onc brain

Phase 3 multicentre RCT (CRUK/18/010), N=205 oropharyngeal SCC, 2:1 IMPT:IMRT, stratified by T-stage, N-stage, p16 status, and smoking history.

Oropharyngeal SCC requiring concurrent chemoradiotherapy with bilateral neck treatment. p16 status was a stratification factor, so both HPV-associated and HPV-independent disease are included.

70 Gy / 56 Gy in 33 fractions over 6.5 weeks, identical for both arms; IMPT vs IMRT is the only difference. Identical planning constraints applied across modalities.

Concurrent cisplatin 100 mg/m² on D1 and D22.

Co-primary PRO: UW-QoL physical composite at 12mo (saliva, taste, chewing, swallowing, appearance, speech). Co-primary clinician: CTCAE grade 3 weight loss (≥20% from baseline) or gastrostomy dependence at 12mo.

No between-arm difference in UW-QoL physical composite at 3/12/24mo, similar from 6 weeks post-CRT, with similar trajectories across multiple PRO questionnaires. No effect size reported in source.

Support for protons in OPSCC has rested on dosimetric and single-institution toxicity data; this randomised HR-QoL readout does not confirm a patient-reported advantage for IMPT.

Only the HR-QoL co-primary is presented; the clinician co-primary (weight loss/gastrostomy) and 5yr late-effects follow-up are unreported. No effect sizes or CIs given. Novel UK proton centres and identical constraints may cap IMPT's achievable edge.

Randomised co-primary QoL null (IMPT≈IMRT), consistent with IMRT-based CRT remaining standard. Only HR-QoL co-primary shown; clinician co-primary and 5yr late effects still maturing.

Phase 3 RCT, N=1465 randomised across 39 UK centres. Primary endpoint: biochemical/clinical failure; the side-effect endpoints presented here are secondary.

Localised prostate cancer; the trial rationale states high-risk localised pts are most likely to benefit from pelvic node RT. Full eligibility criteria not reported in source.

20-fraction moderately hypofractionated IMRT. Arms as received: prostate alone (388), prostate + focal prostate boost (464), prostate + pelvic nodes + boost (462). Boost dose and nodal dose not reported in source.

Reported here: early bowel and bladder side effects (<18 weeks) and late (2-year, 6-24 month) G2+ events. Cancer-outcome follow-up is ongoing.

Nodal RT increased early bowel side effects, which resolved by 18 weeks post-RT. At 2 years G2+ bowel and bladder rates were similar across arms, with the numerically highest late bladder rate in the boost-without-nodes arm.

Late analysis covers only the 973 (74%) with ≥2yr follow-up, and no between-arm p-values are reported in source. The efficacy primary endpoint is unreported, so the toxicity read cannot yet be set against a benefit.

Randomised phase 3, prespecified secondary toxicity endpoint, 2yr follow-up. Efficacy 1° EP not yet reported, so it supports safety only, not a practice change.

Phase III equivalence trial, n=520, 1:1 randomisation, accrued 2005-2013, single institution. Powered on a 5-year estimated IBTR of 3% with a 5% equivalence margin and 80% power. Survival outcomes analysed ITT; toxicity and cosmesis per protocol after 14 withdrawals.

Post breast-conserving surgery, pT <25 mm, final surgical margins ≥5 mm, age >40 years. Nodal status and receptor subtype not specified in the source slides.

APBI arm: 30 Gy in 5 fractions IMRT to the partial breast. WBI arm: 50 Gy in 25 fractions plus a 10 Gy in 5 fraction tumour-bed boost. The comparator is a conventionally fractionated whole-breast course, not a modern hypofractionated 26 Gy/5 or 40 Gy/15 schedule.

IBTR HR 1.57 (95% CI 0.82-3.04), p=0.17 at 15 years. The gap widens across timepoints (5yr 2.3% vs 1.2%, 10yr 4.2% vs 2.7%, 15yr 7.7% vs 4.2%) but never reaches significance.

The only 5-fraction PBI dataset reporting to 15 years. IMPORT LOW and NSABP B-39 support PBI at shorter follow-up with different fractionation, so this trial carries the durability question for the ultrahypofractionated schedule specifically.

Powered for 5-year equivalence, so the 15-year read is descriptive rather than a met endpoint. Single institution. The local relapse vs new primary split that carries the interpretation is investigator-adjudicated, not molecularly confirmed.

Randomised phase III, prespecified 5yr equivalence endpoint, 15yr mature f/u, no significant divergence on any oncologic endpoint. Reinforces PBI as a listed option.

Phase 3 randomised 1:1:1, N=2617 across 76 UK hospitals, accrued 2009-2015. Annual clinical follow-up to 10 years; PROs and photographs collected only to 5 years.

Women ≥18 years after breast conserving surgery for invasive early breast cancer, pT1-3, pN0-pN3a, M0, all requiring tumour bed boost RT. Described by the investigators as a higher-than-average risk group.

Control was 40Gy/15F whole breast plus sequential 16Gy/8F boost. Both experimental arms used a simultaneous integrated boost in 15 fractions over 3 weeks, 48Gy (3.2Gy/F) or 53Gy (3.5Gy/F) to the tumour bed, with a modest dose reduction to whole breast distant from the tumour.

Primary: ipsilateral breast tumour relapse (IBTR), reported here at 10 years. Secondary reporting covers overall survival and clinician-assessed late normal tissue effects.

Moderate/marked AEs at 10 years were low across all randomised groups: breast distortion/shrinkage <18%, induration <10%, telangiectasia <2%, breast oedema <2%. No arm-specific late toxicity split is given in the source.

At 5 years (Coles, Lancet 2023) IBTR was 1.9% / 2.0% / 3.2%, and 48Gy was declared non-inferior in absolute terms. The 10-year data preserve that ordering, and both 40+16Gy and 48Gy stay below the 5% control estimate assumed in the original sample size calculation.

Source reports absolute rates only, no between-arm HRs or non-inferiority p-values at 10 years. PRO and photographic cosmesis stopped at 5 years, so 10-year toxicity is clinician-scored. Conference presentation, not yet a full peer-reviewed 10-year report.

The practical yield is logistic as much as oncologic: SIB collapses boost into the same 15 fractions, cutting visits without paying an IBTR or late-toxicity penalty. Further escalation to 53Gy does not help, which closes the dose-escalation arm of this question in a boost-indicated population.

Randomised 3-arm phase 3, prespecified 10-yr follow-up of a published primary; reaffirms 48Gy/15F SIB rather than changing it. No new comparator.

Pre-planned secondary analysis (ITT) of the HypoG-01 phase III randomised trial. N=1,260, median follow-up 4.8 years.

Randomisation was 40 Gy/15 fractions over 3 weeks vs 50 Gy/25 fractions over 5 weeks, each with a tumour-bed boost. Target volumes followed ESTRO contouring guidelines.

First oncological event: locoregional recurrence (LRR), distant recurrence (DR), or second malignancy. LRR classified against the CTV as in-volume, marginal (outside CTV, ≥50% prescribed dose), or out-of-volume (<50%), with planned dose at the recurrence site re-estimated on the initial RT-plan CT.

118 first events. LRR was the lowest-frequency event type; distant recurrence (n=61) and second malignancy (n=37) dominated. 20/30 recurrence sites were in-volume (67%) and 19/30 nodal sites were mainly levels I and II.

Arm-level event counts are not reported in the source, so the "no obvious difference" claim between arms cannot be checked. With roughly 20 LRR events total, the analysis is descriptive and underpowered to exclude a modest fractionation effect on failure pattern.

The actionable signal is target-volume adequacy rather than fractionation: recurrences clustered inside the treated volume and in axillary levels I-II, which argues the ESTRO CTV is catching the right anatomy rather than that coverage needs widening. Out-of-volume failures would have been the argument for larger fields; they were the minority.

Pre-planned secondary analysis of a randomised phase III; supports moderate hypofractionation and ESTRO contouring. Event count (19 iLRR) too small for a powered arm comparison.

Phase III randomised non-inferiority trial, 1:1, run across Denmark, Norway and Germany with accrual 2009-2014. Median follow-up 12.8 years; these are the prespecified 10-year analyses.

1,882 women with node-negative breast cancer or DCIS. Allocation was 949 to 50 Gy and 933 to 40 Gy after exclusions; 936 and 917 women respectively carried forward in the flow diagram.

Whole-breast RT only: 50 Gy in 25 fractions vs 40 Gy in 15 fractions. No boost, nodal target volume, or technique detail (IMRT vs 3D, prone vs supine) is reported in the source.

Primary: grade ≥2 breast induration at 3 years, scored at two consecutive visits or at final follow-up. Morbidity assessed at years 0, 1, 2, 3, 4, 5 and 10; recurrence and survival were prespecified 10-year secondary analyses.

Induration is the toxicity endpoint here and it favours the hypofractionated arm. No other late-effect domain (cardiac, pneumonitis, cosmesis scoring, second malignancy) is reported in the source.

Consistent with START-B and the UK long-term hypofractionation experience, but adds prospectively scored induration out to 10 years in a trial that also enrolled DCIS.

Locoregional recurrence, distant failure and breast cancer mortality are reported only as not significantly different, with no event counts, HRs, or non-inferiority margin in the source. Induration scoring is clinician-assessed and not blinded to fractionation.

Prespecified 10-yr analysis of a randomised phase III with 12.8-yr median f/u; reinforces moderate hypofractionation already standard worldwide.

EORTC OligoCare prospective real-world registry of SABR for oligometastatic disease, 57 institutions, accrual July 2019 to July 2025. Interim analysis; median follow-up 31 months (minimum 6).

2447 eligible pts with 3533 lesions. Median age 69 (28-94), 69% male. Primary tumors: prostate 1021 (42%), NSCLC 530 (22%), colorectal 518 (21%), breast 378 (15%).

SABR to metastatic sites; lesion locations were lung 807 (23%), non-vertebral bone 869 (25%), non-regional lymph node 558 (16%), spine 515, liver 306 (9%), brain 231 (7%), other 247 (7%). Minimum PTV dose correlated with outcome and is named the most critical technical factor; prescription dose and fractionation not reported in source.

Local in-field progression reported as cumulative incidence. No primary endpoint stated in the source; no survival or systemic-progression endpoints given here.

Local in-field progression 5.0% at 1 year and 11.4% (99% CI 10.0-12.9%) at 3 years, i.e. 88.6% local control at 3 years, 237 events among 2447 pts.

Colorectal primaries failed most (19.6% at 3 years) despite the highest median dose per fraction, which the authors read as relative radioresistance rather than underdosing and a case for dose escalation or combination approaches. De novo oligometastatic disease outperformed repeat OMD, attributed to higher delivered dose.

Registry design with no comparator arm and heterogeneous dose/fractionation across 57 centres; indication and selection bias are unaddressed in source. Safety and toxicity outcomes are not reported in the source content.

Large prospective multi-site registry with explicit histology-stratified analyses, but non-randomised and no comparator; supports rather than tests current oligomet SABR practice.