onc brain

About · curated by Nick Boehling, MD · @nb2276

    2026-05-30 ASCO Annual Meeting 2026

    digest generated 2026-07-19

    ROADS: surgical bed recurrence 1% vs 12% for intraop GammaTile brachy vs post-op cavity SRS in resected brain mets >2cm — challenges the SRS standard.
    TL;DR
    RT drove the day's actionable news: ROADS (CNS) favors intraop brachytherapy over cavity SRS on local control, and Neo-CRAG (upper-GI) revives neoadjuvant chemoRT in gastric cancer (mOS 67.5 vs 37.6mo) where CRITICS/TOPGEAR were null. Prostate ran a genomic-classifier thread on an RT+ADT backbone.

    Bladder

    MIBC bladder-preservation thread: durvalumab added to 55Gy/20fx chemoRT (RAD-IO) plus post-pCR perioperative management.

    Early signal

    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.

    Why it mattersRadiation oncology

    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.

    RAD-IO
    +1 more figure
    Durvalumab (N=54): completed planned treatment 33 (61%), discontinued early 21 (39%).
    Durvalumab (N=54): completed planned treatment 33 (61%), discontinued early 21 (39%).
    8 details 4 trials watching
    Design

    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.

    Population & inclusion

    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.

    Regimen

    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.

    Radiotherapy

    55 Gy in 20 fractions to bladder (hypofractionated). Node-positive expansion added 46 Gy/20 fx elective nodal RT.

    Endpoints

    Primary: 12-month disease-free survival post-chemoRT, read against a GO/NO-GO framework (GO ≥75%, contextual 60-75%, NO-GO <60%).

    Results

    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.

    Safety

    AEs reported in line with component therapies (chemoRT plus durvalumab). 21/54 (39%) discontinued durvalumab early.

    vs leading data

    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.

    Applies to
    T2-T4a N0M0 muscle-invasive urothelial bladder cancer suitable for bladder-preservation chemoRT
    Does not represent metastatic disease, radical-cystectomy-preferred pts, or node-positive disease beyond the 6-patient expansion.
    Limitations

    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.

    Rationale

    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.

    Monday clinic

    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.

    Open questions

    Sourced from @dralvaropinto, @nataliagandur, @katy_beckermann

    📚 Sources · 🐦 3 tweets

    Combined Curative Phase 2 trial Early signal ASCO Annual Meeting 2026

    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.

    Trials discussed

    SWOG 8710ABACUSCHECKMATE-274KEYNOTE-905VOLGANIAGARAVESPERKEYNOTE-B15

    Overall survival: HR 0.50.
    Overall survival: HR 0.50.
    8 details 3 trials watching
    Methods
    • 🔍 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
    Results
    • 📊 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
      TrialSettingComparisonResult
      NIAGARACis-eligibleGem/Cis + periop durvalumab24-mo OS 82.2% vs 75.2%
      VESPERCis-eligibleddMVAC vs Gem/Cis5-yr OS 66% vs 57%
      KEYNOTE-905Cis-ineligiblePeriop EVP vs cystectomy aloneOS HR 0.50
      KEYNOTE-B15Cis-eligiblePeriop EVP vs Gem/CisOS improved (under FDA review)
    Critique
    • ⚠️ Not all pts in perioperative trials completed adjuvant therapy, often due to toxicity
    Open questions

    Sourced from @nataliagandur

    📚 Sources · 🐦 1 tweet

    Combined Curative ASCO Annual Meeting 2026

    Prostate

    Genomic-classifier thread on a fixed RT+ADT/ARPI backbone: Decipher for intensification gating and docetaxel selection, mostly prognostic not predictive.

    Confirmatory

    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.

    Why it mattersRadiation oncology

    ~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.

    Genomic Classifier + NCCN Risk Stratification (Abstract 5000)
    +2 more figures
    Genomic Classifier + NCCN Risk Stratification (Abstract 5000)
    EndpointHR (add AAP)95% CIp
    MFS0.530.44-0.64<0.0001
    OS0.600.48-0.73<0.0001
    Genomic Classifier + NCCN Risk Stratification (Abstract 5000)
    7 details
    Design

    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.

    Population & inclusion

    NCCN high-risk and very-high-risk localized prostate cancer, all planned for definitive RT+ADT.

    Regimen

    CT-HR (≤2 pts) → RT+ADT; CT-VHR (≥3 pts) → RT+ADT+AAP (abiraterone acetate + prednisone) intensification.

    Results

    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.

    ComponentCategoryPoints
    NCCN clinicalHigh-risk+1
    NCCN clinicalVery-high-risk+2
    GC (Decipher)< 0.60
    GC (Decipher)0.6-0.85+1
    GC (Decipher)> 0.85+2
    vs leading data

    AAP intensification magnitude is borrowed from STAMPEDE M0 (Attard, Lancet 2022), not generated here; GC prognostic value aligns with prior Decipher/NRG validation.

    Applies to
    NCCN high-risk and very-high-risk localized prostate cancer on definitive RT+ADT
    Does not represent intermediate- or low-risk disease, node-positive or metastatic disease, or the radical-prostatectomy pathway.
    Limitations

    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.

    Rationale

    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.

    Monday clinic

    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.

    Open questions
    • 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

    Sourced from @chavarriagaj, @nataliagandur

    📚 Sources · 🐦 2 tweets

    Curative Retrospective Confirmatory ASCO Annual Meeting 2026

    Early signal

    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).

    Monday clinic

    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.

    Median time to eugonadal T 9.0mo. T recovery by 18mo 52 (66.7%); treatment-free 18mo 45 (57.7%); primary endpoint (treatment-free + T recovery) 32 (41.0%), 80% CI 33.1-48.9%, one-sided p 0.0249
    Median time to eugonadal T 9.0mo. T recovery by 18mo 52 (66.7%); treatment-free 18mo 45 (57.7%); primary endpoint (treatment-free + T recovery) 32 (41.0%), 80% CI 33.1-48.9%, one-sided p 0.0249
    +2 more figures
    A-DREAM
    A-DREAM
    8 details 4 trials watching
    Design

    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.

    Population & inclusion

    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.

    Endpoints

    Primary: treatment-free with eugonadal testosterone (≥150 ng/dL) at 18 months. Exploratory: rPFS, TTNT, OS, cost.

    Results

    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.

    Discussion

    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.

    Applies to
    metastatic HSPC deep responders (PSA<0.2 after ≥18mo ADT + ≥12mo ARPI), low-volume-predominant
    Does not represent incomplete responders, high-volume disease, or patients unwilling to accept delayed testosterone recovery.
    Limitations

    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.

    Rationale

    Single-arm phase 2, N=78, no randomised comparator vs continued therapy; primary endpoint met but interruption safety needs longer follow-up and randomisation.

    Open questions

    Sourced from @mjuanfi81

    📚 Sources · 🐦 1 tweet

    Systemic Palliative Phase 2 trial Early signal ASCO Annual Meeting 2026

    Confirmatory

    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.

    Monday clinic

    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.

    ARACOG (AFT-47)
    Arm (N)Max-changed domainMedian % changeP
    Darolutamide (48)PALFAM (visual mem/exec)-15.80.009
    Enzalutamide (47)SWM (working mem/exec)-36.1n/a
    +1 more figure
    ARACOG (AFT-47)
    7 details 2 trials watching
    Design

    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.

    Population & inclusion

    Advanced prostate cancer across mHSPC, mCRPC, and nmCRPC. Required acceptable enzalutamide co-pay; predominantly White, with most non-White pts randomized to enzalutamide.

    Regimen

    Darolutamide provided by the study vs enzalutamide through standard of care, an asymmetry that could bias crossover and adherence.

    Endpoints

    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.

    Results

    MCCD median change -36.1 (enza, N=47) vs -15.8 (daro, N=48), P=0.009: greater cognitive decline on enzalutamide.

    vs leading data

    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.

    Applies to
    advanced prostate cancer pts (mHSPC, mCRPC, nmCRPC) choosing between darolutamide and enzalutamide
    Does not represent apalutamide, abiraterone, or head-to-head efficacy comparisons.
    Limitations

    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.

    Rationale

    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.

    Open questions

    Sourced from @katy_beckermann, @nataliagandur

    📚 Sources · 🐦 2 tweets

    Systemic Palliative Phase 2 trial Confirmatory ASCO Annual Meeting 2026

    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.

    Trials discussed

    ENZAMETCHAARTED

    Why it mattersRadiation oncology

    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.

    Biomarker vs clinical-risk concordance in high-risk prostate: 24% discordant (tissue n=427 of 3816).
    Biomarker vs clinical-risk concordance in high-risk prostate: 24% discordant (tissue n=427 of 3816).
    +1 more figure
    Precision Oncology: Applying New Biomarkers in GU Cancers
    9 details 4 trials watching
    Methods
    • 🔍 ENZAMET biomarker cohort: 1,071 consented, GEP N=764, final Decipher cohort N=634 (56% of enrolled)
    Results
    • 📊 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)
    Critique
    • ⚠️ 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
    Notes
    • 🔬 ASCO26 education session (J. Lang): a biomarker is useful only if it changes management; GU therapy selection stays biomarker-limited
    Open questions

    Sourced from @nataliagandur

    📚 Sources · 🐦 1 tweet

    ASCO Annual Meeting 2026

    Caveats dominate

    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.

    Monday clinic

    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.

    ENZAMET + Decipher (Part 2)
    Treatment armDecipher >0.85 vs ≤0.85 OS HRp
    ADT + ENZA3.02 (1.50-5.76)—
    ADT + ENZA + Doce1.08 (0.60-1.71)0.73
    +1 more figure
    ENZAMET + Decipher (Part 2)
    Decipher stratumUnweighted HR (doce vs none)IPTW-weighted HR
    ≤0.852.78 (1.49-5.21)1.94 (0.95-3.96)
    >0.851.13 (0.71-1.79)0.75 (0.43-1.33)
    7 details
    Design

    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.

    Population & inclusion

    Metastatic hormone-sensitive prostate cancer on an ADT + enzalutamide backbone with an available Decipher score. A low-volume subset was analysed separately.

    Regimen

    ADT + enzalutamide ± early docetaxel. Docetaxel was given at investigator discretion (a stratification factor), so the docetaxel comparison is not randomised.

    Results

    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.

    vs leading data

    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.

    Applies to
    mHSPC pts on an ADT + enzalutamide backbone with a Decipher score
    Does not represent pts managed without a Decipher score, or on systemic backbones other than ADT + enzalutamide.
    Limitations

    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.

    Rationale

    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.

    Open questions
    • 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)

    Sourced from @nataliagandur

    📚 Sources · 🐦 1 tweet

    Systemic Palliative Phase 3 RCT Caveats dominate ASCO Annual Meeting 2026

    Confirmatory

    TALAPRO-3

    ForHRR-deficient metastatic prostate cancer

    Imaging-based progression-free survival surrogate

    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.

    Monday clinic

    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.

    TALAPRO-3
    PopulationHR (95% CI)Median rPFS, mo
    ITT0.48 (0.36-0.65)NC vs 45.8
    BRCA0.37 (0.22-0.61)NC vs 35.1
    Non-BRCA0.57 (0.39-0.82)NC vs NC
    6 details 2 trials watching
    Design

    Randomized, placebo-controlled trial: talazoparib+enzalutamide vs placebo+enzalutamide, 300 vs 299 pts. Published NEJM May 30, 2026.

    Population & inclusion

    HRR-deficient metastatic prostate cancer, enzalutamide/ADT backbone both arms. Prespecified BRCA (104/103) and non-BRCA HRR (196/196) strata.

    Regimen

    Talazoparib (PARP inhibitor) added to enzalutamide plus ADT; control substituted placebo for talazoparib on the same ARSI backbone.

    Endpoints

    Primary: imaging-based (radiographic) PFS. OS and other secondaries not reported in source.

    Results

    ITT 3yr rPFS 77% vs 56%, P<0.001; per-population HRs and medians in the figure. Benefit concentrated in the BRCA subgroup.

    vs leading data

    Extends PARP+ARSI combinations (TALAPRO-2, PROpel, MAGNITUDE) that established the class in HRR-altered mCRPC toward the enzalutamide/ADT-backbone metastatic setting.

    Applies to
    HRR-deficient metastatic prostate cancer on an enzalutamide/ADT backbone, BRCA-enriched
    Does not represent HRR-intact disease or PARP-inhibitor use outside HRR alterations.
    Limitations

    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.

    Rationale

    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).

    Open questions

    Sourced from @DrChoueiri

    📚 Sources · 🐦 1 tweet

    Systemic Palliative Phase 3 RCT Confirmatory ASCO Annual Meeting 2026

    Breast

    Pre- vs sub-pectoral implant reconstruction: modest patient-reported chest well-being gain against more unplanned implant loss.

    Confirmatory

    PREPEC

    ForSkin/nipple-sparing mastectomy, implant reconstruction, prevention/therapeutic

    Physical well-being (chest), BREAST-Q, 24mo surrogate

    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%).

    Monday clinic

    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%).

    PREPEC
    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
    PREPEC
    Unplanned implant loss/replacement (24mo)Pre-pectoralSub-pectoralAdj. 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
    Design

    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.

    Population & inclusion

    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.

    Endpoints

    Primary: long-term patient-reported physical well-being (chest), BREAST-Q, at 24 months. Main secondary safety: unplanned loss or replacement of expander/implant.

    Results

    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%.

    Safety

    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.

    Applies to
    women choosing implant-based reconstruction after skin- or nipple-sparing mastectomy, therapeutic or risk-reducing
    Does not represent autologous (flap) reconstruction or non-implant approaches.
    Limitations

    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.

    Discussion

    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.

    Rationale

    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.

    Open questions

    Sourced from @to_be_elizabeth

    📚 Sources · 🐦 1 tweet

    Surgery Phase 3 RCT Confirmatory ASCO Annual Meeting 2026

    CNS

    Intraoperative brachytherapy challenges post-op cavity SRS for large resected brain mets, but watch the outsized OS gap for arm imbalance.

    Challenges SOC

    ROADS

    ForResected brain metastasis > 2 cm, post-op cavity RT candidates

    Time to surgical bed recurrence local control

    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.

    Why it mattersRadiation oncology

    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.

    ROADS
    EndpointGammaTileSRS
    Time to surg bed recurrenceNR17 mo
    Surg bed recurrence-free survivalNR11 mo
    2-yr OS62%36%
    8 details 2 trials watching
    Design

    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.

    Population & inclusion

    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.

    Radiotherapy

    Experimental: intraoperative permanent Cs-131 seed brachytherapy (GammaTile) at resection. Control: post-op cavity SRS. Dose, fractionation, and cavity margin not reported in source.

    Results

    Both primary endpoints and 2yr OS favored GammaTile. Safety: radiation necrosis comparable (8% vs 7%), leptomeningeal disease higher with brachytherapy (10% vs 3%).

    vs leading data

    Post-op cavity SRS is the current standard for resected brain mets (N107C, Mahajan). ROADS challenges it, favoring intraoperative brachytherapy on local control.

    Applies to
    pts with a resected brain metastasis > 2 cm who are candidates for post-op cavity radiotherapy
    Does not represent intact (unresected) brain mets or resection cavities ≤ 2 cm.
    Limitations

    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.

    Rationale

    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.

    Monday clinic

    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.

    Open questions

    Sourced from @PDBrownOnc

    📚 Sources · 🐦 1 tweet

    Radiation Palliative Phase 3 RCT Challenges SOC ASCO Annual Meeting 2026

    Thoracic / Lung

    1L NSCLC: atypical-EGFR durability, a CNS-active EGFR TKI vs osimertinib in brain mets, and a chemo-free TROP2-ADC + IO doublet.

    Early signal

    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.

    Monday clinic

    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.

    Median OS 41.0 mo (95% CI 27.7-NE). Median follow-up 31.3 mo.
    Median OS 41.0 mo (95% CI 27.7-NE). Median follow-up 31.3 mo.
    +1 more figure
    Time on treatment: median 13.3 mo (range <0.1-53.2); 39% on treatment >2 years.
    Time on treatment: median 13.3 mo (range <0.1-53.2); 39% on treatment >2 years.
    8 details
    Design

    Single-arm cohort, n=49, no randomised comparator. Median follow-up 31.3 mo.

    Population & inclusion

    Treatment-naïve (1L) atypical EGFR-mutated advanced NSCLC. Responses durable regardless of demographics, baseline mutations, and disease characteristics.

    Regimen

    IV amivantamab + lazertinib. Median treatment duration 13.3 mo (range <0.1-53.2); 39% on treatment >2 years.

    Results

    Median OS 41.0 mo (95% CI 27.7-NE), ~3.5 years. No clear association between EGFR variant subtype and OS.

    Safety

    With longer follow-up, safety consistent with prior reports; no new safety signals.

    vs leading data

    Extends the durable 1L amivantamab+lazertinib OS signal from common EGFR (exon19del/L858R) to atypical variants.

    Applies to
    treatment-naïve atypical EGFR-mutant advanced NSCLC
    Does not represent common EGFR (exon19del/L858R) or pretreated disease.
    Limitations

    Single-arm, n=49, no randomised comparator. Atypical EGFR is a heterogeneous class; per-variant efficacy not detailed in source.

    Rationale

    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.

    Open questions
    • Efficacy by specific atypical EGFR variant
    • Randomised comparison vs other 1L options in atypical EGFR

    Sourced from @chulkimMD

    📚 Sources · 🐦 1 tweet

    Systemic Palliative Early signal ASCO Annual Meeting 2026

    Early signal

    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.

    Why it mattersRadiation oncology

    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
    Design

    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.

    Population & inclusion

    Treatment-naive (1L) EGFR-mutant NSCLC with brain metastases. Mutation subtype, symptomatic status, and prior brain RT not reported in source.

    Regimen

    Asandeutertinib (next-generation EGFR TKI) vs osimertinib. Dose and schedule not reported in source.

    Results

    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.

    EndpointAsandeutertinibOsimertinibHR (p)
    iORR95.5% (89.8-98.5)79.6% (71.0-86.6)p=0.0004
    Intracranial PFSNR17.5 mo (15.18-NA)HR 0.46, p=0.0020
    Overall PFSNR17.2 mo (15.18-19.55)HR 0.64, p=0.0473
    Safety

    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.

    vs leading data

    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.

    Applies to
    treatment-naive EGFR-mutant NSCLC with brain metastases
    Does not represent EGFR-wildtype disease or brain metastases progressing on a prior EGFR TKI.
    Limitations

    Phase 2 with immature time-to-event data (medians not reached); overall PFS benefit borderline (p=0.0473); no OS; blinding not specified.

    Discussion

    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.

    Rationale

    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.

    Monday clinic

    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.

    Open questions

    Sourced from @DrRishabhOnco

    📚 Sources · 🐦 1 tweet

    Systemic Palliative Phase 2 trial Early signal ASCO Annual Meeting 2026

    Early signal

    OptiTROP-Lung05 NCT06448312

    For1L IIIB/IIIC-IV PD-L1≥1% NSCLC, EGFR/ALK wild-type

    Progression-free survival (BICR) surrogate

    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.

    OptiTROP-Lung05
    ArmPFS events n (%)Median PFSHR (95% CI)
    Sac-TMT+Pembro66 (31.7%)NR (13.6-NE)0.35 (0.26-0.47)
    Pembro128 (62.4%)5.7 mo (4.3-7.0)—
    +2 more figures
    OptiTROP-Lung05
    PD-L1 TPSmPFS combomPFS pembroHR (95% CI)
    ≥50%NR9.5 mo0.47 (0.29-0.77)
    1-49%NR4.3 mo0.28 (0.19-0.41)
    OptiTROP-Lung05
    ArmOS events n (%)Median OSHR (95% CI)
    Sac-TMT+Pembro33 (15.9%)NR0.55 (0.36-0.85)
    Pembro54 (26.3%)NR—
    8 details 2 trials watching
    Design

    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.

    Population & inclusion

    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.

    Regimen

    Sac-TMT (TROP2 ADC) 4 mg/kg Q2W + pembrolizumab 400 mg Q6W vs pembrolizumab alone; pembro capped at 18 cycles.

    Results

    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.

    vs leading data

    Current 1L PD-L1+ NSCLC standard is pembrolizumab ± chemotherapy. This tests a chemo-free ADC+IO doublet; no head-to-head vs chemo-IO.

    Applies to
    1L advanced/metastatic PD-L1≥1%, EGFR/ALK wild-type NSCLC
    Does not represent EGFR/ALK-altered, PD-L1-negative, or previously-treated patients.
    Limitations

    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.

    Rationale

    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.

    Open questions

    Sourced from @HHorinouchi, @dr_yakupergun

    📚 Sources · 🐦 2 tweets

    Systemic Palliative Phase 3 RCT Early signal ASCO Annual Meeting 2026

    Germ Cell / Other GU

    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.

    Trials discussed

    EV209EV309RAMPART

    Why it mattersRadiation oncology

    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.

    vs leading data
    • 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
    Living Longer, Living Better: Can We Have It All?
    Componentn (%)
    Full 55 Gy/20 fx RT delivered54 (100%)
    RT with no extension/delay47 (87%)
    Chemo discontinued early12 (22%)
    Durvalumab completed33 (61%)
    Durvalumab discontinued early21 (39%)
    +1 more figure
    Living Longer, Living Better: Can We Have It All?
    6 details 3 trials watching
    Methods
    • 🔍 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
      FeatureEV209EV309
      PopulationCystectomy-eligibleIneligible / refusing
      StagecT2-4a N0 MIBCcT2-4a N0 MIBC
      N240390
      Regimen9 cycles EV + 1 yr pembro9 cycles EV + 1 yr pembro
      EndpointscCR, 2 yr BIEFSBIEFS, OS
    Results
    • 📊 Adjuvant pembro (Choueiri, ASCO26): ctDNA stratifies DFS better than pathologic features; ctDNA-positive pts fare far worse in both arms
    Critique
    • ⚠️ Feasibility signal only; bladder preservation, function, symptom burden, safety and QoL all await longer f/u
    Notes
    • 🗞️ Rini ASCO26 GU discussant: can curative-intent GU therapy raise cure rates while preserving organ function and QoL?
    Open questions

    Sourced from @nataliagandur

    📚 Sources · 🐦 1 tweet

    Curative ASCO Annual Meeting 2026

    GI Upper

    Neoadjuvant chemoRT is RT-attributable positive in high-risk gastric cancer, reopening a question CRITICS and TOPGEAR left null (though on a XELOX, not FLOT, backbone).

    Challenges SOC

    Neo-CRAG

    ForHigh-risk locally advanced gastric/EGJ (cT3N2-3 to cT4), fit for D2 resection

    Disease-free survival surrogate

    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.

    Why it mattersRadiation oncology

    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.

    Neo-CRAG
    EndpointCRTCTHR (95% CI), P
    Median DFS52.7 mo24.4 mo0.750 (0.607-0.928), P=0.008
    3-yr DFS55.6%42.4%—
    Median OS67.5 mo37.6 mo0.781 (0.628-0.970), P=0.025
    5-yr OS50.1%44.2%—
    7 details 2 trials watching
    Design

    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.

    Population & inclusion

    High-risk locally advanced gastric/EGJ adenocarcinoma: cT3N2-3M0, cT4aN+M0, or cT4bNanyM0; 36.3% EGJ (Siewert II/III). All planned standardized D2 gastrectomy.

    Regimen

    Both arms: 3 cycles preoperative + 3 cycles adjuvant XELOX (oxaliplatin 130, capecitabine 1000 BID D1-14, Q3W) around D2 gastrectomy.

    Radiotherapy

    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.

    Results

    Primary DFS met and secondary OS positive, both favoring CRT; pathologic downstaging, ypN0, and locoregional control also improved (see figure and table).

    vs leading data

    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.

    Applies to
    high-risk locally advanced gastric/EGJ (Siewert II/III) adenocarcinoma, cT3N2-3 to cT4b, fit for D2 gastrectomy on a XELOX backbone
    Does not represent FLOT-backbone, metastatic, or Western populations with lower D2-resection rates.
    Limitations

    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.

    Rationale

    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.

    Monday clinic

    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.

    Open questions

    Sourced from @NiuSanford

    📚 Sources · 🐦 1 tweet

    Combined Curative Phase 3 RCT Challenges SOC ASCO Annual Meeting 2026

    Supportive / QoL

    Post-hoc selection score for celiac-plexus SRS in pancreatic pain; awaits external validation.

    Caveats dominate

    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.

    Why it mattersRadiation oncology

    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
    Design

    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.

    Population & inclusion

    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.

    Radiotherapy

    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.

    Endpoints

    Pain response = ≥2-point reduction in average BPI-SF pain from baseline to 3 weeks. Score performance judged by optimism-corrected AUC.

    Results

    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 scorePain responsen
    032%31
    153%40
    289%19
    PredictorUnivariate ORMultivariate OR
    Neurotoxic chemo exposure5.33 (2.13-13.4), p<0.0015.1, p=0.009
    Baseline pain intensity1.73, p=0.0031.8, p=0.003
    Age1.06, p=0.014dropped (collinearity)
    Therapy line0.65, p=0.04dropped (collinearity)
    Discussion

    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.

    Applies to
    pancreatic-cancer pts with intractable retroperitoneal pain evaluated for celiac plexus SRS
    Does not represent pts already exposed to neurotoxic chemotherapy (lower predicted response) or non-pancreatic retroperitoneal pain.
    Limitations

    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.

    Rationale

    Post-hoc predictor modeling of a single-arm phase 2; internal bootstrap validation only, external validation pending. Associations, not a prospectively validated selection tool.

    Monday clinic

    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).

    Open questions
    • 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

    Sourced from @NiuSanford

    📚 Sources · 🐦 1 tweet

    Radiation Palliative Phase 2 trial Caveats dominate ASCO Annual Meeting 2026