onc brain

Multicenter phase IIR/III, two-step RCT. Step 1: gemcitabine vs gemcitabine + erlotinib. Step 2 (reported here): random assignment to a sixth chemo cycle ± CXRT after 5 progression-free cycles. N=354 (180 CXRT, 174 chemo).

Curative-intent resected pancreatic head adenocarcinoma, progression-free on adjuvant chemo. Median age 63, 55% male, 56% PS 1.

Fluoropyrimidine-sensitized CXRT added to the sixth cycle. Dose, fractionation, and target volume not stated in the source excerpt.

Primary: overall survival. Secondary: DFS. Powered for HR 0.76 (316 events, 80% power, 1-sided α=.05).

Primary OS not met (HR 0.96). The one positive signal was the treatment-by-nodal-status interaction (OS P=.0063, DFS P=.014) favoring CXRT in node-negative pts; subgroup effect size not in source.

No increase in grade 4/5 toxicity. Grade 3 toxicity higher with CXRT: 38% vs 19% (P<.001).

ESPAC-1's older 5-FU-based CXRT suggested inferior outcomes; here modern CXRT shows no OS harm but no all-comer benefit. Backbone predates FOLFIRINOX-type adjuvant chemo, named in the source as current SOC.

Node-negative benefit rests on a subgroup interaction, not the prespecified primary. Trial underwent multiple mid-course modifications (LAP07, accrual, slow event rate), and no local-control or pattern-of-failure endpoint is reported despite RT's locoregional rationale.

Clean negative primary OS (HR 0.96) reinforces no routine adjuvant CXRT; node-negative benefit is a subgroup interaction needing confirmation; gemcitabine backbone predates FOLFIRINOX.

Planned secondary analysis of the TROG 08.03 RAVES randomised trial comparing adjuvant RT with salvage RT delivered at PSA >0.2 ng/ml after radical prostatectomy. Patient-reported QOL collected prospectively across multiple Australian and New Zealand sites.

EORTC QLQ-C30 and QLQ-PR25. The unit of analysis is a minimal clinically important change (MCIC), a decline of >0.5 SD from baseline, in bowel symptoms, urinary symptoms, sexual activity, and sexual functioning.

The aRT arm (n=166) reported more bowel-symptom MCIC at 1-5 yr than sRT pts who never required RT. Against pts in the sRT group who did receive RT, no consistent differences in urinary, bowel, or sexual domains emerged.

Dose, fractionation, and target volume are not reported in the source text. Median follow-up from RT was 2.6 yr in the salvage group who received RT (IQR 1.2-5.2), and aRT pts started RT younger (63.9 vs 66.8 yr, p=0.01).

Self-reported QOL in an unblinded trial, so expectancy cuts toward the arm that knows it was irradiated. Denominators thin sharply by 5 yr (23 sRT pts post-RT; 8 in the no-RT sexual-functioning group), and the scattered significant timepoints in the aRT-vs-sRT comparison are fragile at that N.

Reframes the early-salvage rationale: the QOL dividend is sparing roughly the share of men who never trigger RT, not delaying exposure. That matters because delay was the intuitive mechanism, and the regression data do not support it.

Prespecified secondary QOL analysis of a randomised trial; supports the already-guideline-endorsed early-salvage strategy. Small late-timepoint denominators and unblinded self-report temper it.

IPD meta-analysis of 7 phase 3 RCTs (MARCAP consortium) of CFRT vs MHFRT. Primary efficacy endpoint PFS; co-primary toxicity late G2+ GU and G2+ GI; co-primary PRO urinary/bowel QoL decrement. Two prespecified strata: isodose vs dose-escalated MHFRT.

Localised prostate cancer. CFRT arm required modern dose (≥70 Gy in 2 Gy equivalents); trials lacking published IPD efficacy or late-toxicity data excluded. 3454 pts across 3 isodose trials, 2426 pts across 4 dose-escalated trials.

Isodose MHFRT exemplified by 60 Gy in 20 fractions; dose-escalated MHFRT schedules pooled (specific fractionations not given in source). Median follow-up 5.4 y (isodose) and 7.1 y (dose-escalated).

Efficacy equivalent to CFRT for both strata. The only toxicity separations were in the dose-escalated arm, late G2+ GI and bowel QoL, not isodose (see table).

Reinforces isodose 60/20 (CHHiP-type) as the standard MHFRT regimen and argues against dose-escalating hypofractionated schedules, which buy no efficacy but cost bowel toxicity.

Physician-scored late toxicity carries grading subjectivity, though PRO data corroborate the bowel signal. Dose-escalated stratum pools heterogeneous fractionation; longer follow-up needed to confirm late-toxicity divergence.

IPD meta-analysis of 7 phase 3 RCTs consolidating isodose 60/20 as standard MHFRT; reinforces current practice, no efficacy gained by dose-escalating.

Phase 3, randomized, non-blinded, international; N=698 (SBRT 353 / MH-IMRT 345). Co-primary: disease-free survival (superiority) and EPIC-26 bowel + urinary-irritation QoL at 24 mo. Interim futility analyses prespecified.

Localized intermediate-risk prostate cancer, median age 68. Stratified by Gleason score, PSA, and rectal manipulation (SpaceOAR in ~55%).

SBRT 36.25 Gy/5 fx (7.25 Gy/fx, 2-3×/wk) vs MH-IMRT 70 Gy/28 fx or 60 Gy/20 fx. CTV = prostate ±1 cm proximal SV; SBRT PTV margin 5 mm radial / 3 mm AP. Fiducials, MRI fusion, daily IGRT mandated.

Co-primary DFS powered for a 38% relative improvement (target HR 0.62). Co-primary QoL: absolute reduction in MCID for EPIC bowel (≥4) and urinary irritation/obstruction (≥5) at 24 mo.

DFS superiority not met (futility bound crossed); QoL split, bowel favored SBRT while urinary irritation did not. Effect sizes in the tables above.

Investigator-reported toxicity favored SBRT: fewer G≥3 GU events, less rectal hemorrhage, less fatigue (all p<0.05). Table above.

Consistent with PACE-B: both show lower urinary-incontinence decline with SBRT vs MH-IMRT. MH-IMRT SOC anchored by RTOG 0415.

Non-blinded, so patient-reported QoL endpoints are unblinded. SBRT was designed to prove superiority and failed it; 3y biochemical failure ran numerically higher with SBRT.

Prespecified phase III; SBRT failed DFS superiority (futility crossed) and did not beat MH-IMRT on the urinary-irritation co-primary. Confirms SBRT as a safe equivalent option, not an upgrade.

Phase 3 RCT (EORTC 22033-26033 with NCIC-CTG/TROG/MRC-CTU), N=478 clinical high-risk WHO grade 2 LGG, randomized to RT vs dose-dense TMZ. Mature results, with post-hoc 2021 WHO molecular reclassification in 73% (351/478).

RT 28 × 1.8 Gy, standard fractionation, as the single-modality comparator arm.

Dose-dense TMZ 75 mg/m² once daily, 21 of 28 days, up to 12 cycles.

Primary: progression-free survival; overall survival co-reported. No significant difference in PFS or OS between arms.

Neither PFS nor OS differed by arm overall; molecular-subgroup OS is in the detail table, with only IDH-wildtype favoring TMZ.

Combined-modality (RT + chemo) was not tested here but has since become standard for IDH-mutant astrocytoma (e.g. RTOG 9802, RT+PCV).

Molecular subtypes are post-hoc reclassification (tissue in 73%); the IDH-wildtype subgroup is small (n=64). Combined-modality untested.

Mature phase 3; the null modality comparison confirms combined-modality's rise as SOC. Molecular subgroups reclassified post-hoc, so no single-modality practice change lands.

Phase 3 open-label RCT, N=802 across 8 countries (2014-2018), median follow-up 8 years. Primary: metastasis-free survival (switched from OS mid-trial for fewer-than-expected deaths). Enzalutamide 160mg × 24mo vs conventional NSAA × 6mo, both on 24mo LHRH agonist + EBRT.

High-risk clinically-localized or locally-advanced prostate, EBRT-suitable. 90% Gleason 8-10, 36% PSA >20, 12% cN1 by conventional imaging. 40% planned pelvic RT, 8% brachytherapy boost.

Prostate to 78Gy, or 46Gy + brachy boost. Pelvic nodal RT 46Gy elective + boost to gross nodes, required for cN1, optional (pre-declared) for cN0. Intensive QA: credentialing, real-time review of first 5 plans per site, 20% sampling thereafter.

Primary MFS not met; PFS positive, OS neutral; benefit isolated to the cN1 and pelvic-RT-planned subgroups (see tables).

The cN1 MFS benefit mirrors STAMPEDE abiraterone; the weaker overall effect reflects ENZARAD's more favorable baseline risk (lower cN1 fraction, lower PSA, less cT3-4).

Active NSAA control (not placebo) narrows the measured enzalutamide effect. Subgroup benefits are prespecified but hypothesis-generating, and the pelvic-RT arm is confounded by nodal enrichment. Primary endpoint switched from OS to MFS mid-trial.

Phase 3, prespecified MFS primary, 8yr f/u, active-NSAA control; negative overall reinforces restrained intensification, cN1/pelvic-RT benefit mirrors STAMPEDE. Subgroups prespecified, not practice-defining alone.

Single-centre, randomised, open-label phase 2 (European Institute of Oncology, Milan). N=105 randomised 1:1 (52 SBRT alone, 53 SBRT+ADT); modified ITT, 51/arm analysed. Median follow-up 31 mo.

Metachronous oligorecurrent hormone-sensitive prostate cancer after radical local treatment; ≤3 lesions (pelvic/extra-regional nodal or bone) on PSMA-PET or MRI; ECOG 0-1; median age 70. Stratified by PSMA-DT (≤3 vs >3 mo), site (node vs bone), imaging.

SBRT 30 Gy in 3 fractions every other day (EQD2 98.6 Gy at α/β 1.5, BED >100 Gy), or equivalent by site. All oligometastatic sites treated in both arms.

The SBRT+ADT arm added 6 months of LHRH-analogue ADT starting within 1 week before SBRT.

Primary: clinical progression-free survival. OS and time-to-CRPC were not the primary read.

Adding short ADT roughly doubled median cPFS; effect sizes in the results table.

Near-absent RT toxicity: 1 G1 GI, 1 G3 GU (left ureter stenosis, SBRT+ADT), no late effects. ADT added 22 G1 AEs, all resolved. No treatment-related deaths.

First RCT of adding short ADT to MDT in metachronous oligorecurrent HSPC. STOMP/ORIOLE established MDT vs observation; RADIOSA instead isolates the ADT add-on onto an SBRT backbone.

Single-centre, open-label, N=105. Primary endpoint is clinical PFS, a surrogate; ADT's own progression-delaying effect confounds the SBRT+ADT arm. Optimal ADT duration untested.

Single-centre open-label phase 2, N=105; 1° EP is clinical PFS (surrogate), not OS. Consistent with STOMP/ORIOLE MDT signals; not definitive enough to change practice.

IPD meta-analysis (PROSPERO CRD42023479078) of 7 phase 2 RCTs; the primary MDT-efficacy analysis pooled 6 trials randomizing 472 men to MDT+SOC (n=248) vs SOC (n=224). Median follow-up 40.7 mo (IQR 25.6-53.7).

Oligometastatic (up to 5 mets) prostate cancer; 65% castration-sensitive (n=375), ARTO entirely CRPC and EXTEND baskets CRPC-enriched. 85.5% (n=491) had prior definitive local therapy; median PSA 1.9 both arms.

MDT is delivered per each component trial (EXTEND, STOMP, ORIOLE, ARTO, COMET-SABR), predominantly SBRT-based. Dose, fractionation, target volume, and modality breakdown are not reported in this meta-analysis, so the technique-transfer question can't be answered from source.

Coprimary: PFS and OS. Secondary: rPFS and castration resistance-free survival (CRFS).

MDT plus SOC improved PFS, rPFS, and CRFS across both trial- and patient-level analyses; overall survival did not reach significance (effect sizes in the table above).

STOMP and ORIOLE (observation-controlled SBRT trials) drove the early MDT signal; this pooled IPD extends the PFS/CRFS benefit across 6 trials and shows it persists on a systemic-therapy backbone in the observation-excluded sensitivity analysis.

All 7 component trials are phase 2 with non-blinded randomization ('some concerns' RoB) and open-label PSA-driven endpoints. OS non-significant (p=0.051). SOC arm slightly older (71 vs 68) and more often on 2nd-gen ARPI (59.8% vs 50.4%).

IPD meta-analysis of 6 phase-2 non-blinded RCTs; PFS/rPFS/CRFS clearly hit but OS non-significant. Reinforces the emerging MDT-for-oligomet signal (STOMP, ORIOLE), doesn't establish survival.

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).

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.

RT randomization of NRG/RTOG 0848 phase 3. After curative-intent resection and adjuvant gemcitabine-based chemo without progression, N=354 randomized to no further therapy (n=174) vs fluoropyrimidine-sensitized CXRT (n=180). Primary: overall survival.

Resected pancreatic head adenocarcinoma; mix of N0 (n=91) and N1 (n=263), predominantly T3 (n=288 vs T1/T2 n=66), mostly negative margins (n=295). Only pts completing adjuvant chemo without progression.

Adjuvant systemic backbone gemcitabine-based: gemcitabine alone (n=236), non-oxaliplatin gemcitabine combinations (n=18), gemcitabine+erlotinib (n=100). Added arm was fluoropyrimidine-sensitized CXRT.

CXRT was fluoropyrimidine-sensitized chemoradiotherapy delivered after completion of adjuvant chemo. RT dose, fractionation, and target volume not reported in source text.

Primary: overall survival. Prespecified 5-yr OS subgroup estimates with interaction tests by nodal status, T stage, margins, CA19-9, sex, age, and systemic regimen.

Primary OS negative: HR 0.96 (90% CI 0.79-1.18), p=0.38; median OS 2.6 vs 2.3 yr. Nodal-status interaction p=0.022 with a node-negative gain (see table).

Gemcitabine backbone predates FOLFIRINOX-era adjuvant standard; authors note the node-negative signal needs confirmation in trials using FOLFIRINOX/FOLFOXIRI.

Node-negative OS benefit is a subgroup finding (n=91, interaction p=0.022), hypothesis-generating. Dated gemcitabine backbone; RT technique not reported in source.

Prospective phase III, primary OS endpoint not met (HR 0.96); reinforces omitting adjuvant CXRT. Node-negative benefit is subgroup-only (interaction p=0.022), needs independent confirmation.

Prospective phase 2, multi-institutional (NRG/RTOG), risk-adapted by WHO grade, extent of resection, and recurrence status. 244 consented, 165 protocol-treated. Central pathology review; data cutoff 8/15/2023.

Adults ≥18, Zubrod 0-1, histologically confirmed unifocal WHO grade 1-3 meningioma, any resection extent. Low-risk n=60, intermediate n=52, high-risk n=53.

Intermediate-risk 54 Gy and high-risk 60 Gy, both in 30 fractions, adjuvant. Low-risk received no RT (observation). No hypofractionation or SRS arm.

Primary (3-yr PFS) reported previously. This analysis reports long-term PFS, OS, and cumulative incidence of progression (competing-risk) at ~12-yr median follow-up.

Per-cohort 10-yr PFS, OS, and cumulative-incidence values are in the table above. Median PFS not reached for low- and intermediate-risk.

RT-attributable grade 3+ toxicity 9.6% (intermediate, 5/52) and 15.1% (high-risk, 8/53). The observed low-risk cohort carried no RT toxicity.

No randomised RT-vs-observation trial in grade 2 meningioma has reported. ROAM/EORTC-1308 and NRG-BN003 (GTR grade 2) remain open; RTOG 0539 is the prospective benchmark.

Each risk cohort is single-arm, no randomised RT-vs-observation comparison; modest per-cohort N (~50-60); grading predates molecular integration into WHO CNS grading.

Prospective multi-institutional risk-adapted phase 2, 12-yr mature f/u, sets RT patient-selection benchmark. Each cohort single-arm; no randomised RT-vs-observation comparison.

Prospective practice-pattern study within the Michigan Radiation Oncology Quality Consortium (MROQC), a statewide RT registry. 553 pts across 26 centers, Jun 2020–Nov 2024. Facility modeled as a random intercept (mixed-effects).

Intact, high-risk M0/N0-1 prostate cancer on definitive RT. GG4-5 75.0%, PSA ≥20 40.0%, cN1 19.9%, cT3/4 13.3%. 27.9% met STAMPEDE M0 intensification criteria.

Primary: intended guideline-concordant ADT (≥18mo). Also assessed: ARPI adoption before vs after STAMPEDE M0 publication, facility-level variability, and multivariable predictors of concordance.

91.3% recommended any ADT, 67.0% guideline-concordant. ARPI intensification among STAMPEDE-eligible rose 0% → 23.2% post-publication. Facility variability persisted on MVA (P<.0001).

Benchmarks real practice against the 2022 AUA/ASTRO guideline (18-36mo ADT) and STAMPEDE M0 (ARPI for high-burden high-risk). Documents a persistent adoption gap, not a treatment effect.

Captures intended ADT duration and recommendations, not delivered therapy or adherence. Single-state consortium limits generalizability, and there is no efficacy or outcome endpoint.

Descriptive practice-pattern audit (no efficacy endpoint); reinforces AUA/ASTRO ADT guideline and STAMPEDE M0 as benchmark, documenting under-adoption rather than testing a new effect.

Phase 3 noninferiority RCT, 1:1, N=2766 enrolled (2540 per-protocol), 67 sites across 5 countries; median follow-up 46.8 mo. Reports the prespecified secondary RFS; primary OS not yet reported.

cN0 T1-T3 breast cancer with 1-2 sentinel-node macrometastases (>2mm). Extends eligibility beyond Z0011 to mastectomy, T3, extracapsular extension, and men.

Nodal RT including nodal target volumes reached 89.9% (SNB-only) and 88.4% (cALND). ALND omission was therefore tested within regional nodal irradiation, not as omission of axillary treatment.

Primary: overall survival (not reported in source). This analysis: prespecified secondary recurrence-free survival, per-protocol and modified ITT.

Noninferiority met: the upper confidence bound stayed below the prespecified 1.44 margin (P<0.001) across 191 recurrence-or-death events.

Consistent with Z0011 (breast-conserving + whole-breast RT) and AMAROS (axillary RT replacing ALND), both null for ALND benefit at 10 yr. SENOMAC adds the macromet-only, mastectomy/T3/ECE/male groups in a larger cohort.

This is the secondary RFS endpoint, not the OS primary, at a 46.8-mo median follow-up short for ER+ biology. The HR 1.44 noninferiority margin is generous, and ~90% nodal RT confounds attribution to surgical omission alone.

Randomised phase 3 noninferiority; prespecified secondary RFS met, extends Z0011/AMAROS de-escalation to mastectomy/T3/ECE/men. Primary OS not yet reported.

Phase 3 open-label RCT, 1:1, SWOG/NRG; N=403 eligible (201 S / 202 AS). Stopped at first interim for futility on OS and PFS. Median follow-up 12 mo (0.03-49).

T1-3N0M0 NSCLC ≤7cm, medically inoperable or declined surgery, ≥1 recurrence risk factor (diameter ≥2cm, SUV ≥6.2, moderate/poor/undifferentiated). Median age 73, median tumor 2.3cm, 89% ECOG 0-1.

SBRT both arms (SoC backbone): 3-8 fractions, BED ≥100 Gy. Stratified by central vs peripheral, <4 vs ≥4cm, PS 0-1 vs 2.

Atezolizumab 1200mg IV Q3wk ×8 (neoadjuvant, concurrent, adjuvant); SBRT initiated at cycle 3.

Primary: overall survival. Secondary: PFS, failure patterns, toxicity, QoL. 1-sided stratified log-rank at 2.5%.

G≥3 AEs 12% AS (21 G3, 1 G4, 1 G5 respiratory-failure death) vs 2% S. Excess toxicity with no efficacy gain.

Prior randomized phase 2 (**PMID 37478883, I-SABR, nivolumab+SBRT) suggested benefit adding IO; S1914 with atezolizumab does not confirm** and shows harm signals.

Open-label; stopped early at interim (median f/u 12mo, only 49 deaths). Former/never-smoker harm is an exploratory subgroup; central review of local recurrence ongoing.

Phase 3 stopped for futility; adding IO to SBRT gave no OS/PFS benefit and excess toxicity, reaffirming SBRT-alone SOC and not confirming the prior phase 2 signal.

Prospective nationwide population-based cohort, N=4541, 6 RT centres, treated 2007-14. IMNI assigned by tumour laterality: right-sided → IMNI, left-sided → no IMNI. Median follow-up 13.7 yr.

Node-positive breast cancer, including the 1-3 positive-node low-burden group. Excluded prior malignancy, bilateral cancer, neoadjuvant systemic therapy, pre-RT recurrence, non-standard RT.

Modern systemic backbone: taxane chemotherapy, trastuzumab, aromatase inhibitors, the era hypothesized to shrink absolute IMNI gain.

3D-based RT. IMNI delivered to right-sided tumours only; laterality allocation balances cardiac dose. Dose/fractionation not reported in source.

Primary: overall survival. Secondary: breast cancer mortality, distant metastasis.

IMNI improved all three endpoints (see table). Absolute 15yr OS gain 4.2% (65.0% vs 60.8%).

Confirms DBCG IMN1 (+4.7% abs OS at 14.8 yr) and the EBCTCG meta-analysis (+3% abs 15yr survival, regional node RT); contradicts the negative Korean KROG 06-08 in the modern-therapy era.

Non-randomized: IMNI assigned by tumour laterality rather than randomization, so residual confounding is possible despite balanced baseline characteristics.

Large prospective laterality-allocated cohort, not randomized; confirms IMN1 + EBCTCG that IMNI benefit persists with modern systemic therapy. Non-random design caps it below practice-changing.

Multicenter retrospective cohort, Spain 2010-2022, N=369 treated with definitive TMT (maximal TURBT + concurrent chemoRT). Multivariable logistic regression for predictors of complete local response.

cT2-T4aN0M0 muscle-invasive bladder. Median age 76, 85.1% male. Node-positive and metastatic disease excluded by staging.

Image-guidance quality tracked with local control: weekly portal imaging predicted lower CLR (OR 0.35, p<0.001), favoring daily volumetric IGRT; VMAT showed a non-significant favorable trend. RT dose/fractionation not reported in source.

Concurrent chemoradiotherapy. 5-FU-based CRT predicted higher CLR (OR 4.9, 95% CI 1.1-22.1, p=0.038).

Primary: complete local response (CLR). Secondary: OS, CSS, recurrence patterns, salvage cystectomy.

CLR 63.7%. Disease progression 28.8% (local 10.1%, systemic 10.7%, combined 8.7%). Salvage cystectomy 9.7%.

Retrospective, non-randomised; CLR predictors exploratory and confounded by treatment era. No head-to-head vs radical cystectomy; RT technique detail and CLR-survival effect sizes absent from source.

Retrospective real-world European cohort; no randomised TMT-vs-cystectomy comparator. Reinforces guideline-recognized bladder preservation; predictor findings exploratory.

Systematic review (search date December 15, 2022) of EBRT series meeting prespecified HCC technical standards and reporting OS, followed by individual patient data solicitation from corresponding authors. Kaplan-Meier OS and RMST stratified by BCLC stage and treatment status; random-effects Cox for covariates.

N=4,913 EBRT-treated HCC pts across a multinational author network, median follow-up 5.0 years. Stratified as treatment-naive vs treatment-experienced; BCLC stage, tumor burden, performance status, and Child-Pugh class all captured at patient level.

EBRT delivered per each contributing series; the pooling filter was prespecified technical standards for HCC. Ablative dose was independently associated with reduced risk of death, but specific dose/fractionation schedules and the ablative-dose threshold are not reported in the source abstract.

Median OS 6.8 years for BCLC-0 and 4.6 years for BCLC-A; among treatment-naive pts not reached for BCLC-0 and 5.4 years for BCLC-A. On multivariable modeling, advanced BCLC stage, higher tumor burden, worse performance status, and Child-Pugh B/C raised mortality risk; ablative dose and more recent treatment year lowered it.

The authors position these OS figures as comparable with resection, thermal ablation, and other ablative locoregional therapies. That comparison is across literatures, not within a trial, so the usual selection differences (lesion location, vascular proximity, comorbidity burden) between an EBRT-referred and a resection-eligible population remain unadjusted.

No comparator arm: the resection/ablation equivalence claim is a cross-study inference. IPD came only from authors who responded, and the technical-standard filter selects for expert centers, both biasing toward better outcomes. Year-of-treatment effect confounds technique era with staging and systemic-therapy improvements.

The practical argument here is algorithmic placement: BCLC has historically routed early HCC to resection, ablation, or transplant with EBRT absent, and this is the largest patient-level dataset assembled to contest that omission. The treatment-naive BCLC-0 result matters most, since it isolates first-line EBRT from salvage-after-ablation-failure use.

Large multinational prospective-collected IPD across many sites with stage-stratified analyses, but non-randomised and no head-to-head comparator; supports EBRT's guideline-listed role rather than establishing it.

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.

Randomized, unblinded, phase 3 noninferiority trial across 278 sites in North America and 6 other countries. 2,354 randomized May 2011 to June 2014, 2,255 eligible for analysis. Median follow-up 7.3 years.

Higher risk of IBR after lumpectomy and axillary surgery. Median age 55 (IQR 47-64), 35.6% under 50; 96.8% invasive, 52.7% grade 3, 29.6% ER-negative, 16.3% node-positive, 16.7% LVI, 16.7% close (<2 mm) or focally positive margins. 61.8% received chemotherapy.

Concurrent arm: WBI 40 Gy/15F with concurrent boost 8 Gy/15F at 0.53 Gy per day. Sequential arm: WBI 50 Gy/25F (52.4%) or 42.7 Gy/16F (47.6%), then 12 Gy/6F (84.9%) or 14 Gy/7F. 3DCRT in 59%, photons in 73.8%; QART scored 92.8% of contours and 91.9% of dose plans per protocol or acceptable variation.

Primary: IBR as first recurrence, noninferiority defined as an HR upper 90% CI limit below 2.12. Secondary: DFS, OS, adverse events, and cosmesis (BCTOS, physician Global Cosmesis Score, blinded central digital photo review).

56 IBR events, 24 sequential and 32 concurrent. Noninferiority held on cause-specific hazards, Fine-Gray (HR 1.31, 90% CI 0.84-2.03), and against each sequential WBI fractionation separately; the triggered superiority test was not significant. 7-yr regional nodal recurrence 1.2% (95% CI 0.8-1.7) with no difference by arm, and no differences in DFS, DDFS, or OS.

Toxicity above grade 2 was uncommon, with no significant difference in grade 3-4 events (p=0.81); radiation dermatitis, fatigue, and breast pain were most prevalent. 3-yr excellent/good cosmesis by physician rating 85.9% vs 82.4% (p=0.34) and by central photo review 64.2% vs 72.0% (p=0.11).

IMPORT HIGH tested a simultaneous integrated boost in 15 fractions against a sequential boost in the same setting; its effect sizes are not in this source. This is the larger North American test of the same question, enriched for grade 3 and node-positive disease.

Unblinded. The noninferiority margin (HR 2.12) was set under a protocol redesign against an assumed 1.59% 5-yr IBR, and the point estimate favored sequential (HR 1.31) on 56 total events. Cosmesis response rates fell to 50.5% (physician) and 47.1% (central photo) by 3 years.

Randomized phase 3, prespecified noninferiority met at 7.3-yr median follow-up; wide NI margin (HR 2.12) and a point estimate favoring sequential keep it below practice-changing.