Palliative
TREASURE NCT04462276
ForES-SCLC, ≥stable disease after chemo-IO induction; unselected
6.7 vs 13.4 mo
HR 1.55 (95% CI 0.90-2.69), P=.34; TRT arm worse, ns
TL;DRmOS 6.7 vs 13.4mo (HR 1.55, ns) adding consolidative TRT to atezo maintenance; halted early for SAEs 61% vs 18%.
The harm, not the null OS, is the RT read: SAEs 61% vs 18%, fatal AEs 19% vs 3%, driven by post-TRT lymphocyte depletion and low baseline DLCO in the fatal cases. 30Gy/10fx consolidative TRT on atezo maintenance is net harmful in unselected ES-SCLC; any future use needs lung-function gating.
6 details 1 trial watching
Phase 2 open-label RCT (AIO-TRK-0320), 1:1, 20 sites in Germany/Austria. Planned 104 pts; halted early by the SMC after 68 randomized (34/arm) for excess fatal SAEs in the TRT arm. Recruited 2020-2022, last follow-up Sept 2024, post-hoc survival update April 2026.
ES-SCLC with at least stable disease after induction carboplatin-etoposide-atezolizumab. Baseline well balanced between arms and between pts with vs without SAEs. Unselected for lung function.
Consolidative TRT 30 Gy in 10 fractions added to atezolizumab maintenance (arm A) vs atezolizumab maintenance alone (arm B).
Primary: overall survival. Secondary included PFS and safety.
Primary OS not met: the TRT arm was numerically worse with no PFS difference and sharply higher serious and fatal toxicity (see table).
| Endpoint | +TRT (arm A) | Atezo alone (arm B) | Effect |
|---|---|---|---|
| mOS | 6.7 mo (5.1-9.0) | 13.4 mo (10.7-17.5) | HR 1.55 (0.90-2.69), P=.34 |
| mPFS | 2.4 mo (1.3-3.9) | 2.6 mo (1.2-3.9) | HR 0.92 (0.54-1.55), P=.85 |
| SAEs | 61.3% | 18.2% | P<.001 |
| Fatal AEs | 19.4% | 3.0% | P=.04 |
SAEs dominated by infection and respiratory disorders, linked to radiation-induced lymphocyte depletion; fatal-AE pts in arm A had lower baseline DLCO. No other risk factors identified.
CREST (pre-immunotherapy) showed a modest OS benefit from thoracic RT after chemo; TREASURE tested that strategy on an IMpower133-style IO-maintenance backbone and found harm, not benefit.
Open-label; small N (68) and early termination leave OS underpowered with a wide CI. Phase 2; efficacy conclusions provisional, though the safety signal is robust.
Randomised harm signal (SAEs 61% vs 18%, fatal 19% vs 3%) argues against adding consolidative TRT to IO maintenance, contesting emerging RT enthusiasm; OS worse but underpowered by early stop.
In unselected ES-SCLC with at least stable disease after chemo-IO induction, this evidence argues against routinely adding consolidative thoracic RT to atezolizumab maintenance; it does not address the good-lung-function subset the authors flag as possibly selectable.
- Which lung-function-selected ES-SCLC pts might tolerate consolidative TRT on IO maintenance not yet Adebrelimab Combined with Chemotherapy and Thoracic Radiotherapy for First-line Treatment of ES-SCLC Phase 3n=524 · primary completion 2029-06 · phase 3 consolidative TRT on adebrelimab IO maintenance
- Whether lower-dose or delayed TRT lessens lymphocyte depletion and infection risk
📚 Sources · 📄 1 paper
Abstract
ARTO NCT03449719
ForOligomet CRPC, ≤3 mets, no prior systemic mCRPC therapy, on abiraterone
TL;DRmOS NR vs 50mo, HR 0.55 (0.33-0.92, p=0.021) adding SBRT to all mets to abi+ADT in oligomet CRPC (unplanned OS analysis).
Ablative dose is the transferable read: BED ≥100 Gy in 1-5 fractions to ALL oligomet sites, and MDT added no excess grade 3-4 toxicity (the only treatment-related death was in the control arm). Extends the oligomet-MDT OS signal from hormone-sensitive disease into CRPC on an abiraterone backbone, informing whether to irradiate all sites when starting an ARSI.
Also covered Jun 12
9 details 4 trials watching
Phase 2, open-label, randomised 1:1, N=157, 16 Italian academic/community centres; stratified by centre, ECOG PS, and number of metastases. Median follow-up 53 mo (IQR 43-60). This OS read is an unplanned long-term analysis.
Prostate adenocarcinoma with metastatic castrate-resistant disease, ≤3 metastatic sites, and no prior systemic therapy for mCRPC. Control n=82, experimental n=75.
Both arms received ADT plus oral abiraterone acetate 1000 mg daily. The experimental arm added SBRT.
SBRT to all sites of metastatic disease, 1-5 fractions, biologically effective dose ≥100 Gy (ablative).
Primary: 6-month biochemical response (PSA drop ≥50%), previously met and reported. This paper reports an unplanned overall survival analysis at long-term follow-up.
OS median NR (95% CI 55-NR) experimental vs 50 mo (36-NR) control, HR 0.55 (0.33-0.92), p=0.021.
G3-4 infectious complications 5 (control) vs 0 (experimental); cardiovascular disorders 3 vs 3. One treatment-related death (myocardial failure) in the control arm. No excess toxicity from MDT.
Prior oligomet-MDT RCTs (STOMP, ORIOLE) enrolled castration-sensitive disease; ARTO extends the metastasis-directed RT signal into the CRPC setting on an ARSI backbone.
Unplanned OS analysis with post-hoc power recalculation; the trial was powered for 6-month biochemical response, not survival. Open-label, small N (157), phase 2.
Unplanned OS analysis (trial powered for 6-mo biochemical response, not survival); phase 2, N=157, open-label. Positive but hypothesis-generating pending a survival-powered phase 3.
In oligometastatic CRPC (≤3 sites, no prior systemic mCRPC therapy) starting abiraterone, this supports adding metastasis-directed SBRT; the signal does not extend to higher-volume mCRPC or the castration-sensitive oligomet setting.
- Does the OS benefit hold in a phase 3 powered for survival? recruiting Metastasis-directed Therapy in Oligoprogressive Castration-refractory Prostate Cancer Phase 3n=246 · primary completion 2029-01 · phase 3 MDT in oligoprogressive CRPC
- Optimal SBRT dose, fractionation, and site coverage in oligomet CRPC recruiting HIghly MetAstatic Life Prolonging Therapy-Resistant Prostate Cancer: Role of Stereotactic Radiotherapy for Bone and Lymph Node Metastases (HIMARS) Phase NAn=18 · primary completion 2028-05 · phase 1 SBRT max-tolerated-volume escalationrecruiting OligoCare TwiCs (Trials Within Cohorts) Trial Comparing Acute Toxicity in Single-fraction vs Multiple-fraction SBRT for Metastasis-directed Treatment (SPRINT) Phase NAn=302 · primary completion 2029-02 · single- vs multi-fraction SBRT for oligomets
- Which oligomet CRPC pts benefit most from MDT n=18 · primary completion 2023-07 · PSMA PET tests predictive value for MDT
📚 Sources · 📄 1 paper
Abstract
NRG/RTOG 1112 NCT01730937
ForLocally advanced HCC, macrovascular invasion (74%), 1L systemic candidates
15.8 vs 12.3 mo
HR 0.77 (90% CI 0.59-1.01), 1-sided P=.06, ns; adjusted HR 0.72, P=.04
TL;DRAdding SBRT to sorafenib: mOS 15.8 vs 12.3mo (HR 0.77, 1-sided P=.06, ns primary); mPFS 9.2 vs 5.5mo, HR 0.55, P<.001.
The RT read is PFS, not the ns OS primary: mPFS 9.2 vs 5.5mo (HR 0.55, P<.001), a locoregional-control signal in a cohort 74% macrovascular-invasion, where liver-directed RT is hardest. Personalized 27.5-50Gy/5fx, no excess G3+ toxicity. Open decision: does SBRT still add over a modern IO backbone (sorafenib obsolete)?
8 details 3 trials watching
Phase 3 open-label RCT, 1:1, 193 randomized (177 eligible), stratified by performance status, liver function, degree of metastases, and macrovascular invasion. Accrual stopped early after first-line systemic SOC shifted.
Locally advanced HCC unsuitable for or refractory to standard locoregional therapy, fit for first-line systemic. 84.7% male, median age 66; macrovascular invasion in 74%.
Personalized SBRT, 27.5 to 50 Gy in 5 fractions, dose adapted to liver function, delivered before sorafenib.
Primary: overall survival. Secondary: progression-free survival, adverse events, quality of life.
Primary OS trend favored SBRT but missed the prespecified 1-sided threshold (P=.06); stratification-adjusted OS and the secondary PFS were both significant. See the endpoint table.
| Endpoint | SBRT+sorafenib | Sorafenib | Effect (HR/P) |
|---|---|---|---|
| mOS | 15.8 mo | 12.3 mo | HR 0.77 (90% CI 0.59-1.01), 1-sided P=.06 |
| mPFS | 9.2 mo | 5.5 mo | HR 0.55 (0.40-0.75), P<.001 |
| G3+ TRAE | 47% (39/83) | 42% (37/88) | P=.52 |
G3+ treatment-related AEs similar (47% vs 42%, P=.52). Treatment-related deaths: 2 with sorafenib (liver failure, death NOS), 1 with SBRT+sorafenib (lung infection). No excess RT-attributable toxicity.
Predates modern first-line combinations (atezolizumab-bevacizumab, durvalumab-tremelimumab); the sorafenib-alone comparator is now obsolete, leaving open whether SBRT adds over an IO backbone.
Open-label; accrual stopped early (underpowered); primary OS not significant unadjusted; comparator superseded; QoL assessed in small subsets (n=17-20).
Randomised phase 3 argues for adding SBRT to systemic in MVI-heavy HCC, but primary OS not significant (1-sided P=.06), stopped early, sorafenib comparator obsolete.
In locally advanced HCC with macrovascular invasion refractory to or unsuitable for standard locoregional therapy, this supports adding SBRT to first-line systemic as contested evidence; it does not establish benefit over a modern IO-based first-line backbone.
- Does SBRT add over modern IO-based first-line systemic therapy? recruiting Testing Immunotherapy With or Without Stereotactic Body Radiation Therapy in Patients With Advanced Liver Cancer, HELIO-RT Trial Phase 3n=226 · primary completion 2029-03 · phase 3 IO+SBRT vs IO alone
- Optimal SBRT dose and fractionation with impaired liver function recruiting A Pilot Study of Liver Protection Using Prednisone for Patients Receiving Stereotactic Body Radiation Therapy for Hepatocellular Carcinoma Phase 2n=20 · primary completion 2026-08 · prednisone liver-protection during SBRTn=18 · primary completion 2026-12 · phase 1 repeated-dose SBRT dose escalation
📚 Sources · 📄 1 paper
Abstract
ORIOLE NCT02680587
ForRecurrent HSPC, 1-3 conventional-imaging mets, off ADT ≥6mo
19% vs 61%
P=.005; SABR vs observation
TL;DR6-mo progression 19% vs 61% favoring SABR (P=.005); mPFS NR vs 5.8mo, HR 0.30 (0.11-0.81) in oligomet HSPC.
Surfaced from a review's discussed trials
The RT read is completeness, not SABR alone: among SABR pts, leaving any PSMA-avid lesion untreated collapsed DMFS to 6.0 vs 29.0 mo (HR 0.19, 0.07-0.54). Conventional imaging under-stages, so PSMA-PET staging plus total consolidation, not partial MDT, is the decision this moves. SABR dose/fractionation not reported in source.
9 details 5 trials watching
Phase 2 randomized trial, 2:1 SABR vs observation, N=54 at 3 US radiation centers. Primary: composite progression at 6 mo. Median follow-up 18.8 mo.
Recurrent hormone-sensitive prostate cancer, 1-3 asymptomatic mets ≤5 cm on conventional imaging, prior definitive treatment of the primary. No ADT within 6 mo. Median age 68.
SABR to all conventional-imaging metastases; PSMA-PET obtained but blinded to planning. Dose/fractionation not reported in source. Local control 98.9% at 6 mo.
Because PET was blinded, 16/36 SABR pts had untreated PET-avid lesions; any untreated lesion collapsed DMFS to 6.0 vs 29.0 mo (HR 0.19). Total consolidation, not SABR per se, drove the benefit.
Concordant with STOMP (phase 2 MDT in oligomet PC): both show metastasis-directed therapy delays progression and defers ADT. The pooled ORIOLE+STOMP analysis reinforced the signal.
Phase 2, N=54; composite surrogate primary read at 6 mo, not OS-powered. Open-label observation control. Conventional-imaging staging misses PET-avid disease.
| Endpoint | SABR | Observation | Effect |
|---|---|---|---|
| 6-mo progression (composite) | 7/36 (19%) | 11/18 (61%) | P=.005 |
| 6-mo PSA progression | 4/36 (11%) | 9/18 (50%) | P=.005 |
| Median PFS | Not reached | 5.8 mo | HR 0.30 (0.11-0.81), P=.002 |
| Median biochemical PFS | Not reached | 6.4 mo | HR 0.31 (0.13-0.75), P=.002 |
| Endpoint | No untreated | Any untreated | Effect |
|---|---|---|---|
| 6-mo progression | 1/19 (5%) | 6/16 (38%) | P=.03 |
| Median PFS | Not reached | 11.8 mo | HR 0.26 (0.09-0.76), P=.006 |
| New mets 180d | 3/19 (15.8%) | 10/16 (62.5%) | P=.006 |
| DMFS | 29.0 mo | 6.0 mo | HR 0.19 (0.07-0.54), P<.001 |
Phase 2, N=54; composite progression primary read at only 6mo. Randomised but small, short f/u. Concordant with STOMP MDT signal; awaits phase 3.
In recurrent HSPC with 1-3 conventional-imaging mets and off ADT ≥6mo, this supports metastasis-directed SABR to defer systemic therapy; it does not extend to higher-volume or castration-resistant disease.
- Overall survival benefit of metastasis-directed SABR recruiting Stereotactic Ablative Radiotherapy (SABR) for the Treatment of Patients With Metastatic Cancer, ID-COMET Trial Phase 3n=800 · primary completion 2032-09 · phase 3 SABR vs 3-mo delay, survival endpoint
- Role of PSMA-PET staging before consolidative SABR n=140 · primary completion 2025-05 · PSMA vs fluciclovine PET for RT planningactive Multicenter Randomized Trial of 68Ga-PSMA-11 PET/CT Based SRT After Radical Prostatectomy Phase 3n=193 · primary completion 2027-07 · randomized 68Ga-PSMA PET-guided RT vs standard
- SABR benefit in higher-volume or ADT-dependent disease active Androgen Deprivation Therapy for Oligo-recurrent Prostate Cancer in Addition to radioTherapy Phase 3n=280 · primary completion 2027-10 · phase 3 MDRT ± ADT vs MDRT alone, MPFSrecruiting HIghly MetAstatic Life Prolonging Therapy-Resistant Prostate Cancer: Role of Stereotactic Radiotherapy for Bone and Lymph Node Metastases (HIMARS) Phase NAn=18 · primary completion 2028-05 · SBRT volume-escalation in high-volume mets
📚 Sources · 📄 1 paper
Abstract
ARTO NCT03449719
ForOligometastatic CRPC, ≤3 nonvisceral mets, first-line abiraterone
92% vs 68.3%
OR 5.34 (95% CI 2.05-13.88), P=.001
TL;DRAdding SBRT to abiraterone lifted 6-mo PSA response to 92% vs 68.3% (OR 5.34) and cut progression (PFS HR 0.35) in oligomet CRPC.
Surfaced from a review's discussed trials
The RT read is total metastatic consolidation: SBRT to all ≤3 CRPC sites concurrent with abiraterone more than doubled complete PSA response (56% vs 23.2%) and cut progression risk (HR 0.35). It pushes MDT beyond hormone-sensitive oligomet (ORIOLE/STOMP) into first-line CRPC, moving the decision to irradiate every lesion, not defer.
Also covered Jul 7
6 details 5 trials watching
Multicenter randomized phase II, 1:1, N=157, enrolled Jan 2019-Sep 2022. Primary: 6-month biochemical response.
Oligometastatic castration-resistant prostate cancer with ≤3 nonvisceral metastatic lesions, in the first-line abiraterone setting.
Both arms received abiraterone acetate + prednisone (AAP). The experimental arm added concomitant SBRT.
SBRT to all sites of disease, concomitant with AAP. Dose/fractionation not reported in source.
Primary: biochemical response (PSA drop ≥50% at 6mo). Secondary: complete BR (PSA <0.2 ng/mL), PFS.
Primary endpoint and PFS both met, favoring the SBRT arm (see results table).
| Endpoint (6mo) | AAP+SBRT | AAP alone | Effect size |
|---|---|---|---|
| Biochemical response (PSA ≥50% drop) | 92% | 68.3% | OR 5.34 (2.05-13.88), P=.001 |
| Complete BR (PSA <0.2 ng/mL) | 56% | 23.2% | OR 4.22 (2.12-8.38), P<.001 |
Extends the metastasis-directed SBRT benefit seen in ORIOLE/STOMP (hormone-sensitive oligomet) into first-line CRPC.
Phase II, N=157. Primary endpoint is a PSA surrogate with no OS reported; dose/fractionation and long-term durability not in source.
Randomized phase II, primary hit, named comparator (AAP alone); primary is a PSA surrogate, so supportive of the emerging oligomet MDT paradigm rather than practice-setting.
In oligometastatic CRPC (≤3 nonvisceral mets) starting first-line abiraterone, this supports adding SBRT to all sites for deeper PSA response and longer PFS; it does not extend to visceral or polymetastatic disease.
- OS benefit of adding SBRT in oligomet CRPC recruiting Metastasis-directed Therapy in Oligoprogressive Castration-refractory Prostate Cancer Phase 3n=246 · primary completion 2029-01 · phase 3 MDT vs SOC in oligoprogressive CRPCrecruiting Treatment With Darolutamide +/- Radiation Therapy for Patients With a Castration Resistant Cancer and Metastases Detected by Functional Imaging Phase 3n=336 · primary completion 2029-10 · phase 3 darolutamide ± SBRT in metastatic CRPC
- Optimal SBRT dose/fractionation for CRPC metastases recruiting OligoCare TwiCs (Trials Within Cohorts) Trial Comparing Acute Toxicity in Single-fraction vs Multiple-fraction SBRT for Metastasis-directed Treatment (SPRINT) Phase NAn=302 · primary completion 2029-02 · single- vs multi-fraction SBRT for oligomets
- Does MDT delay next systemic therapy in CRPC? n=102 · primary completion 2027-04 · SBRT to postpone 2nd-line systemic tx in CRPCn=66 · primary completion 2030-11 · SBRT + darolutamide to defer 2nd-line in M0CRPC
📚 Sources · 📄 1 paper
Abstract
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
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
RASolute 302
ForPreviously treated metastatic pancreatic cancer (RAS-mut or WT)
HR 0.40
95% CI 0.30-0.53, P<0.001; mOS 13.2 vs 6.7 mo (overall pop)
TL;DRmOS 13.2 vs 6.7mo, HR 0.40 (0.30-0.53), P<0.001 for daraxonrasib vs investigator's-choice chemo in previously treated metastatic pancreatic cancer.
In previously treated metastatic pancreatic cancer with a RAS mutation, daraxonrasib's OS benefit supports it as a systemic option over chemotherapy; the signal does not extend to treatment-naive or localized disease.
| Population · Arm | Median OS | HR (death) | 12-mo OS |
|---|---|---|---|
| G12 · Daraxonrasib | 13.2 mo (10.0-NR) | 0.40 (0.30-0.54) | 53.3% |
| G12 · Chemo | 6.6 mo (5.4-8.2) | — | 8.7% |
| Overall · Daraxonrasib | 13.2 mo (10.0-NR) | 0.40 (0.30-0.53) | 53.2% |
| Overall · Chemo | 6.7 mo (5.8-8.0) | — | 17.3% |
7 details 1 trial watching
Phase 3 RCT, daraxonrasib vs investigator's-choice chemotherapy in previously treated metastatic pancreatic cancer. Two prespecified populations: RAS G12-mutant and overall (G12/G13/Q61 or no RAS mutation identified).
Previously treated metastatic pancreatic cancer. RAS G12 arm n=228 vs 231; overall n=248 vs 252. Overall population also includes tumors with no identified RAS mutation.
Daraxonrasib, an oral RAS(ON) multi-selective inhibitor targeting active GTP-bound RAS, vs investigator's choice cytotoxic chemotherapy.
Primary OS met: median 13.2 vs 6.7 mo, HR 0.40 (0.30-0.53), P<0.001 (overall); HR 0.40 (0.30-0.54) in RAS G12. 12-mo OS 53% vs 17% (overall). Deaths 32% vs 55-56%.
Chemo control (6.6-6.7 mo) matches the historic 2L metastatic PDAC benchmark; no prior targeted agent has shown an OS signal of this magnitude in this setting.
Data limited to a single ASCO LBA OS figure; full safety and PFS not yet reported. Open-label; daraxonrasib median OS upper CI not reached (10.0-NR), so tail durability is immature.
Randomized phase 3, OS primary hit HR 0.40 in 2L metastatic PDAC where no targeted SOC exists; hard endpoint, unprecedented magnitude. Full LBA data pending.
- Sequencing and combination with 1L chemotherapy recruiting Study of Daraxonrasib and Daraxonrasib + GnP as First-line Treatment in Patients With Metastatic Pancreatic Adenocarcinoma Phase 3n=900 · primary completion 2028-06 · 1L daraxonrasib + gem/nab-paclitaxel combination
- Efficacy across RAS-WT vs RAS-mutant subsets
- Full safety and toxicity profile
📚 Sources · 🐦 1 tweet
#ASCO26
— Nicholas Hornstein (@GIMedOnc) May 31, 2026
This one is special.
This is the hottest paper of 2026 and potentially in the history of pancreatic cancer.
Let’s dive in.
RASolute 302: Daraxonrasib vs investigator’s choice chemotherapy in previously treated metastatic pancreatic cancer
Abstract LBA5 (soon!)… pic.twitter.com/Lq7PEjOWAo
OCEANUS
ForAdvanced/refractory NSCLC on immunoradiotherapy, median age 64, 74% male
TL;DRSequential iRT beat concurrent for real-world OS in newly-dx advanced NSCLC: median 20.3 vs 16.0 mo, HR 0.68 (0.47-0.99), P=.045.
Sequential iRT (ICI and RT not overlapping) beat concurrent for real-world OS in newly-dx advanced NSCLC, HR 0.68 (0.47-0.99), P=.045, favoring temporal separation of RT from ICI. RT dose, fractionation, and target volume aren't in the source, so the signal can't yet transfer to a specific plan. The refractory RT+ICI-maintenance read was NS (P=.20).
7 details 1 trial watching
Territory-wide real-world cohort (OCEANUS, Hong Kong CDARS, >90% population coverage); NSCLC diagnosed 2010-2021 who received iRT. Overlap-weighting propensity score primary, IPTW sensitivity; landmark-based OS with weighted Kaplan-Meier and Cox (restricted mean survival time where PH violated).
335 of 3522 ICI-treated pts received RT: 155 newly-dx advanced, 180 refractory. Median age 64 (34-90), 73.7% male. Refractory analysis required survival ≥90 days (landmark).
RT dose, fractionation, modality, and target volume not reported in source. The variable studied is timing of RT relative to ICI (sequential vs concurrent), not technique.
Both comparisons favored the sequential / ICI-maintenance arm (magnitudes in table). Chemotherapy was associated with longer OS in newly-dx pts only; not significant in refractory disease.
| Setting / comparison | Experimental OS | Control OS | HR / P value |
|---|---|---|---|
| Newly-dx advanced, sequential vs concurrent iRT | 20.3 mo (95% CI 13.3-NR) | 16.0 mo (95% CI 8.3-30.0) | HR 0.68 (0.47-0.99), P=.045 |
| Refractory, RT + ICI maintenance vs RT alone | 11.2 mo (95% CI 7.9-20.6) | 6.7 mo (95% CI 4.4-17.4) | P=.20 (ns) |
Randomized data on iRT sequencing in advanced NSCLC are limited (stated by authors). RT-before-ICI direction is consistent with the PACIFIC consolidation paradigm, but PACIFIC treated curative-intent unresectable stage III with concurrent chemoRT, a different population.
Observational: sequential vs concurrent not randomized, residual confounding by indication despite weighting. Small subgroups (155 newly-dx). Refractory comparison non-significant (P=.20).
Observational real-world cohort; sequential-vs-concurrent not randomized, confounding by indication despite propensity weighting. Small subgroups (155 newly-dx). Authors label it hypothesis-generating.
In newly-diagnosed advanced NSCLC starting immunoradiotherapy, this real-world signal supports separating RT from ICI in time rather than delivering them concurrently; it does not extend to refractory disease, where the RT-plus-ICI-maintenance benefit was not significant.
- Optimal RT-ICI sequencing (sequential vs concurrent) in advanced NSCLC active PD-1 Inhibitor and Chemotherapy With Concurrent Irradiation at Varied Tumour Sites in Advanced Non-small Cell Lung Cancer Phase 3n=327 · primary completion 2026-12 · phase 3 concurrent RT+PD-1 in stage IIIB/IV NSCLC
- Value of ICI maintenance after RT in refractory NSCLC
📚 Sources · 📄 1 paper
Abstract
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
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 |
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| 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
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
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
EXTEND Trial
ForOligometastatic solid tumors, 1-5 mets, on standard systemic therapy
HR 0.54
95% CI 0.41-0.72, p<0.001 (per-protocol, all baskets)
TL;DRMDT+SOC improved PFS across all baskets, HR 0.54 (0.41-0.72), p<0.001; RT delivered 98% of MDT.
The RT-relevant read is that this is essentially an SBRT trial (98% of MDT was radiotherapy) layered on top of continued systemic therapy, so the PFS gain is attributable to local ablation, not a systemic switch. The prostate-excluded HR 0.60 (0.40-0.89) is what matters for referrals outside prostate. Dose and fractionation are not in the source abstract, which gates transfer to practice.
Also covered May 17
9 details 5 trials watching
Multicenter randomized phase II basket trial, accrual 2018 to 2023. Six baskets (breast, pancreas, kidney, two prostate, "Other") each with basket-specific stratification and powering. Median follow-up 53 months.
Patients with 1-5 metastases from solid tumors, randomized to MDT+SOC vs SOC systemic therapy alone. Screened 521, randomized 350, 334 analyzed per protocol (MDT+SOC n=166; SOC n=168).
Radiotherapy was the MDT for 98% of metastases (370/379), so this reads as an ablative RT trial in all but name. Dose, fractionation, and technique are not reported in the source abstract.
Primary: PFS, pre-specified in the per-protocol set within each basket, across all baskets, and across all baskets excluding prostate. Exploratory: ctDNA and immune profiling.
Overall PFS HR 0.54 (0.41-0.72), p<0.001; excluding prostate baskets HR 0.60 (0.40-0.89). Basket-level superiority in pancreas, prostate, and "Other"; breast and kidney inconclusive. Per-basket effect sizes not reported in source.
Detectable ctDNA at enrollment tracked with shorter PFS and survival; 3-month ctDNA clearance tracked with improved survival, raising the option of a ctDNA-refined oligometastatic definition. Systemic immune activation after MDT was most pronounced in the baskets that showed PFS superiority, offered as a candidate mechanism.
Per-protocol, not ITT, primary analysis with 16 of 350 randomized patients excluded. Phase II with six baskets tested, so histology-specific claims are hypothesis-generating; no OS result reported in source.
Randomized phase II, primary PFS endpoint hit with 53mo f/u, but per-protocol analysis and basket design; histology signals explicitly framed as hypothesis-generating for phase III.
In pts with 1-5 metastases from pancreas or prostate primaries already on standard systemic therapy, this supports adding ablative MDT rather than systemic therapy alone; the breast and kidney baskets were inconclusive and do not carry the same read.
- Does MDT-driven PFS gain translate to overall survival recruiting Veterans Affairs Seamless Phase II/III Randomized Trial of STAndard Systemic theRapy With or Without PET-directed Local Therapy for Oligometastatic pRosTate Cancer Phase 2/3n=464 · primary completion 2026-09 · phase 2/3 SST +/- PET-directed local therapy, CRPC-FSn=873 · primary completion 2027-04 · phase 3 MDT +/- ADT/ARTA, n=873, PMFS endpointn=1200 · primary completion 2030-12 · n=1200 prospective LAT cohort, any-histology OMD
- Can ctDNA refine which oligometastatic pts benefit from MDT n=60 · primary completion 2027-12 · SABR cohort with ctDNA dynamics as biomarkerrecruiting Phase II Non-Randomized Study Evaluating POSLUMA-PSMA PET Response After Oligo- Metastatic/Progressive-directed Treatment With Radiotherapy (PROMPT-R) Phase 2n=50 · primary completion 2028-05 · ctDNA change after ablative RT vs PSMA-PET response
- Why were breast and kidney baskets inconclusive
📚 Sources · 📄 1 paper
Abstract
OLIGOMA NCT04495309
ForOligometastatic breast, ≤5 lesions, any line, mostly ER+/HER2- first line
35.8 vs 20.4 mo, HR 0.48
95% CI 0.25-0.91, p=0.021
TL;DRmPFS 35.8 vs 20.4mo, HR 0.48 (0.25-0.91), p=0.021 for MDT to all lesions in oligometastatic breast, QoL non-inferior.
The RT read is who was actually irradiated: 2/3 of lesions were bone and >80% of pts had 1-3 mets, so this is largely bone-directed ablative RT in first-line ER+ disease, not a visceral-oligomet population. Dose and fractionation are not reported in source, which gates transfer to practice. QoL non-inferiority at 12wk (-2.1, margin -10) removes the main argument against adding local therapy to a working systemic backbone.
+3 more figures
| Arm | QLQ-C30 mean at 12wk (95% CI) | Between-group change (ANCOVA) |
|---|---|---|
| Experimental | 72.2 (67.2-77.2) | -2.1 (-9.2-5.1) |
| Control | 74.3 (69.3-79.3) | n/a |
9 details 5 trials watching
Randomised trial (ARO-2021-09, NCT04495309) of systemic therapy alone vs systemic therapy plus local ablative radiotherapy to all metastatic lesions. Randomisation stratified by type of systemic therapy and treatment line. N=87 (43 experimental, 44 control).
Metastatic breast cancer, any treatment line, maximum 5 metastatic lesions, with the systemic regimen determined by multidisciplinary tumour board. Pts requiring palliative RT to all metastases were not eligible, though palliative RT to symptomatic sites was allowed. Median age 58 / 59; ECOG 0 in 76.7% of the experimental arm.
The intervention is local ablative radiotherapy to all metastatic lesions on top of the systemic backbone. Dose, fractionation, modality, and target-volume definition are not reported in the source slides, and 2/3 of treated lesions were bone metastases.
Co-primary: progression-free survival and quality of life (EORTC QLQ-C30) at 12 weeks post-randomisation. Secondary: overall survival, toxicity, compliance, QLQ-C30 and QLQ-BR23, and patient satisfaction with cancer care (EORTC PATSAT C33).
Both co-primaries read out in favour of adding MDT: PFS separated at HR 0.48 and the QoL summary score met non-inferiority against a -10 point margin. See the figure captions for the arm-level values.
Recruitment stopped early at <20% of the initial and <40% of the amended target, leaving N=87 and a wide HR CI (0.25-0.91). Open-label design with a patient-reported co-primary. No OS data reported in source, and the toxicity secondary endpoint is likewise absent from the presented slides.
The presenter frames this as the first RCT showing a PFS benefit from MDT in oligometastatic breast cancer, extending the STOMP / SABR-COMET line of evidence into a histology where systemic control is comparatively good. Eight further randomised trials are accruing, so the magnitude here should be read as provisional.
Randomised but stopped early at <20% of initial accrual target; N=87 with wide HR CI (0.25-0.91). Underpowered for a durable PFS estimate.
In ER+/HER2- breast cancer with 1-3 mostly bony metastases on first-line systemic therapy, this supports discussing ablative RT to all lesions as a PFS-directed addition; it does not extend to >5 lesions, heavily visceral disease, or pts needing palliative RT to every site.
- Does the PFS benefit translate to overall survival n=340 · primary completion 2026-11 · JCOG phase 3 MDT vs systemic alone, 340 pts
- Which oligometastatic breast subgroups benefit most active Standard Treatment +/- SBRT in Solid Tumors Patients With Between 1 and 5 Bone-only Metastases Phase NAn=168 · primary completion 2025-07 · SBRT vs none in 1-5 bone-only mets, breast inclrecruiting BreCLIM-2 - A RCT Investigating Local Treatment for Breast Cancer Liver Metastases Phase 3n=200 · primary completion 2029-12 · RCT of local tx in 1-4 breast liver metsnot yet Adding Surgery and Radiation to the Usual Treatment for HER2-Positive Breast Cancer That Had Already Spread at Diagnosis Phase 3n=562 · primary completion 2032-05 · HER2+ de novo stage IV, 1-5 mets, SBRT added
- Optimal RT dose and fractionation for bone-dominant oligomet breast recruiting OligoCare TwiCs (Trials Within Cohorts) Trial Comparing Acute Toxicity in Single-fraction vs Multiple-fraction SBRT for Metastasis-directed Treatment (SPRINT) Phase NAn=302 · primary completion 2029-02 · single-fraction vs multifraction SBRT, breast incl
📚 Sources · 🐦 3 tweets
📌 Metastases-directed treatment in Patients with Oligometastatic Breast Cancer: Results from the OLIGOMA-trial (ARO-2021-09, NCT04495309) @DavidKrugMD 👏🏻 #ESTRO26 @ESTRO_RT @OncoAlert #OncoAlertAF pic.twitter.com/YDMef0fXRm
— Elisabetta Bonzano MD, PhD (@to_be_elizabeth) May 17, 2026
❗️ The OLIGOMA trial results just dropped at #ESTRO26 and they are massive. A 15-month improvement in median PFS for OMD breast cancer (HR = 0.48). This adds to the growing mountain of evidence that MDT (Metastasis-Directed Therapy) works. Lets’s go 🧵 1/n pic.twitter.com/5uiEVSYtdH
— NonsparseOncologist (@5_utr) May 17, 2026
Here are some details!
— Jeff Ryckman (@jryckman3) May 17, 2026
On OLIGOMA, nearly 3/4 were first line endocrine or chemotherapy. #ESTRO26 #OncTwitter@CJTsaiMDPhD pic.twitter.com/r3kJzNNsyK