onc brain

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.

Phase II randomized trial, 1:1, unmasked, single institution, accrual February 2020 to April 2023, database lock June 2024. 55 randomized, 4 withdrew or were ineligible, 51 analyzed (25 optimized, 26 standard). Randomization used permuted blocks of 2 and 4, stratified by tumor location.

Early-stage NSCLC, pathologically or imaging-confirmed, unable or unwilling to undergo surgery; ECOG 0-2; pre-RT ALC > 0.5 x 10^9 cells/L. Prior-recurrence pts eligible. Excluded prior thoracic RT within 2 years and systemic therapy within the prior year or planned within 6 months post-SBRT. Median age 74 both arms; cT1 in 100% optimized vs 88.5% standard.

SBRT 45-60 Gy in 5 fractions (BED 85.5-132 Gy) by IMRT or VMAT, 6X-FFF, 4DCT-based ITV, PTV margin 5mm radial and 8mm superior-inferior, daily CBCT. Both arms met RTOG 0813/0915 constraints; the optimized arm added heart, great vessels, thoracic spine and lymph-node-stations (Chapet atlas) contoured to a 40 cGy per fraction threshold as competing OARs.

Primary: in vivo lymphocyte depletion (ALC change) at end-of-treatment, 4 weeks and 6 months, plus safety/toxicity comparison. OS and EFS were unplanned subgroup analyses, descriptive only.

Two grade 3 events (lung infection) in the optimized arm vs four in the standard arm (dyspnea, hypoxia, lung infection); all recovered. Grade 2 events in 6 (24%) optimized vs 9 (35%) standard. No grade 2+ pneumonitis and no grade 4+ toxicity in either arm.

The premise rests on the observed link between post-RT lymphopenia and worse outcomes rather than on any prior trial that randomized immune-organ sparing, so there is no comparator trial to place this against. The authors cite lung SBRT plus immunotherapy improving 4-year EFS from 53% to 77% as the alternative route to the same immune endpoint, which is an add-a-drug strategy rather than a planning one.

Chance imbalance runs against the optimized arm on some axes (fewer treatment-naive: 64.0% vs 88.5%) and toward it on others (more central tumors: 36.0% vs 23.1%), and with 51 pts neither is correctable by adjustment. The LN V5 35.4cc OS split is a post-hoc median dichotomy on the same small cohort, so it cannot be read as an independent confirmation of the ALC result. Only 15 central tumors carried the largest effect estimate.

The trial establishes that the dose can be moved, and that ALC follows it, in a setting where the target dose was held fixed. What it does not establish is that the lymphocyte curve translates into disease control, and the OS and EFS signals here are explicitly underpowered and unplanned.

Preprint, single-institution phase II, N=51, endpoint is a lymphocyte surrogate not a clinical outcome; survival analyses unplanned and underpowered.

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.

Phase 2, open-label, randomised 1:1, investigator-initiated, 21 hospitals across Australia, Belgium, Italy, Norway, Spain and Switzerland. Recruited June 11, 2018 to April 30, 2021; median follow-up 50 months (IQR 42-58). Stratified by PET tracer (choline vs PSMA) and MDT type (sLND vs SBRT); participants and investigators unmasked.

Biochemical relapse after radical prostatectomy, postoperative RT, or definitive RT, with up to five PET-detected pelvic nodes (pelvis defined up to the aortic bifurcation, common iliac included). Bone, visceral, or above-bifurcation nodal disease excluded, as was previous RT overlapping current fields. Median age 70-71, median PSA at inclusion 1·00 vs 0·85 ng/mL, 91% and 86% EAU high-risk BCR, and 55-62% had a single positive node.

MDT arm: SBRT 30 Gy in 3 fractions every other day to 90% of the PTV with a 3 mm margin, or salvage lymph node dissection. ENRT arm: 45 Gy in 25 fractions to the whole pelvis on a modified RTOG 2009 template (upper limit L4-L5) with a simultaneous integrated boost to 65 Gy on PET-positive nodes; IMRT or rotational technique mandatory, with a benchmark-case QA programme. Prostate bed RT (≥66 Gy/33 fx) was advised for pT3-4, Gleason ≥8, or positive margins and given to 25% of MDT and 41% of ENRT pts.

Both groups received 6 months of LHRH agonist or antagonist, started no later than the first fraction (or day 1-10 postoperatively after sLND). Every patient who started intended local therapy plus ADT completed it. Physicians were instructed not to restart ADT absent clinical progression.

Primary: metastasis-free survival (any M1 on PET or death), with local or pelvic nodal relapse explicitly NOT counted as an event. Secondary: biochemical RFS, locoregional RFS, ADT-free survival, and late grade 2+ GU/GI toxicity to 48 months. OS, prostate cancer-specific survival, and time to castration resistance had insufficient events and are deferred.

Grade 2+ GU events above baseline at 4 years were 28% MDT vs 31% ENRT (absolute difference 3%, p=0·73) and grade 2+ GI 7% vs 9% (difference 2%, p=0·93). Most common grade 3 events were urinary incontinence (6% vs 10%) and diarrhoea (1% vs 2%). In post-hoc analysis the driver of toxicity was the prostate bed, not the pelvic volume: GI OR 4·6 (95% CI 1·5-15·8), p=0·0085 and GU OR 1·85 (0·95-3·60), p=0·068 with bed inclusion. No treatment-related deaths.

The single-arm GETUG-P07 OLIGOPELVIS reported 3-year bRFS of 45% for ENRT against 57% at 4 years here, though its median PSA was 3-4 ng/mL and staging was choline-based, so the populations differ. Against the ADT-intensification trials, EMBARK and PRESTO enrolled the PSA-doubling-time population that simulations put at up to 40% pelvic nodal relapse on PET, and this trial's median time off ADT exceeded 48 months in MDT and was not reached in ENRT, versus 13-18 months with RT alone and 16-17 months with ADT alone across earlier series.

No central PET review at baseline or follow-up, so the primary endpoint depends on local reads (authors cite κ 0·74 for pelvic nodes). Curves did not separate in year 1 because of the shared 6 months of ADT, which strains the proportional hazards assumption the HR summarises. The open-label design plausibly biased adverse-event attribution in both directions, and prostate bed RT was left to physician discretion, so a treatment that materially changed both toxicity and local recurrence was not randomised.

The result reads as a field-size question answered on pattern of failure rather than on distant control: relapse after MDT was predominantly locoregional, meaning PSMA PET missed nodal disease in at least half of pts treated to visible targets only. That reframes ENRT less as escalation than as compensation for imaging sensitivity that has not caught up with the treatment paradigm it enabled.

Phase 2 powered at α=0·20; primary MFS p=0·063 would not clear conventional significance, and the authors themselves await a phase 3 (POINTER-PC).

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.