onc brain

Global single-arm phase II, registrational. Interim analysis, N=154 enrolled, median f/u 26.3 mo (range 2-36).

dMMR/MSI-H locally advanced rectal cancer. 144 pts had ≥12 mo f/u for investigator-assessed cCR12.

Dostarlimab 500 mg IV q3w for 9 cycles as monotherapy; chemotherapy, radiation and surgery reserved for non-responders.

Key endpoints: sustained cCR for 12 months (cCR12) after end of treatment by investigator and independent central review, and composite cCR12 (INV) + pCR.

cCR12 68% (INV) vs 47% (54/116) (ICR); composite cCR12+pCR 76%. Of 15 resected pts, 12 (80%) had pCR; no recurrences to date after cCR or pCR.

88% completed all 9 cycles. G≥3 immune-mediated AEs in 4 pts.

Post-TNT cCR is cited at 21-41% in LARC broadly; AZUR-1 exceeds that in a biomarker-selected group. It scales up the earlier small dostarlimab study that first showed durable cCR in dMMR LARC.

Investigator and central review diverge on cCR12, and ICR evaluability lagged because cCR was confirmed later. cCR12 is a surrogate for durable organ preservation; local regrowth risk beyond 3 years is unmeasured.

Durable cCR with no recurrences so far makes RT omission a realistic default question in dMMR LARC. Open: how long surveillance must run, and what salvage looks like for late regrowth.

Single-arm interim analysis without a randomised comparator; investigator vs central review cCR12 diverge, and durability beyond 26.3mo median f/u is unproven.

Randomized 2:1, open-label, multicenter phase II, N=85 (56 P+MDT, 29 MDT alone). Median follow-up 17.5 mo.

omRCC after prior nephrectomy, ≤3 metastases within 5 years of Nx or prior metastasectomy, candidates for MDT to all metastatic sites. Baseline characteristics reported as balanced.

Pembrolizumab 400 mg q6w × 9 cycles (1 year), first dose before MDT. Median cycles delivered 6.6.

MDT was SABR in 73% vs 72% and surgery in 23% vs 28%. Dose, fractionation and target definition not reported in source.

Primary: relapse-free survival. Secondary: distant RFS, local relapse, OS, safety; only safety secondaries are reported in the abstract.

Any AE 80% vs 21%, G3 7% vs 3%. P-related AEs 59%, led by hypothyroidism 23%; no G4/5.

KEYNOTE-564 established adjuvant pembrolizumab after Nx and for M1NED within 1 year of Nx. PE-PE moves that into unresected oligomets ablated by SABR or surgery, including relapse up to 5 years out.

No local vs distant relapse split, so the site of benefit is unknown. RFS assessor blinding not stated in an open-label trial, and 2 of the 9 planned cycles went undelivered at the median.

The RFS gain is large but rests on 35 events, with a CI upper bound of 0.92. It does not settle whether IO at MDT beats IO deferred to relapse, which is the comparison that decides treatment-free intervals.

Randomized phase II met its RFS primary, but N=85 with a 29-pt control arm, 17.5-mo median f/u, open-label, and only 2 deaths; abstract-only.

Phase II protocol, single cohort, N=109 assessable of 111 treated, 304 irradiated sites. Response assessed 4-6 wk post-RT then every 3 mo; median follow-up for pts in remission 7 mo.

Symptomatic recurrent B-cell indolent lymphoma; proven transformation and concurrent steroids or chemo excluded. Median age 62, median 2 prior regimens (range 0-11), bulky disease in 52% of pts with size data.

4 Gy as 2×2 Gy 48h apart (n=80) or 1×4 Gy (n=29), megavoltage photons or electrons. Target was the entire nodal area or the node with a 1.5 cm margin, involved sites only; 6 pts had total nodal irradiation.

in-field lymphoma control, response defined by local activity only, worst site counted. Secondary: TP (any progression) and TLP (in-field), Kaplan-Meier from first RT day.

ORR 92%, CR 61%, PR 31%. Median TP 14 mo, TLP 25 mo; CR pts TLP 42 mo. Re-treatment in 41 selected responders: RR 98%, CR 71%.

Toxicity virtually absent: one transient alopecia, one transient hyperpigmentation. Antiemetics for upper abdominal fields; allopurinol for bulky disease, no gout or tumor lysis.

Concordant with Girinsky et al (135 sites, 48 pts) on RR, CR and inferior bulky-site results, but 2yr local PFS in PR pts 46% there vs 10% here. FORT later tested this low-dose approach against conventional-dose RT in a randomized design.

Comparison with pts' own prior regimens is historical and confounded by line of therapy, with power falling as numbers drop. Prognostic CR signals (≤2 sites P=.01, ≤5 cm P=.006) sit amid many tests; mixed target-volume definitions left to physician discretion.

A local, repeatable, near-toxicity-free option for systemic disease, with response rates matching first-line systemic therapy in this cohort. It does not settle whether 4 Gy matches conventional dose for durability, particularly in PR or bulky sites.

Single-cohort phase II, no randomized comparator vs conventional-dose RT or systemic therapy; within-patient historical comparison, 7-mo median follow-up in remitters.

Phase 2, nonblinded, randomized noninferiority trial at one institution, 1:1, N=160 (81 SBRT, 79 MFRT). Stratified by tumor size, bone site and number of sites irradiated. Enrolled September 2014 to June 2018.

Pathologic cancer diagnosis, painful bone mets (score ≥2 of 10), age ≥18, life expectancy >3 mo; up to 3 fields allowed. Excluded prior RT to the site, untreated cord compression, pathologic fracture at the site, and recent radioisotope.

SBRT 12 or 16 Gy x1 by lesion size (4 cm cutoff) vs 30 Gy in 10 fx. PTV = GTV + 5 mm, no CTV; 2D/3D, IMRT or VMAT delivery. Prophylactic 7-day low-dose dexamethasone recommended for SBRT only.

Primary: pain response by international consensus criteria (pain score plus MED), noninferiority margin 10%. Secondary: MDASI QoL, CTCAE toxicity, local control, OS.

No toxicity differences between arms. G3 fatigue 9.9% vs 5.1% (P=.37), fracture 1.2% vs 0% (P=.99); MDASI scores improved in both arms without a difference.

Prior randomized trials found no pain difference between single and multifraction conventional courses, with more retreatment after 8 Gy. RTOG 9714 and the Dutch Bone Metastasis Study are the conventional-dose trials behind that equivalence. This trial escalates the single fraction but never tests it against 8 Gy.

Dexamethasone given asymmetrically to SBRT pts confounds early pain response. The 16 vs 12 Gy contrast is non-randomized and tracks lesion size. Five SBRT pts did not receive treatment due to insurance denial, and median OS of 6.7 mo leaves few pts at risk for late local failure.

The ITT data support noninferiority and a local-control advantage for SBRT; the superiority read depends on per-protocol denominators. The live question is 16 Gy vs 8 Gy in pts selected for longer survival, which needs a phase 3.

Single-institution randomized phase 2 with one-sided alpha 0.20; superiority signals are per-protocol amid heavy attrition, comparator 30 Gy/10 rather than 8 Gy. Authors call for phase 3.

Randomized phase II, 1:1, 3 institutions (MD Anderson, London Health Sciences Center, University of Colorado); unmasked. Closed early by DSMB after 49 of 74 enrolled pts were randomized (94 planned). Median follow-up 38.8 mo (28.3-61.4).

Stage IV NSCLC, ≤3 metastases (primary not counted), ECOG ≤2, no progression after front-line therapy: ≥4 cycles platinum doublet, or ≥3 mo EGFR TKI or crizotinib. Randomization dynamically balanced on met number, response, CNS mets, N stage and EGFR/ALK status.

LCT was RT, surgery or both to all active disease sites, modality chosen by MDT; concurrent chemoRT allowed for primary and regional nodes. Dose and fractionation not reported in source text (Appendix Table A1).

Primary: PFS from randomization. Secondary: OS, toxicity, time to new lesions. Powered (90%) for PFS 4 to 7 mo, HR 0.57; P<.10 deemed significant.

PFS, OS and survival-after-progression gains in the arm table above. Late LCT at progression correlated with OS in a multivariable model, HR 0.44 (0.18-1.06), P=.064; initial LCT HR 0.30 (0.12-0.75).

No additional grade ≥3 toxicity beyond events reported in the initial publication.

The authors state no prior randomized trial had shown an OS benefit from LCT in lung cancer. They align their proposed oligometastatic definition (0-3 metastases, unconstrained by molecular profile) with most pts enrolled on SABR-COMET and the UT Southwestern randomized phase II trial, and point to NRG-LU002 as the phase III test.

Unmasked with heterogeneous physician-chosen maintenance. Post-progression and late-LCT analyses are exploratory, post-randomization, and exclude 3 MT/O pts who crossed over before progression. EGFR/ALK cohort n=8, too small to read.

The OS gain is carried by survival after progression, consistent with a window in which all sites are still treatable. Whether the effect survives IO maintenance and a full-size trial is unsettled.

Randomised phase II closed early for PFS benefit at 49 of 94 planned pts; OS is secondary and tested at P<.10. Needs phase III confirmation (e.g. NRG-LU002).

Prospective, randomized phase II, 1:1 allocation after neoadjuvant chemo. 102 pts targeted and enrolled, anticipating a 15% drop out before surgery; 4 withdrew after enrollment. Median follow-up among all enrolled pts 3.4 [2.6, 5.1] years.

Resectable, borderline, or locally advanced (LA) type A PDAC, ECOG 0-2, > 1 month of neoadjuvant chemo. Median age 65 (34-82); 38%/42%/20% resectable, borderline, and LA type A. Prior chemo was FOLFIRINOX (79%), gemcitabine/nab-paclitaxel (12%), or other (9%), with 92% receiving more than 2 months.

Chemo-RT: 50.4 Gy/28 fractions with weekly gemcitabine or capecitabine. SBRT: 25 Gy/5 to elective nodes and 33-40 Gy in 5 to the primary, without concurrent chemo. Most SBRT pts were treated using 1.5 T adaptive MRI guidance.

Primary: pathologic node positivity, hypothesizing lower rates with chemo-RT. Secondary: PFS, OS, patient-reported QOL (PROMIS), physician-reported toxicity, surgical complications, translational endpoints.

Arm-level figures are in the table. 83/98 (84.7%) completed all intended therapy including surgical resection, equal in both arms.

No difference in surgical complications; no rates given. Physician-reported toxicity was a secondary endpoint but is not reported in the abstract. PROMIS physical function, global physical health, and fatigue were better preserved with SBRT (p = < 0.05).

Alliance A021501 tested preop SBRT or hypofractionated RT against chemotherapy alone, and PREOPANC established gemcitabine-based preop chemo-RT against upfront surgery. Neither compared one RT schedule with another. The authors describe this as the first randomized trial comparing SBRT with chemo-RT in the neoadjuvant setting for PDAC.

Abstract only: no per-arm allocation counts, no QOL magnitudes or timepoints, and no figures for pathologic response or margin negativity despite the conclusion citing them. QOL is patient-reported in an unblinded comparison. Concurrent agent varied in the chemo-RT arm and primary SBRT dose ranged 33-40 Gy.

The trial shows SBRT is deliverable preop with equal resection completion and better QOL, and it does not show nodal sterilization differs. It does not settle survival equivalence: median OS 26.04 vs 42.96 mo and LRR 6 vs 2 point the same direction in a sample too small to resolve them.

Randomised phase II, N=102, built to show chemo-RT superiority on nodal positivity and null. Not an equivalence design; survival and LRR lean numerically toward chemo-RT.

Multicenter randomized phase II, 192 pMMR LARC pts enrolled. Initial results as of January 31, 2026 cover the 148 who completed treatment (70 in Group A, 78 in Group B). Allocation ratio, stratification and follow-up duration are not stated in source.

pMMR LARC, T3-4/N+ M0. Baseline characteristics described as balanced. 96.6% (143/148) had at least one high-risk feature: low tumor location, cT4, cN2, MRF+ or EMVI+.

Group A: 6 cycles of CAPOX plus toripalimab. Group B: SCRT followed by the same 6 cycles. cCR pts were offered W&W, non-cCR pts were recommended for surgery.

SCRT 25Gy/5Fx before immunochemotherapy in Group B. Group A received no neoadjuvant RT, with adjuvant chemoradiotherapy reserved for positive circumferential margins. Target volumes, technique and the interval from SCRT to response assessment are not reported in source.

Primary: complete response rate, defined as pCR plus cCR. Secondary: organ preservation rate, anorectal function, adverse events and survival outcomes.

Thrombocytopenia was the most common grade 3-4 AE, 12.9% in Group A and 14.1% in Group B. No other AE data, and no RT-attributable or surgical toxicity, are reported in source.

TORCH, the same group's predecessor, tested induction vs consolidation sequencing of SCRT with CAPOX and toripalimab; this trial asks instead whether SCRT can be dropped. UNION set SCRT followed by immunochemotherapy against long-course chemoradiotherapy. PROSPECT asked the RT-omission question with chemotherapy alone in a lower-risk population than the one enrolled here.

cCR criteria and the assessment timepoint are not stated, and cCR calls cannot be blinded to arm. The pCR denominator in Group B excludes the 25 cCR pts who went to W&W, so resected-only pCR is not a like-for-like comparison. No chemotherapy-alone arm, so toripalimab's contribution is unmeasured.

The gap in CR is carried mostly by clinical responses, which is the outcome that matters for W&W and also the softer of the two components. The rationale for the no-RT arm was functional sparing, yet 58 of 70 Group A pts went to surgery vs 52 of 78 in Group B, and anorectal function is not yet reported. Regrowth after W&W will decide whether the cCR advantage holds.

Initial results in 148 completers of 192 enrolled; no p-value or CI; CR is an early response endpoint, and organ preservation, function and survival readouts are pending.

Prospective, multi-institutional, single-arm phase II. 63 evaluable pts with 70 lesions from 7 institutions, treated 4/2019-9/2025. Median follow-up after RT 186 days.

Multiple myeloma with an uncomplicated painful bone lesion. Median age 66, 49% female, 89% ECOG 0-1, 79% prior chemo (median 1 line), 40% prior RT to a different area. Median baseline BPI 4.8.

4Gy total, delivered as 2Gy x 2 or 4Gy x 1 (29% received 4Gy x 1). Reirradiation with a clinician-choice regimen could be considered at 4 weeks after initial treatment for inadequately controlled pain (the inequality symbol is garbled in the source). Target volume and technique not stated in source.

Primary: proportion with self-reported pain response at 4 weeks. Response was scored on average BPI and oral morphine equivalent dosing per the International Consensus on Palliative RT, assessed at 4 weeks, 8 weeks and 6 months.

Response rates by timepoint are in the table. Median BPI and OMED decreases were 2.25 and 5mg at 4 weeks and 2.75 and 6.2mg at 8 weeks. Median time to pain relief was 36 days, median duration 148 days, with no difference by fractionation.

No grade 3+ treatment-related toxicity. Lower-grade events and hematologic toxicity are not reported in the source, although marrow sparing was the stated rationale.

The source states there is no consensus on the most effective palliative dose in MM. The ultralow-dose concept comes from indolent lymphoma, where FoRT tested it against a conventional dose. With no comparator arm here, the 59% at 4 weeks cannot be ranked against conventional palliative fractionation.

Missing assessments grow from 2/70 at 4 weeks to 25/70 at 6 months, and reasons are not given, so the late per-protocol rates are vulnerable to informative dropout. Handling of reirradiated lesions in the 6 month response is not stated. Pain response is self-reported in an unblinded single-arm design.

Best read as a strategy: 4Gy first, escalate on failure. A 63% response at 4 weeks after reirradiation suggests the low first dose did not obviously compromise salvage, at the cost of time (median 95 days to relief after reRT). It does not settle whether 4Gy matches conventional dosing up front, or whether it spares marrow.

Single-arm phase II, 63 pts, no comparator against conventional palliative fractionation; late responses rest on a per-protocol denominator with 36% non-completion at 6 mo.

Investigator-initiated randomised phase II, 1:1, two Danish centres, no stratification. N=100 randomised Jan 2019 to Dec 2024; mITT 92. Open-label, with masked 1° endpoint imaging review.

1-3 CRLM, each ≤4.0 cm, Child-Pugh A, liver volume ≥700 mL, no prior liver RT. MDT-deemed suitable for both MWA and SBRT; limited extrahepatic disease allowed if curative strategy feasible. Median lesion 1.2 cm; 78% had a single metastasis.

45 Gy/3 fx preferred, 50 Gy/5 fx when OAR constraints required, prescribed to the 67% isodose; PTV 10 mm craniocaudal, 5 mm radial. BED10 >173 Gy to GTV in all. 88% on MR-linac with daily online adaptation.

Primary: patient-level freedom from local progression of treated lesions (new lesions not events). Secondary: OS, treatment-related G3+ toxicity, late G2+ toxicity; EORTC QLQ-C30.

Acute G2+ 1 (3%) SBRT vs 13 (25%) MWA; G3+ only after MWA, 4 (8%) including one death from hepatic necrosis with capsular perforation. Liver pain G1 in 3 (7.5%) SBRT vs 25 (48%) MWA. QoL did not differ.

Authors cite MWA local control exceeding 90% and 1-yr SBRT LC ranging 50% to 95% in prior, largely retrospective series. Dose here clears Kang's BED10 >117 Gy threshold for ~90% 1-yr LC, so a dose deficit does not explain SBRT's result.

KRAS-mutant disease was 45% vs 24% in the MWA vs SBRT arms, with no molecular stratification; Hong reported KRAS-mutant 1-yr LC 43% vs 72%, a large enough modifier to move arm estimates. Single institutional network; post-protocol systemic therapy uncontrolled.

The trial gives the first randomised head-to-head data, not an equivalence claim; a null HR with CI 0.43-1.74 leaves room for either modality to be meaningfully better. What it settles more firmly is that SBRT avoids the invasive-procedure harms MWA carries.

Randomised but small phase II powered for HR 0.38, not equivalence; null 1° EP with wide CI cannot establish SBRT matches MWA. Toxicity underpowered.

Randomized, placebo-controlled, double-blind, parallel-group phase 2 (SPIRIT), 2 academic centers, 1:1, N=136. Enrollment May 2019 to last visit May 2025; target revised from 142 to 134 with DSMB concurrence.

Men ≥40 post-RP for organ-confined pT2N0M0, Gleason 3+3 or 3+4, preop PSA <10, undetectable PSA ≥2 yr. Hypogonadal (T <275 ng/dL and/or free T ≤70 pg/mL) plus low libido, ED, or fatigue. Mean age 68.6; 38% Gleason 6, 62% Gleason 7.

Testosterone cypionate 100 mg IM weekly × 12 wk vs placebo. Total T rose 349 ng/dL (95% CI 283-415) more than placebo; adherence 95% vs 94%.

Primary efficacy: change in sexual activity (PDQ question 4). Primary safety: biochemical recurrence (≥2 consecutive PSA ≥0.2 ng/mL). Secondary: desire, erectile function, affect, body composition, VO2 peak, stair-climb power.

No biochemical recurrence in either arm. Erythrocytosis in 3 TRT pts; SAEs 1 vs 3; no MACE or VTE. One TRT pt had detectable PSA 0.1 to <0.2 ng/mL during treatment.

Described by the authors as the first randomized placebo-controlled trial of TRT in prostate cancer survivors; prior support for TRT after RP rested on observational series. Many guidelines still list prostate cancer history as a TRT contraindication.

Baseline recurrence risk in this cohort is so low that 0 vs 0 BCR carries little information about harm. Erectile function did not move despite EPIC-26 gains, and no P value adjustment was made across secondaries.

The efficacy case for TRT in this population is now randomized and exceeds the MCID. The safety case remains a short-horizon absence of events, which justifies a larger long-term trial rather than settling the contraindication.

Efficacy primary met in a clean double-blind RCT, but the question that gates practice (oncologic safety) is untestable at N=136 and 12 wk; authors frame it as proof-of-concept.

Prospective randomized phase 2, 1:1, N=106 (55 SIB-CRT, 51 CRT), accrued August 2013 to February 2015. Median follow-up 116.6 months, which is the study's real asset.

Stage II/III rectal adenocarcinoma. Radical surgery planned 6 to 8 weeks after chemoradiotherapy. Perioperative chemotherapy was not randomized, and its receipt defines the subgroup that carries the result.

Both arms received 50 Gy/25 fx to the pelvis. The experimental arm added a simultaneous integrated boost of 56 Gy to PGTV and 60 Gy to lateral metastatic nodes where present, so the escalation targets gross primary and involved lateral nodes rather than the elective volume.

Primary: pCR rate. Secondary: DFS, OS, MFS, LC, CSS and toxicity. Every result the conclusion rests on is secondary.

Acute grade 3 toxicity 14.5% (SIB-CRT) vs 19.6% (CRT), primarily radiation dermatitis. Late toxicity is not reported in the source, which matters most for a boost delivered near bowel and for pts followed nearly a decade.

Neoadjuvant dose escalation in LARC has repeatedly raised pCR without translating to survival; this trial reports the mirror image, a null pCR (15.2% vs 18.4%) with survival separation. The result also sits against the TNT era, where systemic intensification rather than RT dose is the current lever, and the chemo-receiving subgroup here showed no additional benefit.

The survival claim is a secondary-endpoint result from 51 vs 55 pts, so a handful of events moves each HR, and no confidence intervals are reported in the source. The driving subgroup is defined by non-randomized chemotherapy receipt, and the higher rate of curative treatment in the SIB arm (89.1% vs 78.4%) is itself a plausible route to the OS difference independent of dose.

A pelvic boost has a defensible mechanism for LC 87.1% vs 70.1% and essentially none for MFS 70.8% vs 47.2%. The authors attribute the distant benefit to intensified control of micrometastases; the simpler reading is that a small trial with a large curative-treatment imbalance produced correlated secondary endpoints.

Randomized phase 2, N=106, primary endpoint (pCR) missed; survival gains are secondary endpoints with wide implied precision and a non-randomized chemo subgroup driving them.

Randomized phase II, 1:1, stratified by tumor location, permuted blocks, not masked. Enrolled Feb 2020 to Apr 2023; 55 randomized, 51 analyzed (25 vs 26). Survival and subgroup analyses were unplanned and exploratory.

Early-stage NSCLC (AJCC v8), ECOG 0-2, unable or unwilling to undergo surgery; recurrent NSCLC eligible. Excluded RT within 2 yr and systemic therapy within 1 yr prior or 6 mo after. Median age 74 both arms.

45-60 Gy in 5 fx (majority 60 Gy/5), IMRT or VMAT, 4DCT ITV plus 5mm radial / 8mm sup-inf PTV margin. Optimized plans met standard RTOG 0813/0915 criteria while minimizing dose to heart, great vessels, thoracic spine and lymph-node-stations, contoured to a 40 cGy/fx low-dose envelope.

Primary: in vivo lymphocyte depletion at end of treatment, 4 wk and 6 mo; safety/toxicity (co-primary). Algorithm performance reported separately. OS and EFS descriptive only.

Central tumors drove the effect (29.5% overall ALC improvement, p=0.004); peripheral PTV <20cc showed no difference. G3 lymphopenia 0% vs 15.4% (p=0.04).

G3 AEs 2 (lung infection) optimized vs 4 standard (dyspnea, hypoxia, lung infection); all recovered. No G2+ pneumonitis or G4+ events in either arm.

Both arms sat inside RTOG 0813/0915 planning criteria, so the comparison isolates immune-OAR avoidance on top of current SBRT constraints. Prior lymphopenia-outcome links in thoracic RT are largely associative; this is a randomized test that planning alone moves ALC.

Arm imbalance in central (36.0% vs 23.1%) and treatment-naive (64.0% vs 88.5%) pts biases the survival comparison. Tx-naive OS reported as 93.4% and 94.1% in different sections. LN V5 OS split is a non-randomized dosimetric stratification.

Establishes feasibility and an ALC effect, not a clinical one. Whether sparing lymphocytes during SBRT translates to EFS/OS, or to better IO response when combined, needs the multi-institutional powered trial the authors call for.

Preprint, small randomized phase II with unmasked lymphocyte surrogate primary; survival analyses unplanned and unpowered. Arm imbalance in central and treatment-naive pts.

Investigator-initiated phase 2 nonrandomized trial across 21 centers (community, regional, academic), enrolling Jan 2008 to Apr 2010. 310 evaluable pts, median age 68, median follow-up 9 yr. Kaplan-Meier estimation with log-rank comparison of LR vs IR.

172 low-risk (T1b-T2a, Gleason 6, PSA under 10) and 138 intermediate-risk (T1b-T2b, Gleason 7 or Gleason 6 with PSA 10-20), all confirmed by central pathologic review. IR pts subclassified favorable vs unfavorable by MSK criteria. Prostate volume up to 100 cc allowed; prior TURP and baseline AUA score were not exclusions.

40 Gy in 5 fractions (8 Gy x 5, equivalent to ~100 Gy at 2 Gy/fx assuming a/b = 2) on a noncoplanar robotic platform. Fiducial tracking with translational and rotational intrafractional motion correction was mandatory. Androgen suppression was not allowed, so the outcomes are RT-attributable.

Relapse defined as biochemical failure (nadir + 2), clinical failure, or administration of any salvage, antiandrogen, or systemic therapy. Late toxicity was physician-reported, CTCAE v3, events beyond 3 mo. Day 0 was the last day of treatment.

10-yr OS 84% (76-91). Freedom from local failure 96% (93-99) overall. The separation that matters is within IR: favorable 92% vs unfavorable 77%, p = 0.002, whereas LR vs IR overall was not significant (p = 0.19).

Four pts had five grade 3 events, all GU, and no grade 4-5 events occurred. Cumulative 10-yr grade 3 rates were 1.4% LR and 1.5% IR, far below the 10% rate the trial deemed acceptable. Grade 2+ GU 14% exceeds grade 2+ GI 2.1% by roughly sevenfold; no new late grade 3+ events after year 5.

IR relapse-free survival (86%) sits above the 74-78% 10-yr RFS of dose-escalated EBRT in RTOG 0126, and the authors note an updated HYPO-RT-PC now shows superior 10-yr RFS in the 6.1 Gy x 7 arm. Toxicity matched Fuller's CyberKnife trial but was lower than the PACE-B SBRT arm and PATRIOT, both of which treated substantial fractions on a conventional linac.

The toxicity advantage over PACE-B and PATRIOT is confounded by platform, and the sponsor makes that platform, so the comparison cannot separate tracking from delivery-era and case-mix differences. Toxicity is physician-reported CTCAE only, with no patient-reported instrument, which understates GU bother relative to the EPIC-based comparators. Comparator EBRT series (RTOG 0126) predate modern IGRT.

The durability question, not the toxicity question, is what 10 yr answers here: two-thirds of relapses occurred between 5 and 10 yr, in this trial and in Fuller's. That timing means a 5-yr non-inferiority readout is structurally optimistic for both arms, and it reframes what PACE-B's 5-yr result can and cannot settle.

Single-arm nonrandomized phase 2, no concurrent comparator; sponsor-funded with device-specific delivery. Extends existing 5-yr SBRT data rather than testing a new question.

Multicentre phase 2 randomised open-label trial, 16 academic and community centres in Italy, 1:1 by random permuted blocks, stratified by centre, ECOG PS and number of metastases. Enrolment Jan 2, 2019 to Sept 7, 2022; median follow-up 53 months (IQR 43-60). ITT analysis.

Age ≥18 with prostate adenocarcinoma and metastatic castrate-resistant disease, no more than three metastatic sites, and no previous systemic therapy for the mCRPC state. N=157 (control 82, experimental 75). No race or ethnicity data collected.

Both arms received ADT plus oral abiraterone acetate 1000 mg daily. The experimental arm added SBRT; the systemic backbone was identical, so the contrast isolates the radiotherapy.

SBRT delivered to all sites of metastatic disease in one to five fractions at a biologically effective dose ≥100 Gy. Comprehensive ablative intent, not treatment of an index lesion.

Primary: 6-month biochemical response (PSA decline ≥50% from baseline), reported previously. After the primary was met the power calculation was updated post-hoc for overall survival, finalised before unmasking; this report is an unplanned long-term OS analysis.

Most common grade 3-4 events were infectious complications (five control, zero experimental) and cardiovascular disorders (three each). One treatment-related death, in the control group, from myocardial failure. No excess grade 3-4 toxicity attributable to SBRT in the reported events.

STOMP and ORIOLE established MDT in hormone-sensitive oligometastatic disease without a systemic backbone, and SABR-COMET tested SABR across mixed histologies. ARTO is the randomised test in castrate-resistant disease with an ARSI given to both arms, which is the setting those trials leave open.

Open-label with no sham, and the OS power calculation was revised after the primary read, so the alpha spent on this comparison is not the trial's original design. The experimental median is not reached, meaning the reported HR rests on a control-arm curve that is itself only partly mature at 53 months.

A survival signal from comprehensive ablation on top of a modern ARSI backbone is the strongest randomised argument yet that MDT in CRPC is doing more than delaying PSA progression. What it does not settle is whether the benefit tracks the ablative dose, the completeness of coverage, or simply the favourable biology of pts whose disease stayed oligometastatic into castration resistance.

See the OS figures above; per-arm event counts beyond the medians and HR are not reported in source.

Randomised phase 2, but the OS analysis is unplanned with post-hoc power revision and the primary endpoint was 6-month PSA response. N=157.

Prospective, single-group, phase 2 nonrandomized trial across 9 tertiary sarcoma centers in Europe and the US. Enrollment ran November 2010 to May 2020; data analyzed January to December 2025. Median follow-up 66.4 months (IQR 48.8-87.5).

Adults with biopsy-proven and translocation-confirmed localized myxoid liposarcoma of the trunk or extremity. N=90, mean age 47 (SD 13.1), 50 (56%) male.

Preoperative RT to a reduced dose of 36 Gy in once-daily 2-Gy fractions, followed by resection. Delivered per protocol in all patients. Three pts (3%) did not proceed to surgery because of intercurrent metastatic disease.

Long-term local recurrence-free survival, progression-free survival, disease-specific survival, overall survival, and late toxic effects. No single stated primary endpoint for this long-term analysis.

Wound complications in 18 pts (21%), with 14 (16%) requiring intervention. Late toxic effects were grade 2 in 13 pts (15%) and grade 3 in 3 pts (3%).

The authors argue the long-term data support adopting 36 Gy as an option through shared decision-making, explicitly on the grounds that a phase 3 trial is impractical in a rare cancer. That is an argument about feasibility, not about evidence level, and the reader should price it as such.

Fourteen-year accrual window spans changing surgical and imaging practice, so the wound complication rate reflects a long era rather than current technique. Late toxicity is reported only as pooled grade counts, without organ or site attribution, which limits comparison against 50 Gy series.

Single-arm phase 2, no randomised 50 Gy comparator; authors concede phase 3 impractical in a rare histology. Long f/u strengthens but does not replace randomisation.

Single-institution, parallel-cohort, open-label randomized trial across four Emory-affiliated centers, enrolling June 2020 to 2024. ADT-eligible pts randomized 1:1 relugolix vs leuprolide, stratified by ASCVD 10-year risk score; a parallel prospective RT-alone cohort was enrolled as control.

94 men with non-metastatic prostate cancer, intermediate and high risk, all treated with pelvic radiotherapy to the prostate with or without pelvic nodes. Lower-risk men eligible for definitive RT alone without planned ADT formed the parallel arm.

Relugolix 360 mg day 1, then 120 mg daily; leuprolide in 3-month depots. ADT given for at least six months, longer by cancer risk tier.

All pts received pelvic radiotherapy to the prostate with or without the pelvic lymph nodes. Dose, fractionation and technique are not reported in source.

Primary: change in total plaque volume. Secondary: changes in plaque subtypes (non-calcified, calcified, low-attenuation). Serial CCTA at baseline (within 7 days of treatment start) and 12 months, blinded to arm, quantified by the automated HeartFlow tool; 12-month mean difference by ANCOVA adjusted for age, statin use and baseline plaque volume.

The adjusted total-plaque-volume difference of 68.9 mm³ favouring relugolix was driven mainly by non-calcified plaque; calcified and low-attenuation plaque showed no significant difference with low absolute change. Per-arm CIs and p-values are not reported in source.

HERO (2020) showed a lower MACE rate with relugolix vs leuprolide and drove the FDA approval, but offered no mechanism, since both agents suppress testosterone comparably and share the hypogonadal metabolic profile. REVELUTION supplies the candidate mechanism, accelerated coronary atherosclerosis under GnRH agonism, consistent with the 2010s observational signal that agonists carry higher cardiovascular risk than orchiectomy.

The imaging endpoint is validated as a predictor of MACE, not a substitute for it, and 12 months is short for plaque trajectories. The parallel RT-alone cohort was not randomized against either ADT arm, so the no-hormone comparison is observational and cannot isolate radiotherapy's own contribution to plaque change.

If the agonist-antagonist difference is real and mechanistic, the decision it moves is which ADT agent accompanies definitive RT in a man with baseline cardiovascular risk, not whether to give ADT at all. It does not establish that changing agent prevents events; that inference still rests on HERO.

Small single-institution randomized trial with an imaging surrogate (plaque volume), not clinical MACE. Supplies a mechanism for HERO rather than independent outcome evidence.

Multicenter randomized phase 2, 1:1 allocation, N=157 enrolled January 2019 to September 2022. Median follow-up not reported in source.

Oligometastatic castrate-resistant prostate cancer, defined as three or fewer nonvisceral metastatic lesions. Visceral disease excluded by definition.

Both arms received abiraterone acetate and prednisone (AAP). The experimental arm added concomitant SBRT, so AAP is a fixed backbone and the randomized contrast is radiotherapy alone.

SBRT to all sites of disease, delivered concomitantly with AAP. Dose, fractionation and target-volume detail are not reported in the source text, which gates how directly the result transfers to a given SBRT practice.

Primary: biochemical response, PSA decrease ≥50% from baseline at 6 months. Secondary: complete biochemical response (PSA <0.2 ng/mL at 6 months) and progression-free survival. No survival endpoint reported.

No toxicity reported in source, so the added burden of ablating up to three lesions is unquantified. PSA endpoints are mechanically sensitive to removing PSA-producing deposits, and the 6-month timepoint precedes any durability read.

STOMP and ORIOLE established the randomized signal for metastasis-directed therapy in hormone-sensitive oligometastatic disease. ARTO's addition is that the signal persists on an ARSI backbone in castration-resistant disease, a setting those trials did not test.

The PFS HR 0.35 is the more meaningful of the two results, since it is less mechanically coupled to ablating PSA-producing lesions than the primary endpoint. What remains unsettled is whether deferring progression on an ARSI translates into anything durable, which a phase 2 sized for a 6-month PSA readout cannot answer.

Randomized phase 2 with a 6-month PSA surrogate primary endpoint; no OS, no reported toxicity, and phase 3 confirmation in CRPC is absent.

Phase 2, 2-arm randomized trial across 3 US radiation facilities affiliated with one university hospital. 80 men screened, 54 randomized 2:1 to SABR or observation, accrual May 2016 to March 2018, data cutoff May 20 2019. Median follow-up 18.8 months (range 5.8-35.0).

Recurrent hormone-sensitive prostate cancer with 1 to 3 metastases detected on conventional imaging (CT, MRI, or bone scan), asymptomatic, arisen within the prior 6 months, no larger than 5.0 cm. Prior definitive treatment of the primary required; salvage prostate-bed or pelvic RT allowed. No ADT within 6 months of enrollment or 3 or more years total. Median age 68 in both arms; Gleason grade ran higher in the observation arm (mean 8 vs 7).

SABR to metastatic sites, with treatment planning blinded to PSMA-PET, so PET-avid lesions outside the conventional-imaging map were left untreated in 16 of 36 SABR pts. Dose and fractionation are not reported in the source text. Local control 98.9% at 6 months.

Primary: progression at 6 months, a composite of PSA rise, radiographic progression on conventional imaging, symptomatic progression, ADT initiation for any reason, or death. Secondary: SABR toxicity, 6-month local control, PFS, Brief Pain Inventory QoL, and concordance between conventional imaging and PSMA-PET.

No grade 3 or higher adverse events in either arm. No differences in Brief Pain Inventory scores between arms or within either arm over time.

Sits alongside STOMP, the other randomized trial of metastasis-directed therapy versus surveillance in oligorecurrent hormone-sensitive disease, and reaches the same directional conclusion from an independent population. What ORIOLE adds is the PSMA-PET consolidation question, which STOMP's choline-PET-selected design could not isolate.

The composite primary is driven partly by ADT initiation for any reason, a clinician decision made without blinding in an open trial, so the treating team's knowledge of arm allocation can move the endpoint directly. The PET-untreated-lesion comparison is a within-arm post-randomization subgroup (19 vs 16 men), not a randomized contrast, and the men whose conventional imaging missed more disease plausibly had more disease to begin with.

The trial makes two distinct claims and they carry different weight. That SABR beats observation on a 6-month composite in a 54-man phase 2 is a signal, not a standard; that leaving PSMA-avid disease untreated tracks with earlier and more distant failure is the finding that changed how the field plans these treatments, even though it rests on an observational contrast inside one arm.

Phase 2, N=54, 6-month composite primary including ADT initiation, median f/u 18.8mo. Hypothesis-generating for MDT; no OS or definitive endpoint.

Prospective multicentre cohort, N=848 across 17 Dutch centres, accrued 2011-2015, presented at EBCC15 with 10-year follow-up; 838 completed follow-up. Not randomised: every patient received the RT volume their risk group assigned.

Breast tumour under 5 cm with 1 to 3 involved lymph nodes at presentation, treated with neoadjuvant chemotherapy then surgery (BCS or mastectomy). Most underwent axillary lymph node dissection.

Volume was set by post-chemotherapy nodal status. ypN0: breast RT after BCS, none after mastectomy. ypN1: breast or chest wall only, regional nodes omitted. ypN2+: breast or chest wall plus regional nodal irradiation. Dose and fractionation are not reported in source.

24 of 838 (2.9%) had a locoregional recurrence without distant spread at 10 years. Per-group counts appear in the detail table; the rates do not separate across strata.

The randomised test of this exact question is NSABP B-51/RTOG 1304 (NCT01872975), which the investigators expect in about 3 years; until then no trial has randomised ypN0 pts to nodal RT versus omission. Prior nodal-RT evidence (MA.20, EORTC 22922) was built in upfront-surgery populations, so it cannot arbitrate a post-chemotherapy response-adapted rule.

The 2.9% rate is uninterpretable without a comparator: a low event count in a de-escalated cohort is equally consistent with the omitted RT having been unnecessary and with the cohort being low-risk to begin with. ALND staging also means the ypN0 label carries more information than a modern sentinel-node ypN0 does.

The finding that recurrence is flat at 2.4% / 3.2% / 2.8% across escalating risk is the intended signal: the added RT in the higher strata may be doing the work that keeps them level with the low-risk group. It does not settle whether the low-risk group needed any RT, only that the allocation rule did not produce a visible failure.

Single-arm prospective cohort with no randomised comparator; allocation used ALND-era nodal staging. Confirmatory randomised answer (NSABP B-51) still pending.

Non-randomised phase 2, eight hospitals in Australia and the Netherlands, run by TROG and ANZUP. Enrolment July 28 2016 to Feb 27 2020; 71 enrolled, one withdrew consent before treatment. This report is the pre-planned final follow-up at a median of 62 months (IQR 60-72).

Histologically confirmed primary RCC, medically inoperable, high risk, or declined surgery, ECOG ≤2, tumours ≤10 cm, N0-N1. Median age 77 years (70-82), 49 (70%) male. Median tumour size 46 mm (37-55), with 39 (56%) T1b, six (9%) T2a and one (1%) T3a.

Size-adapted prescription: 26 Gy in a single fraction for tumours ≤4 cm, 42 Gy in three fractions 48 h apart for tumours >4 cm. Histological confirmation was required before treatment, so this is a biopsy-proven cohort rather than a radiographic-diagnosis one.

Primary: freedom from local progression by RECIST, assessed in the intention-to-treat population, as was safety.

100% local control at 36, 60 and 84 months, with no local recurrences and no cancer-related deaths reported in the cohort.

Seven (10%) patients had at least one treatment-related grade 3 event within 9 months: pain in four (6%), nausea and vomiting in three (4%), colonic obstruction in two (3%), diarrhoea in one (1%). No grade 4 events and no treatment-related deaths; no new long-term safety signals emerged with extended follow-up.

A 100% point estimate in 70 pts carries a wide confidence bound that the headline hides, and RECIST is an imperfect local-control instrument after ablative RT, where a treated mass commonly persists without viable tumour. Renal function trajectory, the endpoint that actually competes with nephrectomy, is not reported in this source.

Prior SABR evidence in primary RCC was retrospective and pooled, so a prospective multicentre dataset at 84 months is the new contribution rather than the effect size itself. Comparison to partial nephrectomy and thermal ablation remains indirect: no randomised trial has run, and this cohort was selected against surgery by definition.

The finding that transfers is durability at a tumour size where thermal ablation performs worst, with a median of 46 mm and 65% at least T1b. What it does not settle is whether SABR is a choice rather than a fallback, which needs a randomised or matched comparison in operable pts, with renal function as a co-primary.

Single-arm phase 2, N=70, inoperable or surgery-declining pts only. No randomised comparator vs partial nephrectomy or thermal ablation. Maturity gate holds despite 62mo f/u.