended ADT duration and recommendations, not delivered therapy or adherence. Single-state consortium limits generalizability, and there is no efficacy or outcome endpoint.
Descriptive practice-pattern audit (no efficacy endpoint); reinforces AUA/ASTRO ADT guideline and STAMPEDE M0 as benchmark, documenting under-adoption rather than testing a new effect.
In high-risk men (GG4-5, cN1, PSA ≥40, or ≥2 STAMPEDE factors) starting definitive RT, this supports benchmarking ADT to ≥18mo and weighing ARPI intensification when STAMPEDE-eligible; it does not extend to low/intermediate-risk disease or ADT-omission decisions.
- Does intended guideline-concordant ADT translate to delivered treatment and adherence?
- What interventions reduce facility-level variability in ADT recommendations?
- Do Michigan consortium patterns generalize to national practice?
📚 Sources · 📄 1 paper
Abstract
AREST
ForAdequately resected pT1-2N0 oral SCC with ≥1 intermediate-risk feature
HR 0.52
3-yr LRFS 89.2% vs 80.9%, 95% CI 0.30-0.91, p=0.02 (ITT)
TL;DR3-yr LRFS 89.2% vs 80.9%, HR 0.52 (0.30-0.91) p=0.02 favoring adjuvant RT in resected intermediate-risk pT1-2N0 oral SCC; no OS/DFS gain.
The move is observe-vs-treat in adequately resected pT1-2N0 OSCC with one adverse feature: 60Gy/30fx to tumor bed plus at-risk neck cut 3-yr loco-regional failure (HR 0.52), strongest in oral tongue over buccal mucosa (exploratory). The gain is loco-regional only, so weigh it against RT morbidity when baseline LRR risk is low.
| Arm | 3-yr LRFS | HR (95% CI) | p |
|---|---|---|---|
| Adjuvant RT | 89.2% (84.3-93.3) | 0.52 (0.30-0.91) | 0.02 |
| Observation | 80.9% (74.6-86.1) | ref | — |
8 details 2 trials watching
Phase 3, open-label, multicenter RCT (India); 1:1 to adjuvant RT vs observation, N=392 (191 RT, 201 observation), stratified by subsite, PNI/LVE, differentiation. Median follow-up 47.2 months.
pT1-2 pN0 OSCC with ≥1 intermediate-risk feature (DOI 5-10mm, PNI, LVE, or poor differentiation), after adequate surgery: margins ≥5mm and ipsilateral level I-III neck dissection with ≥16 nodes.
60Gy in 30 fractions over 6 weeks to the resected tumor bed and at-risk neck nodal region.
Primary: 3-yr loco-regional recurrence-free survival (LRFS), KM with log-rank. Secondary: DFS, OS, and cumulative incidence of loco-regional failure (competing-risk).
Per-protocol LRFS 91.1% vs 80.9%, HR 0.43 (0.23-0.80), p=0.01. DFS and OS not significantly different between arms.
| Analysis | Adjuvant RT | Observation | HR (95% CI), p |
|---|---|---|---|
| ITT | 10.6% (6.1-15.1) | 18.9% (13.3-24.6) | 0.52 (0.30-0.91), p=0.021 |
| Per-protocol | 8.7% (4.3-13.1) | 18.9% (13.3-24.6) | 0.43 (0.23-0.79), p=0.007 |
Prior evidence for adjuvant RT in this pN0 intermediate-risk setting was retrospective (per the abstract); AREST is the first randomized confirmation.
Open-label, abstract-only; benefit is loco-regional control only, no OS/DFS at 47.2-mo median. Observation LRFS (80.9%) exceeded the 70% powering assumption, so the absolute LRFS gain is modest.
First randomized backing for the guideline-listed retrospective signal that RT cuts LRR in adverse-feature pN0 OSCC; loco-regional benefit only, no OS/DFS, open-label abstract.
In an adequately resected pT1-2N0 oral tongue SCC with a single intermediate-risk feature, this supports adjuvant RT for loco-regional control but not survival, and it does not extend to buccal mucosa (weaker signal) or node-positive disease.
- Does loco-regional control benefit translate to survival with longer follow-up? n=85 · primary completion 2026-08 · postop RT vs PD-1 maintenance, survival endpoint
- Optimal adjuvant approach for buccal mucosa vs oral tongue subsites? recruiting A Study of Radiation Therapy After Surgery in People With Oral Tongue Squamous Cell Carcinoma Phase 2n=24 · primary completion 2027-06 · postop IMRT tailored to oral tongue subsite
- Which single intermediate-risk feature drives the RT benefit?
📚 Sources · 🐦 1 tweet · 📄 1 paper
#ASCO26
— Dr Rishabh Jain (@DrRishabhOnco) May 27, 2026
🗣️ The AREST trial tackles one of the biggest gray zones in oral cavity cancer.
After adequate surgery in pT1-2N0 OSCC with intermediate-risk features:
✅ Adjuvant RT improved loco-regional control
❌ No OS benefit observed
3-year LRFS:
🔹 89.2% vs 80.9%
🔹 HR 0.52… https://t.co/qsALPFX032 pic.twitter.com/F4XzTMETih
Abstract
Concurrent Systemic Therapy + Radiation Timing (Speers)
TL;DRTraffic-light framework for what runs concurrent with breast/CW + RNI RT vs hold: continue endocrine + trastuzumab/pertuzumab, caution T-DXd/CDK4/6i, hold cytotoxics/PARPi.
HERANCCTG N9831APHINITYKATHERINEATEMPTDESTINY-Breast05COMBARTKEYNOTE-522
The actionable RT read: in the DESTINY-Breast05 arm, T-DXd ILD was 10.7% sequential vs 9.6% concurrent, so timing around RT did not change ILD, and concurrency is reasonable with lung-dose limits. The 'do not ignore' signal is T-DM1 plus CNS SRS radionecrosis; hold CDK4/6i for large fields.
+1 more figure
7 details 3 trials watching
ASCO 2026 educational review / Educational Book chapter (Wong, Speers, Schaverien, Table 5). Sorts systemic agents into a continue / caution / hold framework for concurrency with breast/chest-wall + RNI RT. Evidence base is mostly retrospective, post-hoc, or small prospective series.
Context is adjuvant breast/CW + regional nodal irradiation. Plan features that raise the concurrency stakes: large lung volumes, IMN coverage, bolus, reconstruction, and CNS SRS (T-DM1 radionecrosis, T-DXd ILD).
Endocrine therapy and trastuzumab/pertuzumab are safe concurrent; T-DXd and CDK4/6i are plan-dependent; cytotoxics, veliparib, and capecitabine sequence. Default outside protocol is PK-based washout, then RT, then resume.
| Agent class | With RT | Notes / evidence |
|---|---|---|
| Endocrine therapy | Continue | minimal radiosensitization |
| Trastuzumab ± pertuzumab | Continue | concurrent standard (HERA, NCCTG N9831, APHINITY) |
| T-DM1 | Continue | per KATHERINE / ATEMPT; watch dermatitis, pneumonitis, CNS SRS necrosis |
| T-DXd | Caution | ILD dominant; sequence/hold for high lung-dose or active pulmonary disease |
| Pembrolizumab | Continue, monitor | KEYNOTE-522 concurrent tolerated; pneumonitis vigilance |
| CDK4/6i (palbo/ribo/abema) | Hold large fields | mostly retrospective; concurrent only in protocol |
| Olaparib | Sequence | complete RT 2-12 wks before; RadioPARP suggests concurrent safety |
| Veliparib / talazoparib | Avoid concurrent | veliparib severe acute/late tox (TBCRC 024) |
| Capecitabine | Hold / sequence | adjuvant paradigm sequential (CREATE-X) |
| Cytotoxics (anthracycline/taxane/platinum) | Hold | sequence, do not give concurrently |
| Metric | Value |
|---|---|
| ILD, T-DXd 5.4 mg/kg (PI) | ~12%; fatal ~0.9% |
| DESTINY-Breast05 ILD | 9.6% T-DXd vs 1.6% T-DM1 |
| RT timing (T-DXd arm) | 10.7% seq vs 9.6% concurrent, no effect |
| COMBART concurrent RT/SRT | 40 pts; acute tox 20% |
For a HER2+ patient on adjuvant trastuzumab/pertuzumab or T-DM1 needing chest-wall + nodal RT, this supports running HER2 therapy through RT with pneumonitis and CNS-SRS vigilance; it does not extend to concurrent cytotoxics, veliparib, or CDK4/6i in large fields.
- Concurrent CDK4/6 inhibitor safety with regional nodal RT recruiting Safety Assessment of Concurrent Radiotherapy and Novel Systemic Therapy for Breast Cancer Phase NAn=148 · primary completion 2026-01 · concurrent nodal RT + CDK4/6i tolerabilityn=15 · primary completion 2026-09 · preop RT + abemaciclib phase 1b safety
- Optimal T-DXd sequencing around thoracic RT to limit ILD
- Concurrent olaparib with RT in early-stage breast active Radiation Therapy With or Without Olaparib in Treating Patients With Inflammatory Breast Cancer Phase 2n=300 · primary completion 2027-06 · phase 2 RT ± olaparib in non-met breast
📚 Sources · 🐦 1 tweet
#ASCO26
— Yakup Ergün (@dr_yakupergun) June 1, 2026
Which treatments should continue with RT, and which should be held?
From the Great presentation by Dr. Corey W. Speers pic.twitter.com/9B7e0HePDZ
mRCAT-III NCT06507371
ForpMMR/MSS LARC, cT3-4N0/+, tumor ≤10cm from verge, no lateral node
61.0% vs 28.6%
P<0.0001, ITT, blinded central review
TL;DRpCR 61.0% vs 28.6% (P<0.0001) with node-sparing SCRT + tislelizumab + CAPOX vs conventional SCRT + CAPOX in pMMR LARC.
The RT read is a confound, not a green light for nodal omission: the experimental arm changed two things at once, tumor-bed-only targeting AND added tislelizumab, so node-sparing's own contribution to the pCR doubling (61.0% vs 28.6%) can't be isolated. Node-sparing plausibly drove the lower severe-GI toxicity, but this doesn't yet license dropping elective nodal RT.
| Endpoint | Experimental | Control | P |
|---|---|---|---|
| pCR (ITT) | 61.0% (47/77) | 28.6% (22/77) | <0.0001 |
| MPR (TRG0+1) | 77.9% (60/77) | 50.6% (39/77) | <0.0001 |
+1 more figure
6 details 5 trials watching
Open-label, multicenter phase 3 RCT across 17 China hospitals; randomized 1:1, 77 pts per arm, stratified by clinical N stage (cN0 vs cN+). Primary pCR read by blinded independent central review.
pMMR/MSS rectal adenocarcinoma, cT3-4N0/+M0, tumor lower edge ≤10cm from the anal verge, ECOG 0-1, age 18-75, no positive lateral pelvic node.
Both arms CAPOX (oxaliplatin 130mg/m² d1, capecitabine 1000mg/m² d1-14). Experimental adds tislelizumab 200mg d1; control is chemo + RT only.
Both arms short-course 5Gy×5. Experimental is node-sparing (tumor bed only, spares tumor-draining nodes); control is conventional elective-nodal coverage. This target-volume contrast is the RT question.
Primary: pCR (ITT). Secondary: MPR, TRG, organ-preservation rate, EFS, OS, AEs.
Primary pCR and secondary MPR both favored the experimental arm (see figure); EFS, OS, organ-preservation not reported in source.
Experimental arm reported fewer severe GI AEs (author takeaway), plausibly from the smaller node-sparing volume; numeric AE rates not in source.
Control pCR 28.6% matches short-course RT + consolidation chemo benchmarks (RAPIDO ~28%). The novelty is a PD-1 benefit in an MSS population usually IO-refractory, with nodal-RT omission as the immunologic rationale.
Open-label; pCR is a surrogate with EFS/OS immature; the experimental arm confounds node-sparing target volume with added tislelizumab, so the RT-attributable effect can't be isolated; N=154, single country.
Divergent MSS-rectal result from a randomized P3 with blinded-review primary; kept off practice-changing because pCR is a surrogate (EFS/OS immature) and node-sparing is confounded with added tislelizumab.
In pMMR/MSS LARC (cT3-4, tumor ≤10cm from verge), this is a trial-stage signal that neoadjuvant PD-1 may help an IO-resistant group; it does not extend to dMMR disease and does not yet displace conventional elective-nodal short-course RT off-protocol.
- Node-sparing RT's independent contribution vs added tislelizumab
- Whether pCR gain translates to EFS, OS, organ preservation n=30 · primary completion 2025-01 · 1° endpoint organ-retention, MSS/pMMR SCRT+IOrecruiting Node-sparing Radiotherapy Combined With Total Neoadjuvant CAPOX and Sintilimab for MSS Middle and Low Rectal Cancer Phase 2n=37 · primary completion 2027-09 · node-sparing SCRT+PD-1, W&W organ preservation
- PD-1 benefit reproducibility in MSS/pMMR rectal cancer recruiting A Series of Neoadjuvant Chemoradiotherapy Combined With Immunotherapy for Locally Advanced Rectal Cancer Phase 2/3n=375 · primary completion 2026-12 · RCT chemoRT ± tislelizumab, pMMR/MSS LARCrecruiting Neoadjuvant Chemoradiotherapy Plus Tislelizumab With or Without Probio-M9 in pMMR/MSS Locally Advanced Rectal Cancer Phase 2n=50 · primary completion 2027-05 · pMMR/MSS chemoRT+tislelizumab vs CRT-only armnot yet Neoadjuvant Chemoradiotherapy Followed by Chemotherapy With or Without Tislelizumab for Resectable Ultra-low Rectal Cancer: The RELIEVE-02 Study Phase 3n=154 · primary completion 2027-12 · phase 3 chemoRT ± tislelizumab, pMMR/MSS
📚 Sources · 🐦 1 tweet
One of most interesting rectal ca studies at #ASCO26
— Dr. Nina Niu Sanford (@NiuSanford) June 2, 2026
P3 RCT in pMMR LARC: Node-sparing short-course RT + CAPOX + tislelizumab doubled pCR v conventional SCRT + CAPOX (61 v 29%)
Hypothesis = sparing elective node RT preserves antitumor immunity & improves PD1 response @OncoAlert pic.twitter.com/6xvA6ne0mg
LBA8005: Concurrent Thoracic RT + Chemoimmunotherapy in ES-SCLC
ForTreatment-naïve ES-SCLC, stage IV or III ineligible for curative chemoRT
HR 1.14
10.0 vs 11.8 mo, 95% CI 0.84-1.56, p=0.40; OS not met
TL;DROS 10.0 vs 11.8 mo, HR 1.14 (0.84-1.56), p=0.40: concurrent thoracic RT added no benefit to durvalumab-based chemoIO in ES-SCLC.
The tested RT is concurrent (30 Gy/10 fx, day 21-28 with chemoIO), not CREST's consolidative post-chemo RT in responders, so the consolidative question stays open. Even the low-burden subgroup without brain or liver metastases was null (HR 1.10). Adding concurrent thoracic RT to chemoIO carries no OS benefit.
| Arm | Median OS | HR (95% CI) | p |
|---|---|---|---|
| ChemoIO + TRT | 10.0 mo | 1.14 (0.84-1.56) | 0.40 |
| ChemoIO | 11.8 mo | n/a | n/a |
+2 more figures
| Subgroup | ChemoIO+TRT | ChemoIO | HR (95% CI) | p |
|---|---|---|---|---|
| Completed 4 chemoIO courses | 11.9 mo | 12.1 mo | 1.02 (0.72-1.44) | 0.92 |
| No brain/liver mets | 11.9 mo | 13.2 mo | 1.10 (0.65-1.87) | 0.72 |
| Arm | Median PFS | HR (95% CI) | p |
|---|---|---|---|
| ChemoIO + TRT | 5.1 mo | 1.10 (0.84-1.45) | 0.49 |
| ChemoIO | 5.0 mo | n/a | n/a |
7 details 5 trials watching
Randomized phase III, 1:1 (chemoIO+TRT n=115, chemoIO n=113). Stratified by liver and brain metastases. Primary: overall survival; secondary ORR, PFS, toxicity.
Treatment-naïve ES-SCLC, stage IV or stage III ineligible for curative chemoRT, ECOG 0-1, ≥1 measurable thoracic lesion. Asymptomatic or stable brain metastases allowed.
Four cycles durvalumab 1500 mg + carboplatin AUC 5 + etoposide (100 mg/m² IV days 1-3, or 200 mg/m² PO days 2-4) Q3W, then durvalumab 1500 mg Q4W maintenance.
Concurrent thoracic RT 30 Gy in 10 fractions, starting day 21-28. PCI 25-30 Gy offered to responders in both arms; WBRT 20-30 Gy for brain metastases per routine.
Primary OS not met and numerically favored chemoIO alone; PFS and both prespecified subgroups (course completers, no brain/liver metastases) were also null. Effect sizes in figures.
CREST (Slotman, Lancet 2015) used the same 30 Gy/10 fx but as consolidative RT after chemotherapy in responders, before immunotherapy, and suggested a survival benefit. Adding RT concurrently to chemoIO shows none.
Open-label (RT cannot be blinded). Tests only the concurrent schedule, not the consolidative timing prior data supported. No toxicity or RT-delivery data in source to explain the numerically inferior OS.
Randomised phase III, prespecified OS primary, null; contests the CREST-era expectation that thoracic RT benefits ES-SCLC, now tested concurrently with chemoIO.
In treatment-naïve ES-SCLC beginning durvalumab plus platinum/etoposide, this questions adding concurrent thoracic RT (no OS benefit); it does not extend to consolidative thoracic RT given after chemotherapy in responders.
- Does consolidative thoracic RT after chemoimmunotherapy still benefit ES-SCLC? n=150 · primary completion 2025-03 · RT to all residual lesions after chemoIO in ES-SCLCrecruiting Phase II Trial of Consolidative Thoracic Radiotherapy for ES-SCLC After Standard Care of Chemo-immunotherapy Phase NAn=104 · primary completion 2025-09 · single-arm consolidative TRT after PD-1/L1 chemoIOrecruiting Association of Thoraco-mediastinal Radiotherapy With Maintenance Immunotherapy Treatment With Atezolizumab Phase 2n=37 · primary completion 2026-12 · thoraco-mediastinal RT + maintenance atezolizumab
- Optimal timing and sequencing of thoracic RT with chemoimmunotherapy active Low-dose Radiotherapy Combined With Durvalumab, Chemotherapy(EP) in the Treatment of ES-SCLC Phase 2n=30 · primary completion 2023-02 · low-dose RT concurrent with 1L durvalumab chemon=46 · primary completion 2027-12 · sequential TRT after 1L durvalumab chemoIO
📚 Sources · 🐦 1 tweet
🚨 #ASCO26 | #️⃣LBA8005⁰☢️ Concurrent thoracic radiotherapy + chemoimmunotherapy in ES-SCLC
— Masahiro TORASAWA, MD. PhD. (@M_Torasawa) June 2, 2026
👥 ES-SCLC⁰Durvalumab + platinum/etoposide⁰± concurrent thoracic radiotherapy⁰TRT: 30 Gy / 10 fractions, starting day 21–28
📊 Randomized phase III⁰ChemoIO + TRT: n=115⁰ChemoIO… pic.twitter.com/TDA5amz59e
ctDNA and Local Regrowth/Distant Mets in Nonoperative Management of Stage II-III Rectal Cancer
ForMSS stage II-III rectal adenoca in cCR/nCR on watch-and-wait after TNT
TL;DRctDNA sensitivity 41% for local regrowth vs 74% for distant mets; positive result predicts both but can't replace endoscopy/MRI surveillance in rectal NOM.
The asymmetry is the actionable read: ctDNA caught only 41% of local regrowths vs 74% of distant mets, so for post-TNT organ-preservation surveillance it flags distant-met risk but can't replace endoscopy/MRI. ctDNA+ at regrowth also tracked more advanced ypT3-4 salvage pathology (75% vs 21%).
7 details 1 trial watching
Prospective single-center cohort (MD Anderson INTERCEPT program), N=110, 2020-2024. Serial tumor-informed ctDNA (Signatera Exome), 669 samples; median follow-up 25 mo (IQR 18-37).
MSS stage II-III rectal adenocarcinoma in cCR (69) or nCR (41) after NAT, managed non-operatively. Median age 56; cT3 in 72 and cN1-2 in 60 of 110; NAT almost entirely TNT (104/110).
Regrowth-free and distant-metastasis-free survival by longitudinal and first-post-NAT ctDNA; per-sample diagnostic accuracy (±90d of each draw); salvage-surgery pathology by ctDNA status. No registered primary endpoint (observational).
Local regrowth in 23 (21%), distant mets in 12 (11%). Ever-positive ctDNA tracked worse regrowth-free and distant-met-free survival (log-rank p=0.0002 and p<0.0001). Per-sample sensitivity 41% local regrowth vs 74% distant mets.
| Endpoint | Sensitivity | Specificity | Accuracy |
|---|---|---|---|
| Local regrowth | 41% (12/29) | 94% (480/509) | 91% (492/538) |
| Distant metastasis | 74% (31/42) | 97% (611/627) | 96% (642/669) |
Consistent with the emerging ctDNA-as-prognostic signal in rectal NOM, but quantifies a sensitivity ceiling (41%) that limits its use for local-regrowth surveillance.
Single-center, N=110 with only 29 regrowth- and 42 distant-met-associated samples driving diagnostic estimates. Assay-specific (Signatera tumor-informed); no comparison vs imaging-alone surveillance.
Single-center prospective cohort (N=110), no interventional comparator; prognostic association consistent with emerging ctDNA-in-NOM data and reaffirms imaging/endoscopy surveillance can't be replaced.
Applies to the MSS stage II-III rectal pt in cCR/nCR pursuing watch-and-wait after TNT, in whom a negative ctDNA still can't exclude local regrowth; it does not extend to MSI-H tumors or pts not pursuing organ preservation.
- Does ctDNA-guided surveillance improve organ-preservation outcomes vs imaging alone n=100 · primary completion 2025-12 · candidate match
- Can serial ctDNA kinetics raise local regrowth sensitivity above 41%
- Generalizability beyond single-center tumor-informed Signatera cohort
📚 Sources · 🐦 1 tweet
Important study re: ctDNA for non-op surveillance in rectal ca.
— Dr. Nina Niu Sanford (@NiuSanford) June 1, 2026
Pos ctDNA associated w regrowth (60%) & distant mets (60%), but neg ctDNA doesn't exclude local regrowth (sensitivity only 41%)
ctDNA good for risk stratification but not surveillance replacement #ASCO26 @OncoAlert pic.twitter.com/UQQub5QfNB
DeLLphi-304
ForRelapsed SCLC with brain mets, >70% prior CNS-directed therapy
TL;DRIntracranial: time-to-CNS-progression HR 0.54 ITT; in brain-mets pts CNS PFS 6.5 vs 4.2mo (HR 0.40), CNS CR 15% vs 5% for tarlatamab.
The RT read is intracranial control without new radiation: brain-mets CNS PFS 6.5 vs 4.2mo (HR 0.40) and CNS CR 15% vs 5%. But >70% had prior CNS-directed therapy, so this is salvage intracranial activity, not a defer-brain-RT signal in RT-naive disease. Informs sequencing systemic ahead of repeat cranial RT.
| Arm | Median CNS PFS | HR (95% CI) |
|---|---|---|
| Tarlatamab (n=254) | NE (13.7-NE) | 0.54 (0.39-0.75) |
| Chemotherapy (n=255) | 7.2 mo (5.6-NE) | n/a |
+2 more figures
| Arm | Median CNS PFS | HR (95% CI) |
|---|---|---|
| Tarlatamab (n=67) | 6.5 mo (4.3-13.7) | 0.40 (0.24-0.66) |
| Chemotherapy (n=56) | 4.2 mo (2.9-5.5) | n/a |
| CNS endpoint | Tarlatamab (n=67) | Chemotherapy (n=56) |
|---|---|---|
| Complete response | 10 (14.9%) | 3 (5.4%) |
| Disease control rate | 52 (77.6%) | 40 (71.4%) |
| Median duration CNS disease control | 8.2 mo | 5.2 mo |
5 details 2 trials watching
Post hoc intracranial analysis of DeLLphi-304, a phase 3 RCT of tarlatamab vs chemotherapy in relapsed SCLC. CNS endpoints were not prespecified primary. Data cutoff Jan 29 2025; median follow-up 11.4 mo (tarlatamab), 11.5 mo (chemo).
Relapsed SCLC. ITT CNS cohort n=254 tarlatamab vs 255 chemo; brain-mets subgroup n=67 vs 56. >70% of brain-mets pts had prior CNS-directed therapy.
Time to CNS progression or death (ITT, RECIST per investigator); brain-mets CNS PFS by mRANO-BM (BICR); best CNS response, CNS disease control rate, and response durations.
ITT time to CNS progression HR 0.54 (0.39-0.75), median NE vs 7.2 mo. Brain-mets CNS PFS and response detail in figures.
First DLL3xCD3 bispecific intracranial signal in SCLC; CNS control historically relied on WBRT/SRS and prophylactic cranial irradiation, not a systemic agent.
Post hoc, unstratified brain-mets HRs, small subgroup N. >70% prior CNS therapy confounds de novo intracranial activity. No new safety data in source.
Post hoc CNS analysis; brain-mets HRs unstratified with small N (67 vs 56), and >70% had prior CNS-directed therapy, confounding de novo intracranial activity.
For relapsed SCLC with previously-treated brain mets, this supports systemic intracranial control as an option before committing to repeat cranial RT; it does not inform RT-naive or symptomatic brain mets, where upfront local therapy still applies.
- Durability of intracranial response beyond current follow-up
- Activity in RT-naive or untreated brain metastases n=35 · primary completion 2029-02 · candidate match
- Sequencing tarlatamab vs cranial radiotherapy in SCLC brain mets n=39 · primary completion 2027-12 · candidate match
📚 Sources · 🐦 1 tweet
Dr. @g_mountzios #ASCO26 presents CNS outcomes with 2L tarlatamab in DeLLphi-304. Improved time to CNS progression overall (HR 0.54). In pts with brain nets, tarlatamab vs chemo CNS CR rate 15% vs 5% with DCR 78% vs 71% and time to CBS progression 6.5m vs 4.2m, HR 0.40 pic.twitter.com/5i8jL1zlKW
— Stephen V Liu, MD (@StephenVLiu) June 1, 2026
RAD-IO
ForT2-T4a N0M0 muscle-invasive urothelial bladder cancer
TL;DR12-mo DFS 40/50 (80%, 95% CI 0.67-0.89) cleared the pre-set ≥75% GO bar for durvalumab added to 5FU/MMC chemoRT in MIBC.
RT is standard and transferable: 55Gy/20fx to bladder, plus 46Gy/20fx elective nodal coverage in the node-positive expansion, extending durvalumab-chemoRT preservation to N+ disease. 12-mo DFS 80% (40/50, 95% CI 0.67-0.89) cleared the pre-set ≥75% GO bar vs BC2001. Moves whether to layer IO onto a hypofractionated preservation backbone.
+1 more figure
8 details 4 trials watching
Single-arm, multi-stage feasibility and safety trial testing durvalumab added to 5FU/MMC chemoradiation for bladder preservation. Benchmarked against BC2001 historical CRT data, not a randomised comparator.
T2-T4a N0M0 urothelial muscle-invasive bladder cancer, stratified by prior neoadjuvant chemotherapy (yes vs no). A stage-1 expansion added the first 6 node-positive pts.
Durvalumab 1500 mg given neoadjuvant, synchronous, and adjuvant to 12 months post-chemoRT. Concurrent 5-FU 500 mg/m²/24h ×5 days and mitomycin C 12 mg/m².
55 Gy in 20 fractions to bladder (hypofractionated). Node-positive expansion added 46 Gy/20 fx elective nodal RT.
Primary: 12-month disease-free survival post-chemoRT, read against a GO/NO-GO framework (GO ≥75%, contextual 60-75%, NO-GO <60%).
12-mo DFS 40/50 (80%), 95% CI 0.67-0.89, clearing the ≥75% GO bar. 33/54 (61%) completed planned durvalumab; investigators reported very high bladder-preservation and DFS vs prior trial data.
AEs reported in line with component therapies (chemoRT plus durvalumab). 21/54 (39%) discontinued durvalumab early.
Benchmarked against BC2001 (James, JCO 2016), where adding 5FU/MMC to RT gave DFS HR 0.78 (0.60-1.02), p=0.07. RAD-IO's 80% 12-mo DFS is claimed higher than prior data, but the comparison is non-randomised.
Single-arm with a historical benchmark and no concurrent IO comparator; 12-mo DFS is an early surrogate; small N (~50 evaluable); node-positive experience limited to 6 pts.
Single-arm feasibility stage, no randomised IO comparator; benchmarked against historical BC2001. 12-mo DFS an early surrogate at small N; met pre-set GO bar for further evaluation only.
In T2-T4a N0M0 MIBC opting for bladder preservation, this supports durvalumab layered onto 5FU/MMC chemoRT as worth further evaluation; it does not yet establish that IO improves on chemoRT alone, and node-positive experience rests on only 6 expansion pts.
- Does durvalumab add over chemoRT alone in a randomised trial n=11 · primary completion 2026-02 · randomised chemoRT ± durvalumab in node+ MIBC
- Durability of bladder preservation and DFS beyond 12 months active Treating Muscle-invasive Bladder Cancer With A Non-surgical Method Consisting of Anti-PD-1 Therapy and Chemoradiation Phase 2n=71 · primary completion 2025-12 · IO+chemoRT bladder preservation, phase 2recruiting Enfortumab Vedotin in Combination With Pembrolizumab vs. Concurrent Chemoradiotherapy (cCRT) in People With Muscle Invasive Bladder Cancer (EV-309) Phase 3n=390 · primary completion 2030-03 · phase 3 EV+pembro vs cCRT bladder preservation
- Efficacy in node-positive MIBC beyond the 6-patient expansion n=11 · primary completion 2026-02 · durvalumab+chemoRT in node-positive bladder ca
📚 Sources · 🐦 3 tweets
RAD-IO: chemoradiation (5FU+MMC) + Durva in MIBC. #ASCO26 pic.twitter.com/yTyhkdjCox
— Álvaro Pinto (@dralvaropinto) May 30, 2026
#ASCO26 🔬 Abstract 4504 | RAD-IO
— Dra. María Natalia Gandur Quiroga (@nataliagandur) May 30, 2026
Durvalumab + chemoradiotherapy in muscle-invasive bladder cancer
Presented by Nicholas D. James, PhD, MBBS, FRCP@OncoAlert@ASCO
Bladder preservation in MIBC remains one of the most important curative-intent questions in GU oncology.
The key… pic.twitter.com/W6JqzTVsJ3
RAD-IO at #ASCO26: durvalumab added to chemoradiation in muscle-invasive bladder cancer cleared its efficacy bar in a bladder-preservation approach. Single-arm, benchmarked against prior CRT data.
— Katy Beckermann (@katy_beckermann) May 30, 2026
Durvalumab given before, during, and 12 months after chemoRT (55Gy/20Fr +… pic.twitter.com/UXxwoZzaMC
Management of MIBC After Pathologic Complete Response
TL;DRReview of perioperative MIBC management after pCR: sandwich IO regimens continue adjuvant regardless of response, cisplatin-chemo alone moves to surveillance.
SWOG 8710ABACUSCHECKMATE-274KEYNOTE-905VOLGANIAGARAVESPERKEYNOTE-B15
8 details 3 trials watching
- 🔍 pCR used as primary endpoint in signal-seeking phase 2 trials
- 🔍 pCR co-primary (not standalone) endpoint in phase 3 registrational trials
- 🔍 High-risk residual disease (≥ypT2 or N+) post-neoadjuvant chemo → adjuvant therapy (CHECKMATE-274)
- 💊 Post-pCR management by regimen
- Sandwich IO (NIAGARA, EVP): continue planned adjuvant regardless of pathologic response
- NIAGARA: resume durvalumab 8 mo post-cystectomy
- Cisplatin-based chemo alone: surveillance after pCR is standard
- 📊 pCR (pT0N0) post-neoadjuvant chemo = strong prognostic marker: SWOG 8710 85% 5-yr OS if pT0
- 📐 Meta-analysis: pooled RR 0.19 for RFS with pCR
- 📊 Perioperative regimens across trials
Trial Setting Comparison Result NIAGARA Cis-eligible Gem/Cis + periop durvalumab 24-mo OS 82.2% vs 75.2% VESPER Cis-eligible ddMVAC vs Gem/Cis 5-yr OS 66% vs 57% KEYNOTE-905 Cis-ineligible Periop EVP vs cystectomy alone OS HR 0.50 KEYNOTE-B15 Cis-eligible Periop EVP vs Gem/Cis OS improved (under FDA review)
- ⚠️ Not all pts in perioperative trials completed adjuvant therapy, often due to toxicity
- Relative contribution of pre- vs post-operative therapy components
- Can adjuvant therapy be de-escalated by pCR or biomarker n=761 · primary completion 2025-06 · adjuvant atezo gated by ctDNA+ post-cystectomyrecruiting Surveillance of the Genetic Signature in Circulating Tumor DNA for Guiding Adjuvant Chemotherapy in Urothelial Carcinoma Phase 2n=20 · primary completion 2025-09 · ctDNA-guided adjuvant gem/cis in urothelialn=992 · primary completion 2030-09 · ctDNA-guided adjuvant IO after cystectomy
📚 Sources · 🐦 1 tweet
#ASCO26 GU Oncology Spotlight 🚨
— Dra. María Natalia Gandur Quiroga (@nataliagandur) May 30, 2026
🔬 Management in Bladder Cancer After Pathologic Complete Disease Response
Presented by Brendan J. Guercio, MD@OncoAlert@ASCO
In muscle-invasive bladder cancer, pCR after neoadjuvant therapy is one of the most powerful prognostic signals we… pic.twitter.com/sMd2In7X3p
Genomic Classifier + NCCN Risk Stratification (Abstract 5000)
ForNCCN high-risk/very-high-risk localized prostate cancer
TL;DR22-gene GC independently prognostic (MFS/DM/OS, p<0.001); combined NCCN+GC score reclassifies ~¼ of high-risk pts to gate AAP intensification on an RT+ADT backbone.
~¼ of NCCN ≥HR pts are clinical/GC-discordant, so the 22-gene GC reclassifies who reaches CT-VHR (≥3 pts) and has AAP added onto the fixed RT+ADT backbone. The intensification it triggers carries STAMPEDE M0 magnitude (MFS HR 0.53, OS HR 0.60). It sharpens the intensification decision, not RT dose or target.
+2 more figures
| Endpoint | HR (add AAP) | 95% CI | p |
|---|---|---|---|
| MFS | 0.53 | 0.44-0.64 | <0.0001 |
| OS | 0.60 | 0.48-0.73 | <0.0001 |
7 details
Retrospective validation of the 22-gene GC (Decipher) layered on NCCN clinical risk in NCCN ≥ high-risk localized prostate (NRG cohort), externally benchmarked to STAMPEDE M0 curves (Attard, Lancet 2022). Not a prospective RCT.
NCCN high-risk and very-high-risk localized prostate cancer, all planned for definitive RT+ADT.
CT-HR (≤2 pts) → RT+ADT; CT-VHR (≥3 pts) → RT+ADT+AAP (abiraterone acetate + prednisone) intensification.
GC is independently prognostic for MFS, DM, and OS over clinical variables (multivariable, p<0.001). Roughly one-quarter of NCCN ≥HR pts are clinical/GC-discordant, reclassifying risk band and the intensification call.
| Component | Category | Points |
|---|---|---|
| NCCN clinical | High-risk | +1 |
| NCCN clinical | Very-high-risk | +2 |
| GC (Decipher) | < 0.6 | 0 |
| GC (Decipher) | 0.6-0.85 | +1 |
| GC (Decipher) | > 0.85 | +2 |
AAP intensification magnitude is borrowed from STAMPEDE M0 (Attard, Lancet 2022), not generated here; GC prognostic value aligns with prior Decipher/NRG validation.
Prognostic, not predictive: no randomized biomarker×treatment interaction showing CT-VHR pts gain more from AAP. Intensification benefit imported from an external trial's average effect.
Retrospective GC prognostic validation, not a randomized predictive-biomarker trial; consistent with prior Decipher/NRG data. Intensification benefit borrowed from STAMPEDE, not shown to be GC-predictive.
In NCCN high-risk/very-high-risk localized prostate planned for definitive RT+ADT, this supports GC-informed CT-VHR (≥3 pts) selection for AAP intensification; it does not extend to intermediate-/low-risk disease or change RT dose or target.
- Does GC-guided AAP intensification improve outcomes prospectively?
- Is GC predictive of differential AAP benefit, not just prognostic?
- Optimal AAP intensification threshold in clinical/GC-discordant pts
📚 Sources · 🐦 2 tweets
#ASCO26 Dr. Patel presented a clinically practical framework integrating NCCN clinical risk + a 22-gene genomic classifier to guide treatment intensification in high-risk localized prostate cancer.
— Julian Chavarriaga (@chavarriagaj) May 30, 2026
Key findings:
🔹 The genomic classifier independently improved prognostic… pic.twitter.com/fRcdTmfBec
#ASCO26 GU Oncology Spotlight 🚨
— Dra. María Natalia Gandur Quiroga (@nataliagandur) May 30, 2026
🔬 Abstract 5000 | High-risk prostate cancer
Clinico-transcriptomic risk stratification to guide abiraterone intensification
Presented by Krishnan R. Patel, MD, MHS@Krishnan_Patel@OncoAlert@ASCO
In high-risk localized prostate cancer,… pic.twitter.com/pZSCiTyGB8
A-DREAM
FormHSPC deep responder (PSA<0.2) after 18-24mo ADT + ≥12mo ARPI
TL;DR41% remained treatment-free with eugonadal testosterone recovery at 18mo after interrupting ADT+ARPI in deep-responding mHSPC (1° EP met, one-sided p=0.0249).
In metastatic HSPC deep responders (PSA<0.2 after ≥18mo ADT and ≥12mo ARPI, predominantly low-volume), this supports discussing a monitored ADT+ARPI holiday with scheduled PSA/imaging; it does not extend to incomplete responders or high-volume disease.
+2 more figures
8 details 4 trials watching
Phase 2 single-arm Alliance trial. N=78 eligible metastatic HSPC deep responders interrupt ADT+ARPI. Enrolled 07/2022-03/2024; median follow-up 26.9mo.
Entry required PSA<0.2 (stable/falling) after 18-24mo ADT and ≥12mo ARPI. Median age 70 (49-90); 64.9% low-volume, 35.1% high-volume (CHAARTED); 51.3% had prior local radiation, 29.5% metastasis-directed radiation.
Primary: treatment-free with eugonadal testosterone (≥150 ng/dL) at 18 months. Exploratory: rPFS, TTNT, OS, cost.
Primary met: 32/78 (41.0%) treatment-free and eugonadal at 18mo (80% CI 33.1-48.9%, one-sided p=0.0249). 57.7% were treatment-free at 18mo and 66.7% recovered testosterone; median time to eugonadal T 9.0mo.
Disease control held through interruption: rPFS 15/78 events, OS 4/78 events, both medians not reached. The 41% primary is capped by slow testosterone recovery, not progression, so the endpoint understates short-term oncologic safety in this older cohort.
Single-arm with no randomised comparator against continued therapy, so the survival cost of interruption is unquantified. Median follow-up 26.9mo is short for mHSPC; durability of treatment-free intervals is unproven.
Single-arm phase 2, N=78, no randomised comparator vs continued therapy; primary endpoint met but interruption safety needs longer follow-up and randomisation.
- Survival cost of interruption vs continued ADT+ARPI active A Study of an Intermittent ADT Approach With Apalutamide Monotherapy in Participants With mCSPC Phase 3n=420 · primary completion 2026-10 · intermittent post-response, rPFS non-inferiorityn=1600 · primary completion 2035-05 · phase 3 intermittent vs continuous, OS endpoint
- Durability of treatment-free interval beyond 27 months
- Which deep responders can safely interrupt active A Study of an Intermittent ADT Approach With Apalutamide Monotherapy in Participants With mCSPC Phase 3n=420 · primary completion 2026-10 · restricted to PSA <0.2 deep respondersrecruiting Optimal PSA Triggered Individual Management of Androgen Sensitive Prostate Cancer Phase 2n=160 · primary completion 2030-10 · intermittent ARPI in optimal PSA responders
📚 Sources · 🐦 1 tweet
Can treatment be safely stopped in selected patients with mHSPC?
— MJosé Juan (@mjuanfi81) May 30, 2026
Phase II A-DREAM trial, 41% of responders remained treatment-free with testosterone recovery 18m after stopping ADT/ARPI. At a median FU of 21 months, 35% of patients required treatment re-initiation.@OncoAlert pic.twitter.com/iW2VDBWWhN
ARACOG (AFT-47)
ForAdvanced prostate cancer (mHSPC/mCRPC/nmCRPC) starting an ARSI
TL;DRMCCD -36.1 (enza) vs -15.8 (daro), P=0.009 at 24 wk: enzalutamide worse for cognition; randomized open-label phase 2, N=111 advanced prostate.
In advanced prostate cancer pts where cognitive tolerability drives ARSI selection, this randomized head-to-head supports darolutamide over enzalutamide for cognitive sparing; it does not address efficacy or compare against apalutamide or abiraterone.
| Arm (N) | Max-changed domain | Median % change | P |
|---|---|---|---|
| Darolutamide (48) | PALFAM (visual mem/exec) | -15.8 | 0.009 |
| Enzalutamide (47) | SWM (working mem/exec) | -36.1 | n/a |
+1 more figure
7 details 2 trials watching
Randomized open-label phase 2, N=111, darolutamide vs enzalutamide, stratified by age (<65, 65-80, >80). US academic centers only; enrolled 8/2021 to 3/2025, crossover permitted.
Advanced prostate cancer across mHSPC, mCRPC, and nmCRPC. Required acceptable enzalutamide co-pay; predominantly White, with most non-White pts randomized to enzalutamide.
Darolutamide provided by the study vs enzalutamide through standard of care, an asymmetry that could bias crossover and adherence.
Primary: between-arm % change from baseline to 24 wk in Maximally Changed Cognitive Domain (MCCD), from 5 remotely delivered CANTAB tests. Crossovers scored at crossover in their randomized arm.
MCCD median change -36.1 (enza, N=47) vs -15.8 (daro, N=48), P=0.009: greater cognitive decline on enzalutamide.
First randomized head-to-head of cognition for these two ARSIs; direction fits darolutamide's minimal blood-brain-barrier penetration vs enzalutamide's CNS exposure.
Open-label with a functional endpoint; enzalutamide via standard of care may have altered crossover. CANTAB is a research tool, not a clinical diagnostic; small N and race-by-arm imbalance limit inference.
Randomized head-to-head met its prespecified cognitive endpoint; aligns with darolutamide's known low CNS penetration. Phase 2, open-label, small N keep it below practice-changing.
- Does the cognitive advantage translate to functional outcomes or efficacy? n=102 · primary completion 2026-04 · tracks functional status + cognition on ARPIs
- Darolutamide vs apalutamide or abiraterone on cognition? n=102 · primary completion 2026-04 · cognitive outcomes across daro/apa/abi ARPIs
- Durability of the cognitive difference beyond 24 weeks
📚 Sources · 🐦 2 tweets
ARACOG (AFT-47) met its primary endpoint: enzalutamide caused significantly greater cognitive decline than darolutamide at 24 weeks in advanced prostate cancer.
— Katy Beckermann (@katy_beckermann) May 30, 2026
Randomized open-label phase 2, 111 pts (mHSPC, mCRPC, nmCRPC), DAR vs ENZ.
Cognition was measured with CANTAB, a… pic.twitter.com/kj4vfGRVyp
#ASCO26 GU Oncology Spotlight 🚨
— Dra. María Natalia Gandur Quiroga (@nataliagandur) May 30, 2026
🔬 Abstract 5005 | ARACOG / AFT-47
Cognitive effects of darolutamide vs enzalutamide
Presented by Alicia K. Morgans, MD, MPH, FASCO@CaPsurvivorship @OncoAlert@ASCO
In prostate cancer, we often discuss AR pathway inhibitors through the lens… pic.twitter.com/vpZr1w6kc6
Precision Oncology: Applying New Biomarkers in GU Cancers
TL;DRBiomarker round-up: tissue HRR/tumor-suppressor testing is SOC, but genomic classifiers show 24% clinical-risk discordance and lack ARPI-era validation.
ENZAMETCHAARTED
For RT readers using genomic classifiers to gate ADT intensification with salvage or definitive RT, the session's caution transfers: Decipher was discordant with clinical risk in 24% of high-risk pts (tissue available in only 427 of 3816), and its validation cohorts predate ARPIs. Treat the score as hypothesis-generating, not a settled gate.
+1 more figure
9 details 4 trials watching
- 🔍 ENZAMET biomarker cohort: 1,071 consented, GEP N=764, final Decipher cohort N=634 (56% of enrolled)
- 📊 Tissue-panel testing for HRR + tumor-suppressor loss is called SOC in prostate
- 📊 Landscape-slide annotations, approx. eligible fraction: Lu-177 PSMA ~90%, PARP inhibitors ~10-20%, pembrolizumab ~3%
- 📊 Decipher genomic classifier discordant with clinical risk in 24% of high-risk events
- 📊 Decipher DPMC ≤0.85 subgroup: ADT+enza+docetaxel had worse OS than ADT+enza (triplet cohort N=320)
- ⚠️ Discordance from tissue-available subset (n=427) of n=3816; representativeness of full trial population uncertain
- ⚠️ Source classifier trials predate ARPIs; applicability to current ARPI-based SOC questioned
- ⚠️ Confounded: docetaxel not randomized, with more high-volume disease + older pts → selection bias, not a validated predictor
- 🔬 ASCO26 education session (J. Lang): a biomarker is useful only if it changes management; GU therapy selection stays biomarker-limited
- Do genomic classifiers retain validity in ARPI-era standard of care? n=240 · primary completion 2023-07 · validates Decipher accuracy across ancestryrecruiting Genomics and Efficacy of Post-prostatectomy Salvage Radiotherapy With 'Extreme' Hypofractionationn=103 · primary completion 2027-11 · prospective Decipher validation, salvage RTactive Genomics in Michigan to AdJust Outcomes in Prostate canceR (G-MAJOR) for Men With Newly Diagnosed Favorable Risk Prostate Cancer Phase NAn=805 · primary completion 2028-03 · RCT of gene expression classifier clinical impactn=1000000 · primary completion 2030-12 · prospective registry testing Decipher utility
- Is Decipher predictive of docetaxel benefit in metastatic HSPC?
📚 Sources · 🐦 1 tweet
#ASCO26 GU Oncology Spotlight 🚨
— Dra. María Natalia Gandur Quiroga (@nataliagandur) May 30, 2026
🔬 Precision Oncology: How to Apply New Biomarkers in Clinical Practice
Excellent discussion by Joshua M. Lang, MD, MS@JoshLangMD@OncoAlert@ASCO
This session captured the real challenge of precision oncology in GU cancers:
A biomarker is only… pic.twitter.com/ubfk49XPiM
ENZAMET + Decipher (Part 2)
FormHSPC on ADT + enzalutamide, Decipher genomic classifier available
TL;DRDecipher >0.85 predicts docetaxel OS benefit on an ADT+enza backbone (HR 0.75 vs 1.94, interaction p=0.04); ≤0.85 can skip docetaxel.
In mHSPC starting ADT + enzalutamide, a Decipher score >0.85 is where the docetaxel OS benefit concentrates while ≤0.85 sees little added benefit; the read informs docetaxel selection, not any radiotherapy decision.
| Treatment arm | Decipher >0.85 vs ≤0.85 OS HR | p |
|---|---|---|
| ADT + ENZA | 3.02 (1.50-5.76) | — |
| ADT + ENZA + Doce | 1.08 (0.60-1.71) | 0.73 |
+1 more figure
| Decipher stratum | Unweighted HR (doce vs none) | IPTW-weighted HR |
|---|---|---|
| ≤0.85 | 2.78 (1.49-5.21) | 1.94 (0.95-3.96) |
| >0.85 | 1.13 (0.71-1.79) | 0.75 (0.43-1.33) |
7 details
Preplanned biomarker analysis of the phase 3 ENZAMET RCT. Decipher genomic classifier (DPMC, cutpoint >0.85) applied to the ADT + enzalutamide backbone cohort, N=320.
Metastatic hormone-sensitive prostate cancer on an ADT + enzalutamide backbone with an available Decipher score. A low-volume subset was analysed separately.
ADT + enzalutamide ± early docetaxel. Docetaxel was given at investigator discretion (a stratification factor), so the docetaxel comparison is not randomised.
Two-part signal: Decipher >0.85 is prognostic for worse OS on ADT+enza, and by IPTW interaction (p=0.04) predicts OS benefit from added docetaxel; ≤0.85 derives little benefit. Effect sizes in the figures.
Consistent with docetaxel OS benefit in CHARTED and STAMPEDE for high-volume/high-risk mHSPC; positions Decipher as a molecular refinement of that selection. Presented as Level 1B evidence.
Docetaxel not randomised (IPTW-weighted, residual imbalance after scoring); the high-Decipher benefit's CI crosses 1 and rests on a subgroup interaction. Hypothesis-generating, not yet practice-defining.
Post-hoc biomarker-by-docetaxel interaction; docetaxel not randomised (IPTW-weighted, residual imbalance acknowledged). High-Decipher benefit CI crosses 1, rests on interaction p=0.04, strengthened only after weighting.
- Prospective validation of Decipher-guided docetaxel selection in mHSPC
- Whether DPMC ≤0.85 pts can safely omit docetaxel
- Decipher predictive value across other intensification agents (ARSI, PARP)
📚 Sources · 🐦 1 tweet
#ASCO26 GU Oncology Spotlight 🚨
— Dra. María Natalia Gandur Quiroga (@nataliagandur) May 30, 2026
🔬 ENZAMET + Decipher | Part 2
Can genomics guide docetaxel intensification in mHSPC?
Outstanding presentation by @ChrisSweeney1.@OncoAlert@ASCO
After Part 1, the key question was:
➡️ Can a genomic classifier identify which patients with… pic.twitter.com/nJYMxuXelV
TALAPRO-3
ForHRR-deficient metastatic prostate cancer
HR 0.48
95% CI 0.36-0.65, P<0.001; 3yr rPFS 77% vs 56% (ITT)
TL;DR3yr rPFS 77% vs 56%, HR 0.48 (0.36-0.65), adding talazoparib to enzalutamide/ADT in HRR-deficient metastatic prostate cancer.
In HRR-deficient metastatic prostate cancer, this supports intensifying enzalutamide/ADT with talazoparib, benefit steepest in the BRCA subgroup; it does not extend to HRR-intact disease.
| Population | HR (95% CI) | Median rPFS, mo |
|---|---|---|
| ITT | 0.48 (0.36-0.65) | NC vs 45.8 |
| BRCA | 0.37 (0.22-0.61) | NC vs 35.1 |
| Non-BRCA | 0.57 (0.39-0.82) | NC vs NC |
6 details 2 trials watching
Randomized, placebo-controlled trial: talazoparib+enzalutamide vs placebo+enzalutamide, 300 vs 299 pts. Published NEJM May 30, 2026.
HRR-deficient metastatic prostate cancer, enzalutamide/ADT backbone both arms. Prespecified BRCA (104/103) and non-BRCA HRR (196/196) strata.
Talazoparib (PARP inhibitor) added to enzalutamide plus ADT; control substituted placebo for talazoparib on the same ARSI backbone.
Primary: imaging-based (radiographic) PFS. OS and other secondaries not reported in source.
ITT 3yr rPFS 77% vs 56%, P<0.001; per-population HRs and medians in the figure. Benefit concentrated in the BRCA subgroup.
Extends PARP+ARSI combinations (TALAPRO-2, PROpel, MAGNITUDE) that established the class in HRR-altered mCRPC toward the enzalutamide/ADT-backbone metastatic setting.
Primary endpoint is rPFS, a surrogate; OS not reported in source. Non-BRCA benefit is modest, so the HRR-wide result leans on BRCA. Talazoparib medians not reached, so follow-up is immature.
Randomized phase 3, rPFS primary hit (HR 0.48); but rPFS is a surrogate and OS not reported. Aligns with PARP+ARSI direction (TALAPRO-2, PROpel, MAGNITUDE).
- Overall survival benefit, given rPFS is the surrogate primary endpoint n=1054 · primary completion 2022-10 · mature phase 3, same combo vs enza, mCRPC
- Whether non-BRCA HRR alterations derive benefit comparable to BRCA recruiting A Study of Talazoparib With or Without Enzalutamide in People With Prostate Cancer Who Have Previously Received Abiraterone Acetate Phase 2n=126 · primary completion 2029-03 · talazoparib in broad HRR-mutant mCRPC
📚 Sources · 🐦 1 tweet
JUST In: TALAPRO-3 published in @NEJM
— Toni Choueiri, MD (@DrChoueiri) May 30, 2026
Adding #talazoparib to enzalutamide/ADT
=>3-year rPFS: 77% vs 56% in HRR-deficient metastatic prostate cancer !
Looking forward to full presentation by @neerajaiims who keeps changing SOC, one trial at a time. @ASCO #ASCO26 @OncoAlert pic.twitter.com/nXiPk4DIXg
PREPEC
ForSkin/nipple-sparing mastectomy, implant reconstruction, prevention/therapeutic
Δ4.8 pts (79.2 vs 74.3)
95% CI 1.0-8.7, p=0.01; 24mo, pre- vs sub-pectoral
TL;DRPre-pectoral implant improved 2yr chest well-being +4.8 pts (BREAST-Q, p=0.01) vs sub-pectoral, but more unplanned implant loss (21% vs 15%).
In pts undergoing skin- or nipple-sparing mastectomy (therapeutic or risk-reducing) who choose implant reconstruction, this supports pre-pectoral placement for better 2yr patient-reported chest well-being, weighed against numerically higher unplanned implant loss (21% vs 15%).
| Endpoint (24mo) | Pre-pectoral (N=191) | Sub-pectoral (N=189) | Difference |
|---|---|---|---|
| Physical well-being, chest (BREAST-Q) | 79.2 (75.5-82.8) | 74.3 (70.7-78.0) | 4.8 (1.0-8.7), p=0.01 |
+1 more figure
| Unplanned implant loss/replacement (24mo) | Pre-pectoral | Sub-pectoral | Adj. difference (95% CI) |
|---|---|---|---|
| Crude % (n/N) | 21.1% (41/194) | 14.5% (27/186) | 5.7% (-2.4 to 13.8) |
8 details 3 trials watching
International randomized phase 3 trial (OPBC-02): pre- vs sub-pectoral implant reconstruction after skin- or nipple-sparing mastectomy. Open-label; patient-reported primary endpoint analyzed by multiple imputation and linear mixed models.
Women undergoing skin- or nipple-sparing mastectomy for cancer treatment or risk reduction, opting for implant reconstruction. Primary QoL analysis N=191 pre- vs 189 sub-pectoral.
Primary: long-term patient-reported physical well-being (chest), BREAST-Q, at 24 months. Main secondary safety: unplanned loss or replacement of expander/implant.
BREAST-Q chest well-being 79.2 vs 74.3 at 24mo, difference 4.8 (95% CI 1.0-8.7, p=0.01), favoring pre-pectoral. Longitudinal completion 83-95%.
Point estimate showed more implant loss with pre-pectoral (21.1% vs 14.5%), failing the trial's non-inferiority safety hypothesis; the adjusted-difference 95% CI (-2.4 to 13.8) crosses zero.
Open-label with a patient-reported primary endpoint, so awareness of implant type could bias PROs. The 4.8-point gain is significant but modest, and the safety signal trended against pre-pectoral.
A major RCT in an area of genuine equipoise. It supports pre-pectoral for patient-reported chest well-being while flagging a higher implant-loss signal, so the choice reads as a real trade-off, not a clean win.
Randomized phase 3, primary endpoint met, but a modest patient-reported surrogate and an unmet non-inferiority safety endpoint keep it short of practice-changing.
- Durability of the QoL benefit and implant-loss gap beyond 24 months n=300 · primary completion 2024-12 · prepectoral vs subpectoral head-to-head, n=300n=88 · primary completion 2025-03 · prepectoral vs subpectoral breast satisfaction
- Do outcomes differ in patients receiving post-mastectomy radiation? n=104 · primary completion 2027-03 · prepectoral recon in adjuvant RT patients
- Which patients accept higher implant-loss risk for better chest well-being?
📚 Sources · 🐦 1 tweet
📌 Surgical de-escalation of implant-based breast reconstruction after mastectomy for breast cancer treatment or prevention: The international randomized phase I|I
— Elisabetta Bonzano MD, PhD (@to_be_elizabeth) May 30, 2026
PREPEC trial (ОРBC-02).
Presented by Walter Weber ✨#ASCO26 @OncoAlert #OncoAlertAF #BreastCancer pic.twitter.com/WE20JcBQG0
ROADS
ForResected brain metastasis > 2 cm, post-op cavity RT candidates
NR vs 17 mo
Surg bed recurrence 1% GammaTile vs 12% SRS
TL;DRSurgical bed recurrence 1% vs 12% and 2yr OS 62% vs 36% favoring intraoperative GammaTile brachytherapy over post-op SRS for resected brain mets >2cm.
The safety tradeoff the headline buries: leptomeningeal disease ran 10% with GammaTile vs 3% with SRS, even as surgical-bed recurrence fell to 1% vs 12%. Radiation necrosis was comparable (8% vs 7%). This moves the intraoperative-brachytherapy-vs-staged-cavity-SRS decision for resected mets >2 cm, where SRS local control is weakest.
| Endpoint | GammaTile | SRS |
|---|---|---|
| Time to surg bed recurrence | NR | 17 mo |
| Surg bed recurrence-free survival | NR | 11 mo |
| 2-yr OS | 62% | 36% |
8 details 2 trials watching
Randomized trial, N=230, resected brain metastasis > 2 cm. GammaTile (Cs-131 collagen-tile brachytherapy) placed in the cavity at resection vs post-op stereotactic radiosurgery. ASCO 2026 final results. Primary: time to surgical bed recurrence and surgical-bed recurrence-free survival.
Resected brain metastasis > 2 cm, the larger-cavity setting where single-fraction post-op SRS local control is weakest. Histology / primary tumor not specified in source.
Experimental: intraoperative permanent Cs-131 seed brachytherapy (GammaTile) at resection. Control: post-op cavity SRS. Dose, fractionation, and cavity margin not reported in source.
Both primary endpoints and 2yr OS favored GammaTile. Safety: radiation necrosis comparable (8% vs 7%), leptomeningeal disease higher with brachytherapy (10% vs 3%).
Post-op cavity SRS is the current standard for resected brain mets (N107C, Mahajan). ROADS challenges it, favoring intraoperative brachytherapy on local control.
Abstract-only, not yet peer-reviewed; open-label. The 2yr OS advantage is large for a local therapy and OS was not a stated primary endpoint, raising the question of baseline arm imbalance.
Randomized, primary endpoint (surg bed control) hit favoring intraop brachy over the post-op SRS standard; but abstract-only, open-label, and the large OS gain warrants scrutiny.
In pts with a resected brain metastasis >2 cm needing cavity radiotherapy, this supports intraoperative brachytherapy as an alternative to post-op SRS for local control; it does not extend to intact (unresected) mets or cavities ≤2 cm.
- Whether the large OS gain reflects arm imbalance vs true benefit active Post-Surgical Stereotactic Radiotherapy (SRT) Versus GammaTile-ROADS (Radiation One and Done Study) Phase 3n=230 · primary completion 2029-08 · randomized phase 3 GammaTile vs SRT
- Leptomeningeal failure risk with intraoperative brachytherapy active Intracavitary Carrier-embedded Cs131 Brachytherapy for Recurrent Brain Metastases: a Randomized Phase II Study Phase 2n=103 · primary completion 2026-12 · randomized brachytherapy vs surgery-alone safety
- Applicability to resection cavities ≤ 2 cm
📚 Sources · 🐦 1 tweet
🚨🚨 ASCO 2026 Final Results Randomized trial resected brain met Brachytherapy vs Post-Op SRS🚨
— PDBrown (@PDBrownOnc) May 30, 2026
- Incredible Surg Bed Control with Brachy (↑↑OS as well)
- Surg bed recurrence 12% SRS vs 1% GammaTile pic.twitter.com/PCTsCluyUd
CHRYSALIS-2
ForTreatment-naïve atypical EGFR-mutant advanced NSCLC
TL;DRmOS 41.0 mo (95% CI 27.7-NE) with 1L amivantamab + lazertinib in treatment-naïve atypical EGFR-mutant NSCLC; single-arm, n=49.
In treatment-naïve atypical EGFR-mutant advanced NSCLC, a population with few standard targeted options, this single-arm 41-mo median OS supports amivantamab+lazertinib as a candidate 1L regimen; it does not extend to common EGFR (exon19del/L858R) disease, where randomised data already guide practice.
+1 more figure
8 details
Single-arm cohort, n=49, no randomised comparator. Median follow-up 31.3 mo.
Treatment-naïve (1L) atypical EGFR-mutated advanced NSCLC. Responses durable regardless of demographics, baseline mutations, and disease characteristics.
IV amivantamab + lazertinib. Median treatment duration 13.3 mo (range <0.1-53.2); 39% on treatment >2 years.
Median OS 41.0 mo (95% CI 27.7-NE), ~3.5 years. No clear association between EGFR variant subtype and OS.
With longer follow-up, safety consistent with prior reports; no new safety signals.
Extends the durable 1L amivantamab+lazertinib OS signal from common EGFR (exon19del/L858R) to atypical variants.
Single-arm, n=49, no randomised comparator. Atypical EGFR is a heterogeneous class; per-variant efficacy not detailed in source.
Single-arm cohort (n=49), no randomised comparator in atypical EGFR NSCLC; durable but single-arm design caps the read at early-signal despite 31-mo follow-up.
- Efficacy by specific atypical EGFR variant
- Randomised comparison vs other 1L options in atypical EGFR
📚 Sources · 🐦 1 tweet
Amivantamab + lazertinib achieved a median OS of 41.0 months in treatment-naïve atypical EGFR-mutant NSCLC, with no clear association between EGFR variant subtype and outcome. A compelling option. Meanwhile, amivantamab continues evaluation across multiple tumor types. #ASCO26 pic.twitter.com/aWn3Ja60Ji
— Chul Kim (@chulkimMD) May 29, 2026
ESAONA
ForTreatment-naive EGFR-mutant NSCLC with brain metastases
TL;DRiORR 95.5% vs 79.6% (p=0.0004) and icPFS HR 0.46 favoring asandeutertinib over osimertinib in 1L EGFR-mut NSCLC brain mets.
The RT-relevant read is upfront local therapy: iORR 95.5% vs 79.6% and intracranial PFS not reached (HR 0.46) strengthen deferring upfront SRS/WBRT in favor of TKI in EGFR-mut brain mets. No head-to-head vs radiosurgery, so it moves sequencing, not RT omission at progression.
7 details 5 trials watching
Randomised phase 2, N=224 (111 asandeutertinib vs 113 osimertinib), 1L EGFR-mutant NSCLC with brain metastases. All efficacy endpoints BICR-assessed. Blinding not specified in source.
Treatment-naive (1L) EGFR-mutant NSCLC with brain metastases. Mutation subtype, symptomatic status, and prior brain RT not reported in source.
Asandeutertinib (next-generation EGFR TKI) vs osimertinib. Dose and schedule not reported in source.
Intracranial endpoints (response, icPFS) drove the result and cleared significance more decisively than the borderline overall PFS benefit. Full arm comparison in the table above.
| Endpoint | Asandeutertinib | Osimertinib | HR (p) |
|---|---|---|---|
| iORR | 95.5% (89.8-98.5) | 79.6% (71.0-86.6) | p=0.0004 |
| Intracranial PFS | NR | 17.5 mo (15.18-NA) | HR 0.46, p=0.0020 |
| Overall PFS | NR | 17.2 mo (15.18-19.55) | HR 0.64, p=0.0473 |
Any TRAEs 99.1% vs 95.6%; serious TRAEs numerically higher with asandeutertinib (10.8% vs 7.1%). Fatal and discontinuation rates not reported in source.
Osimertinib is the established CNS-active 1L EGFR TKI (FLAURA). Asandeutertinib raises the intracranial bar in phase 2, but no OS or phase 3 head-to-head yet.
Phase 2 with immature time-to-event data (medians not reached); overall PFS benefit borderline (p=0.0473); no OS; blinding not specified.
Strong intracranial activity revives whether a CNS-active TKI can defer upfront brain-directed RT/SRS in EGFR-mutant NSCLC. Phase 3 confirmation vs osimertinib, plus OS and durability, is needed before displacing the standard.
Randomised phase 2; strong intracranial ORR but time-to-event immature (medians NR), overall PFS borderline (p=0.0473), no OS. Needs phase 3 before displacing osimertinib.
In treatment-naive EGFR-mutant NSCLC with brain metastases, this supports a TKI-first, SRS-deferred read; it does not extend to EGFR-wildtype disease or brain mets progressing on a prior EGFR TKI.
- Overall survival vs osimertinib recruiting TY-9591 in the Patients With EGFR Mutations in Advanced NSCLC With Brain Metastases Phase 2n=420 · primary completion 2025-06 · 1L TY-9591 vs osimertinib, EGFR brain metsn=380 · primary completion 2029-03 · phase 3 furmonertinib vs osimertinib in brain mets
- Durability of intracranial response with longer follow-up
- Head-to-head efficacy vs upfront radiosurgery n=162 · primary completion 2024-12 · osimertinib +/- early SRS, asymptomatic BMactive Study of Osimertinib + SRS vs Osimertinib Alone for Brain Metastases in EGFR Positive Patients With NSCLC Phase 2n=40 · primary completion 2025-04 · randomized osimertinib +/- upfront SRS, 1Lrecruiting Observation or Upfront Cranial RT in Oncogene Mutated NSCLC With Asymptomatic BM: A Phase III RCT Phase 3n=190 · primary completion 2025-12 · phase 3 upfront cranial RT vs obs on TKI
📚 Sources · 🐦 1 tweet
#ASCO26 🧠🌍
— Dr Rishabh Jain (@DrRishabhOnco) May 30, 2026
Could a next-generation EGFR TKI outperform osimertinib in patients with brain metastases?
The phase II ESAONA trial suggests the answer may be yes.
🧪 LBA2007 | ESAONA
1L EGFR-mutated NSCLC with brain metastases
👥 n=224
⚔️ Asandeutertinib vs Osimertinib
Key… https://t.co/mEOKGNKgf7 pic.twitter.com/pUQuH6i2cV
OptiTROP-Lung05 NCT06448312
For1L IIIB/IIIC-IV PD-L1≥1% NSCLC, EGFR/ALK wild-type
HR 0.35
95% CI 0.26-0.47, p<0.0001; median NR vs 5.7 mo
TL;DRmPFS NR vs 5.7 mo, HR 0.35, adding Sac-TMT (TROP2 ADC) to pembrolizumab in 1L PD-L1+ NSCLC.
| Arm | PFS events n (%) | Median PFS | HR (95% CI) |
|---|---|---|---|
| Sac-TMT+Pembro | 66 (31.7%) | NR (13.6-NE) | 0.35 (0.26-0.47) |
| Pembro | 128 (62.4%) | 5.7 mo (4.3-7.0) | — |
+2 more figures
| PD-L1 TPS | mPFS combo | mPFS pembro | HR (95% CI) |
|---|---|---|---|
| ≥50% | NR | 9.5 mo | 0.47 (0.29-0.77) |
| 1-49% | NR | 4.3 mo | 0.28 (0.19-0.41) |
| Arm | OS events n (%) | Median OS | HR (95% CI) |
|---|---|---|---|
| Sac-TMT+Pembro | 33 (15.9%) | NR | 0.55 (0.36-0.85) |
| Pembro | 54 (26.3%) | NR | — |
8 details 2 trials watching
Phase 3, open-label, multicenter RCT (NCT06448312); 1:1, N=413. Primary PFS by BICR crossed its interim efficacy boundary at 194 events; median follow-up 10.5 mo.
1L stage IIIB/IIIC or IV NSCLC, PD-L1 TPS ≥1% (22C3), EGFR/ALK wild-type, ECOG 0-1. Stratified by histology, PD-L1 (1-49 vs ≥50), ECOG.
Sac-TMT (TROP2 ADC) 4 mg/kg Q2W + pembrolizumab 400 mg Q6W vs pembrolizumab alone; pembro capped at 18 cycles.
ORR 70.2% vs 42.0%. PFS gain held across PD-L1 strata, strongest in TPS 1-49% where pembro monotherapy is weakest. OS immature, formal testing pending.
Current 1L PD-L1+ NSCLC standard is pembrolizumab ± chemotherapy. This tests a chemo-free ADC+IO doublet; no head-to-head vs chemo-IO.
Open-label; OS immature at 10.5-mo follow-up and formally untested; PFS reported at an interim efficacy boundary. No safety data in source.
PFS crossed an interim efficacy boundary; key-secondary OS descriptive/immature at 10.5-mo f/u; open-label. Strong but not yet mature enough to move 1L SOC.
- Will the OS benefit mature and hold? n=30 · primary completion 2026-06 · candidate match
- How does the chemo-free ADC+IO doublet compare to chemo+IO? n=30 · primary completion 2026-06 · candidate match
- Safety of adding a TROP2 ADC to pembrolizumab
📚 Sources · 🐦 2 tweets
🔁REVIEW #ASCO26 #LCSM Oral
— Hidehito HORINOUCHI (@HHorinouchi) May 30, 2026
🔥OptiTROP-Lung05: 1L Sac-TMT + Pembro vs Pembro in PD-L1+ NSCLC
✅mPFS NR vs 5.7m (HR 0.35)
✅ORR 70.2% vs 42.0%
✅OS HR 0.55 (95%CI 0.36-0.85, immature)
🎙️Dr. Caicun Zhou
🔗 https://t.co/DcbK1dGrhO@OncoAlert @Larvol @ASCO @IASLC https://t.co/512k6dZviW pic.twitter.com/Vdo86N50h9
Right patient. Right treatment. Right timing.
— Yakup Ergün (@dr_yakupergun) May 30, 2026
The result: curves like these👇#ASCO26 https://t.co/72KByLKz90
Living Longer, Living Better: Can We Have It All?
TL;DRASCO26 GU discussant on curative-intent trade-offs: bladder-sparing chemoRT + IO feasibility, and ctDNA over pathology for adjuvant RCC selection.
EV209EV309RAMPART
The RT read is delivery feasibility: layering durvalumab onto 55 Gy/20 fx chemoRT left radiotherapy fully intact (100% completed full dose), so the 39% early durvalumab stops reflect IO tolerability, not RT. Supports adding IO to bladder-preservation chemoRT, but bladder-intact and QoL endpoints remain immature.
- RAMPART (adjuvant RCC): non-clear-cell subgroups have few pts/events and wide CIs; no proven adjuvant IO benefit in non-clear-cell RCC
- Session throughline: organ sparing (bladder) and biomarker-refined de-escalation (ctDNA over pathology) without sacrificing cure
| Component | n (%) |
|---|---|
| Full 55 Gy/20 fx RT delivered | 54 (100%) |
| RT with no extension/delay | 47 (87%) |
| Chemo discontinued early | 12 (22%) |
| Durvalumab completed | 33 (61%) |
| Durvalumab discontinued early | 21 (39%) |
+1 more figure
6 details 3 trials watching
- 🔍 Bladder preservation thread: durvalumab added to mitomycin C / 5-FU chemoRT (55 Gy/20 fx) in MIBC
- 💊 Durvalumab drove the early discontinuations (toxicity / PD); chemoRT delivery itself was not compromised
- 🔍 EVP (enfortumab vedotin + pembrolizumab) bladder-sparing trials in MIBC
Feature EV209 EV309 Population Cystectomy-eligible Ineligible / refusing Stage cT2-4a N0 MIBC cT2-4a N0 MIBC N 240 390 Regimen 9 cycles EV + 1 yr pembro 9 cycles EV + 1 yr pembro Endpoints cCR, 2 yr BIEFS BIEFS, OS
- 📊 Adjuvant pembro (Choueiri, ASCO26): ctDNA stratifies DFS better than pathologic features; ctDNA-positive pts fare far worse in both arms
- ⚠️ Feasibility signal only; bladder preservation, function, symptom burden, safety and QoL all await longer f/u
- 🗞️ Rini ASCO26 GU discussant: can curative-intent GU therapy raise cure rates while preserving organ function and QoL?
- Long-term bladder preservation, function, and QoL after durvalumab chemoRT active Carboplatin, Nab-Paclitaxel, Durvalumab Before Surgery and Adjuvant Therapy in Head and Neck Squamous Cell Carcinoma Phase 2n=39 · primary completion 2022-02 · candidate match
- ctDNA vs pathology for selecting adjuvant IO in RCC n=30 · primary completion 2027-06 · candidate match
- Enfortumab vedotin bladder-sparing efficacy (BIEFS, OS) in MIBC n=30 · primary completion 2025-09 · candidate match
📚 Sources · 🐦 1 tweet
#ASCO26 GU Oncology Spotlight 🚨
— Dra. María Natalia Gandur Quiroga (@nataliagandur) May 30, 2026
🔬 Living Longer, Living Better: Can We Have It All?
Discussant: Brian I. Rini, MD, FASCO@OncoAlert@ASCO
This GU session captured one of the central tensions in curative-intent oncology:
Can we improve cure rates while preserving quality of… pic.twitter.com/AMwrRZZM2Q
Neo-CRAG
ForHigh-risk locally advanced gastric/EGJ (cT3N2-3 to cT4), fit for D2 resection
mDFS 52.7 vs 24.4 mo
HR 0.750 (95% CI 0.607-0.928), P=0.008
TL;DRAdding neoadjuvant chemoRT (45Gy/25fx) to periop XELOX improved mDFS 52.7 vs 24.4mo (HR 0.75) and mOS 67.5 vs 37.6mo in high-risk LAGC.
The RT read is clean attribution: both arms share the XELOX backbone and the CRT arm got dose-reduced chemo during RT, yet locoregional recurrence halved (9.4% vs 18.3%) with more ypN0 and downstaging. On 45Gy/25fx, this revives neoadjuvant chemoRT for high-risk D2-resected gastric/EGJ, on a non-FLOT backbone.
| Endpoint | CRT | CT | HR (95% CI), P |
|---|---|---|---|
| Median DFS | 52.7 mo | 24.4 mo | 0.750 (0.607-0.928), P=0.008 |
| 3-yr DFS | 55.6% | 42.4% | — |
| Median OS | 67.5 mo | 37.6 mo | 0.781 (0.628-0.970), P=0.025 |
| 5-yr OS | 50.1% | 44.2% | — |
7 details 2 trials watching
Phase 3 open-label RCT, 1:1, N=620 (310/arm), 13 Chinese referral centers, enrolled 2013-2022. Primary: disease-free survival; secondary OS, pCR, R0, safety.
High-risk locally advanced gastric/EGJ adenocarcinoma: cT3N2-3M0, cT4aN+M0, or cT4bNanyM0; 36.3% EGJ (Siewert II/III). All planned standardized D2 gastrectomy.
Both arms: 3 cycles preoperative + 3 cycles adjuvant XELOX (oxaliplatin 130, capecitabine 1000 BID D1-14, Q3W) around D2 gastrectomy.
CRT arm only: concurrent 45 Gy/25 fx begun after chemo cycle 1, with dose-reduced XELOX (oxaliplatin 100, capecitabine 825) during RT. RT is the sole added variable between arms.
Primary DFS met and secondary OS positive, both favoring CRT; pathologic downstaging, ypN0, and locoregional control also improved (see figure and table).
Contrasts with CRITICS and TOPGEAR, where adding radiotherapy to a chemo backbone did not improve survival. A positive DFS/OS here reopens neoadjuvant chemoRT in high-risk, D2-resected LAGC.
Open-label; non-FLOT XELOX backbone limits transfer to current perioperative standard. Single-country (China) with high D2-resection quality; DFS (not OS) was the primary endpoint.
Randomised phase 3, primary DFS and OS both hit, but positive chemoRT diverges from negative CRITICS/TOPGEAR; non-FLOT XELOX backbone limits transfer to current SOC.
In high-risk cT3N2-3/cT4 gastric or EGJ adenocarcinoma planned for D2 gastrectomy on a XELOX backbone, these data support a DFS/OS and locoregional-control benefit from adding neoadjuvant chemoRT; the signal does not extend to FLOT-backbone or metastatic patients.
- Incremental benefit of RT on a FLOT chemo backbone n=776 · primary completion 2023-06 · candidate match
- Generalizability beyond high-quality-D2 Asian centers
- Whether EGJ and distal gastric benefit equally n=4 · primary completion 2024-03 · candidate match
📚 Sources · 🐦 1 tweet
Neo-CRAG: Ph3 RCT (n=620, gastric/GEJ) - adding neoadj chemoRT to peri-op XELOX improved OS (68 v 38 mo).
— Dr. Nina Niu Sanford (@NiuSanford) May 30, 2026
Limitation=non-FLOT, BUT still relevant IMO b/c:
1) DFS/OS benefit substantial.
2) Improvements in pCR, downstg, LRR supports plausible RT effect on OS. #ASCO26 @OncoAlert pic.twitter.com/eeM0Z8p20M
SPIN Score (Celiac Plexus SRS) NCT03323489
ForPancreatic cancer, intractable retroperitoneal pain, celiac SRS candidates
TL;DR89% pain response at SPIN 2 vs 32% at SPIN 0 for celiac SRS; post-hoc selection score, n=90.
Response is threshold-gated on baseline pain (>6 → 65.8%, rising to 85.7% at >8), and the strongest predictor was neurotoxic-chemo exposure (multivariate OR 5.1). The RT decision this moves is timing: refer for celiac SRS before neurotoxic agents. SRS dose/fractionation not reported in source (parent Lancet Oncol trial).
9 details
Post-hoc predictor analysis of the pivotal single-arm phase 2 celiac plexus SRS trial (NCT03323489, Lancet Oncol 2024). 90 evaluable pts; univariate/multivariate logistic regression with 500-iteration bootstrap internal validation.
Pancreatic-cancer pts with intractable retroperitoneal (celiac) cancer pain treated on the phase 2 SRS trial. Age and BMI were the prior-reported predictors; median baseline values not in source.
Celiac plexus radiosurgery, target D12-L2. Dose and fractionation not reported in source (specified in the parent Lancet Oncol trial), so transferability of the technique can't be judged here.
Pain response = ≥2-point reduction in average BPI-SF pain from baseline to 3 weeks. Score performance judged by optimism-corrected AUC.
Two independent predictors (severe baseline pain, no prior neurotoxic chemo) build a 0-2 score with a monotonic response gradient (see tables). Discrimination modest, AUC 0.714 corrected.
| SPIN score | Pain response | n |
|---|---|---|
| 0 | 32% | 31 |
| 1 | 53% | 40 |
| 2 | 89% | 19 |
| Predictor | Univariate OR | Multivariate OR |
|---|---|---|
| Neurotoxic chemo exposure | 5.33 (2.13-13.4), p<0.001 | 5.1, p=0.009 |
| Baseline pain intensity | 1.73, p=0.003 | 1.8, p=0.003 |
| Age | 1.06, p=0.014 | dropped (collinearity) |
| Therapy line | 0.65, p=0.04 | dropped (collinearity) |
Celiac plexus SRS is a novel non-invasive palliative option recently added to NCCN guidelines. This analysis converts the parent trial's flat response into an actionable selection score and argues for earlier use, before neurotoxic chemotherapy.
Post-hoc, single-arm data; predictors are associative. Internal bootstrap validation only (optimism-corrected AUC 0.714), external validation required. Subjective 3-week pain endpoint; score not prospectively tested.
Post-hoc predictor modeling of a single-arm phase 2; internal bootstrap validation only, external validation pending. Associations, not a prospectively validated selection tool.
In pancreatic-cancer pts with severe retroperitoneal pain and no prior neurotoxic chemo (SPIN 2), this supports earlier celiac plexus SRS, where 89% (n=19) achieved pain response; it does not extend to SPIN-0 pts, whose response was 32% (n=31).
- External validation of the SPIN score in an independent cohort
- Whether earlier SRS before neurotoxic chemo improves outcomes prospectively
- Durability of pain response beyond 3 weeks
📚 Sources · 🐦 1 tweet
Celiac SRS = convenient, effective tx for intractable pain, but who benefits most?
— Dr. Nina Niu Sanford (@NiuSanford) May 30, 2026
Post-hoc Ph2 analysis identified 2 response predictors (SPIN score): severe baseline pain & no prior neurotoxic chemo.
Supports earlier use before potential chemo neuropathy. #ASCO26 @OncoAlert pic.twitter.com/3qFYU6N1iD
Wait or Treat? NCT05236946
ForAsymptomatic brain mets, EGFR/ALK-mutant metastatic NSCLC, on TKI + chemo
Sub-HR 0.35
95% CI 0.21-0.59, p<0.001; favors upfront RT
TL;DRUpfront cranial RT cut 2y intracranial progression (21.7% vs 50%, sub-HR 0.35) but no OS gain; survival numerically favored delayed (HR 1.45).
The primary endpoint actually favored upfront RT (2y intracranial progression 21.7% vs 50%, sub-HR 0.35), yet OS trended toward delayed (2y 48% vs 60%) with 6% radiation necrosis vs none. Better CNS control bought no survival and added toxicity, so upfront cranial RT can be safely deferred to intracranial progression.
| Endpoint | Upfront RT | Delayed RT |
|---|---|---|
| Events | 20 | 47 |
| 1-yr intracranial PD | 8.7% (2.9-14.5) | 25.7% (16.8-34.7) |
| 2-yr intracranial PD | 21.7% (12.6-30.8) | 50% (39.2-60.9) |
| Sub-HR (95% CI) | 0.35 (0.21-0.59), p<0.001 | ref |
8 details 4 trials watching
Phase 3 open-label RCT, 1:1, N=208 (105 upfront cranial RT vs 103 delayed) at a single center (Tata Memorial). Median follow-up 30.6 mo; stratified by GPA and synchronous vs metachronous BM.
Metastatic EGFR- or ALK-mutant NSCLC with radiologically measurable, completely asymptomatic brain metastases, ECOG 0-2. Both arms received TKI + chemotherapy.
Delayed arm held cranial RT until intracranial progression or patient request, with MRI brain q3mo for year 1 then q6mo. RT dose, fractionation, and technique (SRS vs WBRT) not reported in source.
Primary: intracranial PFS. Secondary: OS, PFS, toxicity, ORR, neurocognition, PROM.
Primary endpoint met for intracranial control but did not translate to survival; the OS trend and radiation-necrosis signal both favored deferral. See the intracranial-progression figure and survival table for effect sizes.
First randomized evidence on RT timing in this population. Consistent with the CNS-active TKI era (osimertinib, alectinib, lorlatinib), where strong systemic intracranial control supports deferring RT.
Open-label and single-institution. Powered for intracranial PFS, not OS, so the survival and necrosis signals favoring deferral are secondary. RT technique not reported.
Randomized phase 3, primary intracranial-PFS endpoint met, but no OS benefit and less necrosis with deferral; backs the emerging TKI-first, defer-RT approach in oncogene-driven NSCLC.
In asymptomatic brain metastases from EGFR/ALK-mutant metastatic NSCLC on TKI plus chemo, this supports deferring cranial RT until intracranial progression; it does not extend to symptomatic brain mets or oncogene-negative NSCLC.
- Neurocognition and PRO outcomes by RT timing (not reported in source)
- Does RT technique (SRS vs WBRT) change the deferral tradeoff? n=115 · primary completion 2026-07 · randomizes SRT vs hippocampal-sparing WBRT
- Durability of TKI-first intracranial control beyond 2 years n=162 · primary completion 2024-12 · osi alone vs early SRS, asymptomatic BMactive Study of Osimertinib + SRS vs Osimertinib Alone for Brain Metastases in EGFR Positive Patients With NSCLC Phase 2n=40 · primary completion 2025-04 · osimertinib-alone arm tests TKI-first controlrecruiting Early or Delayed Intervention of Brain Radiotherapy Combined With Almonertinib in EGFR Mutated NSCLC With Brain Metastases Phase 3n=232 · primary completion 2028-12 · randomizes early vs delayed RT on EGFR-TKI
📚 Sources · 🐦 3 tweets
#ASCO26 | Wait or Treat? Brain RT in EGFR/ALK+ NSCLC
— OncLive.com (@OncLive) May 29, 2026
Presented by Dr Anil Ramakant Tibdewal.
A landmark Phase III randomized trial from @TataMemorial addressed a long-standing question: should asymptomatic brain metastases in oncogene-driven NSCLC receive upfront cranial RT or… pic.twitter.com/lRy9CfyQ8r
Should asymptomatic brain mets await systemic response in front line within EGFR/ALK context? I think yes. Despite reducing icPD, delayed brain RT OS looked better and radiation necrosis didn’t occur vs 6% #ASCO26 pic.twitter.com/O6d7GrvtU4
— Dr Riyaz Shah (@DrRiyazShah) May 29, 2026
No improvement in survival with up front radiation. OS favored delayed radiation with 2y OS 48% with early radiation vs 60% in late (OS HR 1.45). Also, radiation necrosis less common and less severe in delayed arm. Each case unique but delayed approach appealing #ASCO26 pic.twitter.com/wIhjqxhSaq
— Stephen V Liu, MD (@StephenVLiu) May 29, 2026