Palliative
ES-SCLC Concurrent TRT + Chemoimmunotherapy (LBA8005)
ForES-SCLC, treatment-naΓ―ve, ECOG 0-1, measurable thoracic lesion
TL;DRmOS 10.0 vs 11.8mo, HR 1.14, p=0.40: concurrent TRT adds no OS benefit to chemoIO in ES-SCLC.
- vs CREST (Lancet 2015): TRT 30 Gy/10 fr post-induction improved 1yr OS in pre-IO ES-SCLC; not replicated here in IO era
| Arm | Median OS | 95% CI | HR (95% CI) | p |
|---|---|---|---|---|
| ChemoIO + TRT | 10.0 mo | 8.3-11.7 | 1.14 (0.84-1.56) | 0.40 |
| ChemoIO | 11.8 mo | 10.0-13.6 | ref | n/a |
+3 more figures
| Arm | Median PFS | 95% CI | HR (95% CI) | p |
|---|---|---|---|---|
| ChemoIO + TRT | 5.1 mo | 4.7-5.4 | 1.10 (0.84-1.45) | 0.49 |
| ChemoIO | 5.0 mo | 4.6-5.4 | ref | n/a |
| Subgroup | ChemoIO+TRT median OS | ChemoIO median OS | HR (95% CI) | p |
|---|---|---|---|---|
| Completed all 4 cycles | 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 |
6 details
- π Phase III RCT, N=228 (115 vs 113); TRT 30 Gy/10 fr concurrent from day 21-28 of cycle 1
- π Eligibility: stage IV SCLC or stage III ineligible for curative CRT, ECOG 0-1, measurable thoracic lesion required
- π PCI 25-30 Gy optional for responders per local routine; durvalumab 1500 mg Q4W maintenance until PD
CONSORT flow
- β οΈ Control arm mOS (11.8mo) consistent with CASPIAN durvalumab arm (~12.9mo); TRT arm numerically inferior at 10.0mo
- β οΈ Pre-specified OS subgroups (completed all 4 cycles, no brain/liver mets) both null, consistent with ITT
- β οΈ PCI optional per local routine; differential PCI use between arms unreported, potential survival confound
- Whether consolidative rather than concurrent TRT sequencing improves outcomes
- Role of PCI in IO-era ES-SCLC given uncontrolled differential use in this trial
- Optimal ES-SCLC subpopulation (if any) for TRT in the IO era
π Sources Β· π¦ 1 tweet
π¨ #ASCO26 | #οΈβ£LBA8005β°β’οΈ Concurrent thoracic radiotherapy + chemoimmunotherapy in ES-SCLC
— Masahiro TORASAWA, MD. PhD. (@M_Torasawa) June 2, 2026
π₯ ES-SCLCβ°Durvalumab + platinum/etoposideβ°Β± concurrent thoracic radiotherapyβ°TRT: 30 Gy / 10 fractions, starting day 21β28
π Randomized phase IIIβ°ChemoIO + TRT: n=115β°ChemoIOβ¦ pic.twitter.com/TDA5amz59e
DeLLphi-304 (tarlatamab CNS outcomes)
For2L ES-SCLC; brain mets subgroup β₯1 BM at baseline, >70% prior CNS treatment
TL;DRCNS PFS HR 0.54 (ITT), HR 0.40 in brain mets; CNS CR 14.9% vs 5.4% with tarlatamab vs chemo 2L SCLC.
- DeLLphi-304 primary results: tarlatamab OS + PFS benefit in 2L SCLC; CNS data extends intracranial signal
| Arm | n | Median CNS PFS (mo) | HR (95% CI) |
|---|---|---|---|
| Tarlatamab | 67 | 6.5 (4.3-13.7) | 0.40 (0.24-0.66) |
| Chemotherapy | 56 | 4.2 (2.9-5.5) | ref |
+2 more figures
| Arm | n | Median CNS PFS (mo) | HR (95% CI) |
|---|---|---|---|
| Tarlatamab | 254 | NE (13.7, NE) | 0.54 (0.39-0.75) |
| Chemotherapy | 255 | 7.2 (5.6, NE) | ref |
| Endpoint | Tarlatamab (n=67) | Chemo (n=56) |
|---|---|---|
| CNS CR | 10 (14.9%) | 3 (5.4%) |
| Non-CR/Non-PD | 42 (62.7%) | 37 (66.1%) |
| CNS DCR | 52 (77.6%) | 40 (71.4%) |
| Median duration CNS CR (mo) | NE | 3.6 |
| Median duration CNS DC (mo) | 8.2 | 5.2 |
5 details
- π Post-hoc subgroup analysis of DeLLphi-304 phase 3 RCT; ITT n=509 (254 tarlatamab / 255 chemo)
- π Brain mets subgroup: n=67 (tarlatamab) vs n=56 (chemo); >70% had prior CNS treatment
- π Data cutoff Jan 29 2025; median f/u 11.4 mo (tarlatamab), 11.5 mo (chemo)
- π Ongoing CNS complete response at cutoff: 5 (50%) tarlatamab vs 0 chemo
- β οΈ CNS outcomes not prespecified; interpretability limited without a confirmatory prospective CNS endpoint
- Does tarlatamab CNS activity change the role of PCI in ES-SCLC?
- Confirmatory prospective CNS endpoint needed from DeLLphi-304 or successor trial
- Durability of CNS CR beyond 11mo median f/u
π Sources Β· π¦ 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
ForPrev-treated metastatic PDAC, RAS G12 mutation, β₯1 prior systemic line
TL;DRDaraxonrasib vs IC chemo in 2L RAS G12 mPDAC: mOS 13.2 vs 6.6 mo, HR 0.40 (0.30-0.54), p<0.001.
- 2L PDAC historical: IC chemo (FOLFOX, nalirinotecan-based regimens) mOS ~5-7 mo; daraxonrasib more than doubles median in RAS G12-selected pts
| Daraxonrasib | Chemotherapy | |
|---|---|---|
| RAS G12: N | 228 | 231 |
| RAS G12: mOS (95% CI) | 13.2 mo (10.0-NR) | 6.6 mo (5.4-8.2) |
| RAS G12: HR (95% CI), p | 0.40 (0.30-0.54), p<0.001 | ref |
| RAS G12: 12-mo OS | 53.3% | 8.7% |
| Overall: N | 248 | 252 |
| Overall: mOS (95% CI) | 13.2 mo (10.0-NR) | 6.7 mo (5.8-8.0) |
| Overall: HR (95% CI), p | 0.40 (0.30-0.53), p<0.001 | ref |
| Overall: 12-mo OS | 53.2% | 17.3% |
6 details
- π Phase 3 RCT; RAS G12 primary analysis N=459 (228 vs 231); overall N=500 (248 vs 252); control: investigator's choice chemotherapy
CONSORT flow
- π 1Β° EP (RAS G12 population): mOS 13.2 mo (95% CI 10.0-NR) vs 6.6 mo (5.4-8.2); HR 0.40 (0.30-0.54), p<0.001
- π 12-mo OS (RAS G12): 53.3% daraxonrasib vs 8.7% chemo
- π Consistent in overall population (all RAS mutations + no-mutation pts, N=500): HR 0.40 (0.30-0.53), p<0.001; mOS 13.2 vs 6.7 mo
- β οΈ Event maturity asymmetric at datacut: 32% events in daraxonrasib arm vs 55% chemo; upper OS CI not reached (NR); follow-up ongoing
- β οΈ G12 variant breakdown (G12D vs G12V vs G12R) not reported in source
- Activity by specific G12 variant (G12D vs G12V vs G12R)
- Durability beyond current f/u; upper OS CI not yet reached
- Optimal sequencing and potential 1L investigation
π Sources Β· π¦ 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.
Letβs dive in.
RASolute 302: Daraxonrasib vs investigatorβs choice chemotherapy in previously treated metastatic pancreatic cancer
Abstract LBA5 (soon!)β¦ pic.twitter.com/Lq7PEjOWAo
A-DREAM (ALLIANCE mAPMS)
FormHSPC achieving PSA<0.2 after β₯18-24mo ADT+ARPI, low-volume predominant
TL;DRADT+ARPI interruption in mHSPC: 41% treatment-free with eugonadal T at 18mo (1Β° EP); 38.5% still off-tx at 26.9mo FU.
- Intermittent ADT established in earlier hormone-sensitive trials; A-DREAM is first prospective signal for ADT+ARPI interruption in mHSPC
+2 more figures
9 details
- π Single-arm phase II, N=78 enrolled 07/2022-03/2024; PSA<0.2 after β₯18-24mo ADT + β₯12mo ARPI
- π Re-initiation triggers: PSA β₯5 ng/mL, radiographic change (PCWG3), or PrCa-related sx
- π Primary EP: 80% CI 33.1-48.9%, one-sided p=0.0249; pre-specified 80% CI threshold (not 95%)
- π Median time to eugonadal T recovery: 9.0mo (95% CI 8.4-12.4)
- π Disposition at 26.9mo: 38.5% still off-tx; 37.2% resumed ADT+ARPI per protocol; 9.0% started non-protocol tx
- π rPFS from interruption: 15/78 events, median NE (32.5-NE); 12-mo est 94.6% (89.6-99.9%)
- π OS: 4/78 events, median NE; causes: prostate cancer, MDS, influenza, MI
- β οΈ Single-arm; no randomized comparator vs continuous ADT+ARPI
- β οΈ 64.9% low-volume CHAARTED, 84.6% White; high-volume and diverse pts underrepresented
- Impact on long-term OS vs continuous ADT+ARPI: randomized trial needed
- Optimal re-initiation criteria in high-volume vs low-volume disease
- Biomarker predictors of durable treatment-free interval
π Sources Β· π¦ 1 tweet
Can treatment be safely stopped in selected patients with mHSPC?
— MJosΓ© 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
ENZAMET + Decipher Biomarker Analysis
FormHSPC, ADT + enzalutamide backbone, tumor tissue available for Decipher testing
TL;DRDecipher >0.85 identifies mHSPC pts with OS benefit from docetaxel intensification; IPTW interaction p=0.04, HR 0.75 (0.43-1.33).
- Framed as Level 1B evidence; consistent with CHARTED and STAMPEDE docetaxel predictive patterns
| Analysis | Decipher | Docetaxel HR (95% CI) | p | Interaction p |
|---|---|---|---|---|
| Unweighted | β€0.85 | 2.78 (1.49, 5.21) | 0.001 | 0.02 |
| Unweighted | >0.85 | 1.13 (0.71, 1.79) | 0.60 | β |
| IPTW | β€0.85 | 1.94 (0.95, 3.96) | 0.07 | 0.04 |
| IPTW | >0.85 | 0.75 (0.43, 1.33) | 0.33 | β |
+1 more figure
| Decipher | OS HR triplet vs doublet (95% CI) | p |
|---|---|---|
| β€0.85 | 3.02 (1.50-5.76) | β |
| >0.85 | 1.08 (0.60-1.71) | 0.73 |
4 details
- π Biomarker analysis within ENZAMET phase 3 RCT; ADT+enza+doce cohort N=320 with evaluable Decipher; DPMC 0.85 cutoff per statistical analysis plan
- β οΈ Individual arm HRs non-significant in IPTW-MVA (Decipher >0.85: HR 0.75, p=0.33; Decipher β€0.85: HR 1.94, p=0.07); signal rests on interaction term only
- β οΈ Tissue available in only ~427/3816 ENZAMET pts; representativeness of the analyzed subset uncertain
- β οΈ ENZAMET predated current ARSI-doublet SOC; Decipher model trained pre-ARPI β applicability to modern ADT+ARSI backbone unvalidated
- Prospective Decipher-guided triplet selection trial in ARPI-era mHSPC needed
- Optimal DPMC cutoff in pts receiving ADT+ARSI (not ENZA) doublets
π Sources Β· π¦ 2 tweets
#ASCO26 GU Oncology Spotlight π¨
— Dra. MarΓa Natalia Gandur Quiroga (@nataliagandur) May 30, 2026
π¬ ENZAMET + Decipher | Part 2
Can genomics guide docetaxel intensification in mHSPC?
Outstanding presentation by @ChrisSweeney1.@OncoAlert@ASCO
After Part 1, the key question was:
β‘οΈ Can a genomic classifier identify which patients withβ¦ pic.twitter.com/nJYMxuXelV
#ASCO26 GU Oncology Spotlight π¨
— Dra. MarΓa Natalia Gandur Quiroga (@nataliagandur) May 30, 2026
π¬ 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
TALAPRO-3
ForHRR-deficient metastatic hormone-sensitive prostate cancer
TL;DR3yr rPFS 77% vs 56% (HR 0.48, p<0.001) favoring talazoparib+enza+ADT in HRR-deficient mHSPC.
- vs TALAPRO-2 (talazoparib+enza, mCRPC, HRR+, HR ~0.46): class effect now established in hormone-sensitive setting
| Subgroup | n (exp/ctrl) | Median rPFS exp | Median rPFS ctrl | HR (95% CI) |
|---|---|---|---|---|
| ITT | 300/299 | NC (NC-NC) | 45.8 (37.7-NC) mo | 0.48 (0.36-0.65), p<0.001 |
| BRCA | 104/103 | NC (NC-NC) | 35.1 (18.6-NC) mo | 0.37 (0.22-0.61) |
| Non-BRCA | 196/196 | NC (NC-NC) | NC (40.5-NC) mo | 0.57 (0.39-0.82) |
3 details
- π Phase 3 RCT; N=599; HRR-deficient mHSPC; talazoparib+enza+ADT vs placebo+enza+ADT
CONSORT flow
- β οΈ Primary endpoint imaging-based rPFS, not OS; OS maturity not reported in source
- β οΈ Non-BRCA HRR effect attenuated (HR 0.57 vs BRCA HR 0.37); non-BRCA HRR subset heterogeneous
- OS benefit magnitude and maturity
- Which non-BRCA HRR alterations drive clinically meaningful rPFS benefit
- Post-progression sequencing in PARP-pretreated pts transitioning to mCRPC
π Sources Β· π¦ 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
CHRYSALIS-2 (1L Ami+Laz, Atypical EGFR+)
ForAdvanced NSCLC, atypical EGFR mutation, treatment-naive
TL;DRMedian OS 41.0 mo (95% CI 27.7-NE) with ami+laz in 1L atypical EGFR+ advanced NSCLC; single-arm, n=49.
- Yang JCH NEJM 2025 (ami+laz 1L common EGFR): durable OS now reported in both common and atypical EGFR-mutated NSCLC populations
+1 more figure
7 details
- π Single-arm, n=49; 1L atypical EGFR-mutated advanced NSCLC
- π Median treatment duration 13.3 mo (range <0.1-53.2)
- π 39% remained on treatment >2 years
- π Median OS 41.0 mo (95% CI 27.7-NE); median follow-up 31.3 mo
- β οΈ Single-arm; no randomized comparator vs osimertinib or chemotherapy
- β οΈ Small N (49) limits any subgroup analysis by EGFR variant subtype
- β οΈ No clear EGFR variant subtype-outcome association found; underpowered to confirm or exclude
- Randomized trial vs osimertinib in atypical EGFR needed to confirm benefit
- CNS penetration and activity across atypical EGFR variant subtypes
- SC amivantamab formulation (COPERNICUS) applicability in this population
π Sources Β· π¦ 1 tweet
Amivantamab + lazertinib achieved a median OS of 41.0 months in treatment-naΓ―ve 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
For1L EGFR-mutated NSCLC with active brain metastases
TL;DRIntracranial ORR 95.5% vs 79.6% (p=0.0004), iPFS HR 0.46 favoring asandeutertinib over osimertinib in 1L EGFR+ NSCLC with brain mets.
- Osimertinib established 1L SOC via FLAURA; ESAONA is first randomized head-to-head with a next-gen EGFR TKI in the brain-met-enriched setting
| Endpoint | Asandeutertinib | Osimertinib | HR / p |
|---|---|---|---|
| iORR (BICR) | 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 |
5 details
- π Phase II, randomized, N=224; 1L EGFR-mutated NSCLC with brain mets, asandeutertinib (n=111) vs osimertinib (n=113)
- π Asandeutertinib: next-generation EGFR TKI evaluated head-to-head vs established osimertinib SOC
CONSORT flow
- β οΈ Safety (TRAEs)
- Any TRAEs: 99.1% (asandeutertinib) vs 95.6% (osimertinib)
- Serious TRAEs: 10.8% vs 7.1% β slightly higher in experimental arm
- β οΈ Phase 2 only, N=224; PFS medians not reached in experimental arm (immature); OS data not reported in source
- β οΈ Primary EP was iORR (response endpoint), not PFS or OS; longer follow-up required for survival readout
- Phase 3 OS confirmatory data needed before practice adoption
- Activity after progression on prior osimertinib unknown
- Optimal sequencing vs osimertinib + chemo (FLAURA2) in brain-met population
π Sources Β· π¦ 1 tweet
#ASCO26 π§ π
— 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.
π§ͺ LBA2007 | ESAONA
1L EGFR-mutated NSCLC with brain metastases
π₯ n=224
βοΈ Asandeutertinib vs Osimertinib
Key⦠https://t.co/mEOKGNKgf7 pic.twitter.com/pUQuH6i2cV
OptiTROP-Lung05 NCT06448312
ForStage IIIB-IV NSCLC, PD-L1 TPS β₯1%, no EGFR/ALK, treatment-naive, ECOG 0-1
TL;DRmPFS NR vs 5.7mo, HR 0.35 (0.26-0.47), p<0.0001 favoring sac-TMT + pembro in 1L PD-L1+ NSCLC.
- Converges with TROPION-Lung08 (Dato-DXd+durvalumab vs pembro, TPSβ₯50%): ADC+IO > IO-mono signal emerging in 1L NSCLC
| Arm | Events n (%) | Median PFS (95%CI) | HR (95%CI) | p |
|---|---|---|---|---|
| Sac-TMT+Pembro (n=208) | 66 (31.7%) | NR (13.6, NE) | 0.35 (0.26, 0.47) | <0.0001 |
| Pembro (n=205) | 128 (62.4%) | 5.7mo (4.3, 7.0) | ref | β |
+3 more figures
| PD-L1 TPS | Sac-TMT+Pembro median PFS | Pembro median PFS | HR (95%CI) |
|---|---|---|---|
| β₯50% | NR (NE, NE) | 9.5mo (6.9, 13.8) | 0.47 (0.29, 0.77) |
| 1-49% | NR (11.1, NE) | 4.3mo (2.9, 5.5) | 0.28 (0.19, 0.41) |
8 details
- π Phase 3 open-label RCT; N=413; stage IIIB/IIIC/IV NSCLC; PD-L1 TPS β₯1%; no EGFR/ALK; ECOG 0-1
- π Sac-TMT 4mg/kg Q2W + pembro 400mg Q6W vs pembro 400mg Q6W; max 18 pembro cycles
CONSORT flow
- π 1Β° EP PFS by BICR: median NR (13.6, NE) vs 5.7mo (4.3, 7.0), HR 0.35 (95%CI 0.26-0.47), p<0.0001
- π ORR 70.2% vs 42.0%
- π Descriptive OS (immature): HR 0.55 (95%CI 0.36-0.85); events 33 (15.9%) vs 54 (26.3%); median f/u 10.5mo
- π PFS benefit consistent across both PD-L1 TPS subgroups (β₯50% and 1-49%)
- β οΈ OS immature at primary PFS analysis (10.5mo median f/u); definitive OS benefit not yet established
- β οΈ Control is pembro mono; for TPS 1-49%, pembro+platinum chemo is also SOC β no head-to-head vs chemo-IO doublet
- Will PFS benefit translate to OS with longer follow-up?
- Superiority vs. pembro + platinum chemo for TPS 1-49%?
- Predictive biomarker beyond PD-L1 TPS for TROP2 ADC benefit?
π Sources Β· π¦ 2 tweets
Right patient. Right treatment. Right timing.
— Yakup ErgΓΌn (@dr_yakupergun) May 30, 2026
The result: curves like theseπ#ASCO26 https://t.co/72KByLKz90
πREVIEW #ASCO26 #LCSM Oral
— Hidehito HORINOUCHI (@HHorinouchi) May 30, 2026
π₯OptiTROP-Lung05: 1L Sac-TMT + Pembro vs Pembro in PD-L1+ NSCLC
β mPFS NR vs 5.7m (HR 0.35)
β ORR 70.2% vs 42.0%
β OS HR 0.55 (95%CI 0.36-0.85, immature)
ποΈDr. Caicun Zhou
π https://t.co/DcbK1dGrhO@OncoAlert @Larvol @ASCO @IASLC https://t.co/512k6dZviW pic.twitter.com/Vdo86N50h9
Wait or Treat β NCT05236946 (Upfront vs Delayed Brain RT in Oncogene-mutated NSCLC) NCT05236946
ForMetastatic NSCLC, EGFR or ALK mutant, completely asymptomatic BM, ECOG 0-2
TL;DRUpfront brain RT halves icPD (HR 0.35, p<0.001) but OS numerically favors delayed (HR 1.45, 2yr 60% vs 48%) in EGFR/ALK+ mNSCLC.
- First RCT on this question; supports emerging TKI-first approach (osimertinib/alectinib CNS penetration)
| Upfront RT (n=105) | Delayed RT (n=103) | |
|---|---|---|
| Events | 20 | 47 |
| 1-yr cumulative icPD | 8.7% (2.9%, 14.5%) | 25.7% (16.8%, 34.7%) |
| 2-yr cumulative icPD | 21.7% (12.6%, 30.8%) | 50% (39.2%, 60.9%) |
| Sub-HR (95% CI) | 0.35 (0.21, 0.59) | ref |
| p-value | <0.001 | β |
+1 more figure
7 details
- π Phase III open-label RCT, N=208; EGFR/ALK+ mNSCLC, completely asymptomatic BM, ECOG 0-2
- π Both arms: TKIs + chemotherapy; delayed arm: RT at intracranial PD or patient request
- π Stratification: GPA score (0-2 vs >2); synchronous vs metachronous BM
CONSORT flow
- π OS HR 1.45 favoring delayed; 2yr OS 48% upfront vs 60% delayed (secondary endpoint)
- β οΈ Radiation necrosis: 6% upfront vs 0% delayed
- β οΈ OS HR p-value not reported in source; trial takeaway: 'timing of RT does not affect survival'
- β οΈ TKI + chemo backbone may not reflect current osimertinib or alectinib monotherapy practice
- Does icPD reduction with upfront RT translate to QoL or neurocognitive benefit?
- SRS vs WBRT in upfront arm: impact on radiation necrosis rate?
- Which pts (high GPA, many lesions) benefit most from upfront cranial RT?
π Sources Β· π¦ 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 didnβt 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
OLIGOMA NCT04495309
ForMetastatic breast, β€5 mets, any systemic therapy line
TL;DRmPFS 35.8 vs 20.4 mo, HR 0.48; first RCT positive for MDT in oligometastatic breast cancer.
- Claimed first RCT positive for MDT PFS specifically in oligomet breast; confirmatory trials ongoing (TAORMINA, STEREO-SEIN, LARA, CLEAR)
+2 more figures
5 details
- π Randomised; metastatic breast any line, β€5 lesions; systemic Β± ablative RT to all mets
- π >80% had 1-3 mets; 2/3 of lesions bone mets; majority ER/PR+, HER2- in 1st-line
CONSORT flow
- π QoL 12-wk co-primary met: QLQ-C30 diff -2.1 (-9.2 to 5.1), NI margin -10 pts (n=64)
- β οΈ Stopped early: enrolled <20% of initial, <40% of amended target; N=87 total
- β οΈ HR CI very wide (0.25-0.91); no OS data reported
- Which subgroups benefit most (therapy line, met burden, histology subtype)?
- OS benefit not yet demonstrated; durability of PFS gain uncertain
- Will confirmatory data from ongoing breast-specific MDT RCTs align?
π Sources Β· π¦ 3 tweets
π Metastases-directed treatment in Patients with Oligometastatic Breast Cancer: Results from the OLIGOMA-trial (ARO-2021-09, NCT04495309) @DavidKrugMD ππ» #ESTRO26 @ESTRO_RT @OncoAlert #OncoAlertAF pic.twitter.com/YDMef0fXRm
— Elisabetta Bonzano MD, PhD (@to_be_elizabeth) May 17, 2026
βοΈ 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. Letsβs go π§΅ 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