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Prospective comparative effectiveness study (COMPPARE, PCORI-funded), non-randomized proton vs photon cohorts across 51 centers. 2524 accrued July 2018-October 2022. Early results, short follow-up.

De novo localized prostate cancer, excluding very-high-risk and metastatic. Proton cohort n=1500, photon (IMRT) cohort n=1000.

Proton therapy vs IMRT; rectal spacer use captured as a covariate (FDA-approved 2015). Dose/fractionation and target volume not reported in source.

Co-primary patient-reported bowel urgency and frequency (EPIC) and ≥G2 GI toxicity (CTCAE v5), each powered 90%. Exploratory: 3-yr freedom from PSA progression.

No significant proton advantage on any endpoint (all p ≥ 0.28). Observed toxicity fell far below design assumptions (hypothesized IMRT GI tox 29%, actual 5.6%).

Rectal spacer reduced 2-yr cumulative G2+ GI toxicity in both arms (p=0.009); the spacer effect exceeded any proton-vs-IMRT difference.

Directionally consistent with PARTIQoL (randomized proton vs IMRT, localized prostate), which found no bowel-QoL advantage for protons.

Non-randomized cohorts (selection bias, residual confounding); short follow-up leaves late GU/GI toxicity and long-term control unanswered; dose/fractionation not reported.

Prospective but non-randomized cohorts (selection bias); early results, short f/u leave late toxicity and long-term control open. Null aligns with randomized PARTIQoL non-superiority.

Prospective single-arm phase I, N=50, Fudan University Shanghai Cancer Center. Data cutoff Dec 31 2025; median follow-up 19.9 mo (95% CI 16.4-23.4).

MSS rectal cancer, primary ≤10cm from anal verge, synchronous unresectable mets. 76% male, median age 57; 52% liver, 8% lung, 40% both; RAS/BRAF-mut 56%.

RT delivered first as an immune primer: HFRT to the primary, HFRT or SBRT to metastases. Dose, fractionation, and target volumes not reported in source.

Post-RT, biomarker-gated: FOLFOX-bevacizumab-tislelizumab (RAS/BRAF-mut) or FOLFIRI-cetuximab-tislelizumab (WT); tislelizumab 200mg Q2W. Resection/metastasectomy if converted, watch-and-wait if primary cCR.

Primary: ETS rate (≥20% target shrinkage at 8wk). Secondary: DCR, DOR, OS, PFS, safety.

ETS 76.0%, ORR 68.0%, DCR 88.0%; 18% (9/50) reached NED. Median OS 23.2mo, PFS 9.3mo, DOR 8.0mo (endpoints in table).

Single-arm phase I, N=50, no comparator to isolate RT's contribution. Surrogate primary (ETS at 8wk), short median DOR (8mo), and near-universal lymphopenia (95.9%).

Single-arm phase I, N=50; surrogate primary (ETS at 8wk); no comparator to isolate RT's contribution to the immune-priming effect.

Single-arm, multi-stage feasibility and safety trial testing durvalumab added to 5FU/MMC chemoradiation for bladder preservation. Benchmarked against BC2001 historical CRT data, not a randomised comparator.

T2-T4a N0M0 urothelial muscle-invasive bladder cancer, stratified by prior neoadjuvant chemotherapy (yes vs no). A stage-1 expansion added the first 6 node-positive pts.

Durvalumab 1500 mg given neoadjuvant, synchronous, and adjuvant to 12 months post-chemoRT. Concurrent 5-FU 500 mg/m²/24h ×5 days and mitomycin C 12 mg/m².

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

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

12-mo DFS 40/50 (80%), 95% CI 0.67-0.89, clearing the ≥75% GO bar. 33/54 (61%) completed planned durvalumab; investigators reported very high bladder-preservation and DFS vs prior trial data.

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

Benchmarked against BC2001 (James, JCO 2016), where adding 5FU/MMC to RT gave DFS HR 0.78 (0.60-1.02), p=0.07. RAD-IO's 80% 12-mo DFS is claimed higher than prior data, but the comparison is non-randomised.

Single-arm with a historical benchmark and no concurrent IO comparator; 12-mo DFS is an early surrogate; small N (~50 evaluable); node-positive experience limited to 6 pts.

Single-arm feasibility stage, no randomised IO comparator; benchmarked against historical BC2001. 12-mo DFS an early surrogate at small N; met pre-set GO bar for further evaluation only.

Phase 2 single-arm Alliance trial. N=78 eligible metastatic HSPC deep responders interrupt ADT+ARPI. Enrolled 07/2022-03/2024; median follow-up 26.9mo.

Entry required PSA<0.2 (stable/falling) after 18-24mo ADT and ≥12mo ARPI. Median age 70 (49-90); 64.9% low-volume, 35.1% high-volume (CHAARTED); 51.3% had prior local radiation, 29.5% metastasis-directed radiation.

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

Primary met: 32/78 (41.0%) treatment-free and eugonadal at 18mo (80% CI 33.1-48.9%, one-sided p=0.0249). 57.7% were treatment-free at 18mo and 66.7% recovered testosterone; median time to eugonadal T 9.0mo.

Disease control held through interruption: rPFS 15/78 events, OS 4/78 events, both medians not reached. The 41% primary is capped by slow testosterone recovery, not progression, so the endpoint understates short-term oncologic safety in this older cohort.

Single-arm with no randomised comparator against continued therapy, so the survival cost of interruption is unquantified. Median follow-up 26.9mo is short for mHSPC; durability of treatment-free intervals is unproven.

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

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

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

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

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

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

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

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

Single-arm cohort (n=49), no randomised comparator in atypical EGFR NSCLC; durable but single-arm design caps the read at early-signal despite 31-mo follow-up.

Phase 3, open-label, multicenter RCT (NCT06448312); 1:1, N=413. Primary PFS by BICR crossed its interim efficacy boundary at 194 events; median follow-up 10.5 mo.

1L stage IIIB/IIIC or IV NSCLC, PD-L1 TPS ≥1% (22C3), EGFR/ALK wild-type, ECOG 0-1. Stratified by histology, PD-L1 (1-49 vs ≥50), ECOG.

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

ORR 70.2% vs 42.0%. PFS gain held across PD-L1 strata, strongest in TPS 1-49% where pembro monotherapy is weakest. OS immature, formal testing pending.

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

Open-label; OS immature at 10.5-mo follow-up and formally untested; PFS reported at an interim efficacy boundary. No safety data in source.

PFS crossed an interim efficacy boundary; key-secondary OS descriptive/immature at 10.5-mo f/u; open-label. Strong but not yet mature enough to move 1L SOC.

Pooled retrospective analysis of 3 institutions (Peter MacCallum, Cleveland Clinic, Roswell Park). N=1687 (1200 primary NSCLC, 487 pulmonary oligometastases). No randomisation, no comparator arm; survival curves out to 60 months.

Primary NSCLC (n=1200) and pulmonary oligometastases (n=487) treated with single-fraction SABR. Stage, tumour location, and specific eligibility criteria not reported in source.

Single-fraction SABR across all pts. The Gy dose is not reported in source (single fraction only), so the specific regimen behind these outcomes is unknown, gating whether the result transfers to a given practice.

No prespecified primary endpoint stated. Reported: local control, overall survival, PFS, and adverse events.

2y local control 90-93%; isolated local/locoregional failure very uncommon. Median PFS 30 mo (NSCLC) vs 11 mo (oligomets). OS by cohort shown in the figure.

G3+ AEs 2-3% (23/789, 2.9% in the assessed NSCLC subset); G2+ 124/789 (15.7%), any AE 215/789 (27%). AE data from 2 of 3 sites only (no Roswell Park).

Consistent with SAFRON II (TROG 13.01) and RTOG 0915 supporting single-fraction lung SABR, but those were randomised; this pooled cohort carries no comparator.

Retrospective, no randomised/matched comparator. Single-fraction Gy dose unstated. AE denominator excludes one of three sites (n=789 of 1687).

Pooled retrospective single-arm cohort, no randomised or matched comparator vs multi-fraction SABR; single-fraction Gy dose unstated. Consistent with SAFRON II / RTOG 0915.

Phase 3 international non-inferiority RCT, 1:1, biochemical failure (Phoenix) primary, NI margin 12%. Interim analysis at 142 analyzed of 456 planned; median follow-up 59.7 mo.

Localized low- to intermediate-risk prostate cancer, IPSS <12. 82.4% intermediate-risk; stratified by risk, gland volume (<60 vs 60-80cc), and ADT. 28% received ADT (≤6 mo, both arms).

AHRT 36.25 Gy/5 fx (7.25 Gy/fx) + GTV SIB to 40 Gy vs EHRT 70.2 Gy/26 fx (2.7 Gy/fx), IMRT in all patients.

AHRT non-inferior to EHRT for biochemical failure: 7% vs 7.4%, P non-inferiority=0.007 at 4.25y.

Acute G2+ GI toxicity lower with AHRT. No significant difference in late G2+ GI or acute/late G2+ GU toxicity. Supportive-med use (laxatives, psyllium) counted as G2.

First RCT comparing AHRT vs EHRT 1:1 with modern IMRT and ADT. Prior ultrahypofractionation trials (HYPO-RT-PC, PACE-B, NRG-GU005) used heterogeneous or no-ADT controls.

Interim analysis at roughly one-third of planned accrual; full pre-specified primary pending. Small analyzed N (142); biochemical, not clinical, endpoint.

Interim analysis at 142 of 456 planned pts; non-inferiority met but full pre-specified primary analysis pending. Underpowered vs accrual goal.

Patient-level pooled analysis of two prospective trials of involved nodal RT, INRT-AIR and DARTBOARD. N=117, median follow-up 3.4 years. No randomised ENI comparator arm.

HNSCC of oropharynx, larynx, and hypopharynx, stage I-IVB, excluding T1-2N0 larynx. Completed PET/CT and neck CT required for entry.

INRT omits elective nodal irradiation, treating involved nodes only, with an artificial-intelligence model assisting identification of suspicious lymph nodes. Dose, fractionation, and margin not reported in source.

5-yr solitary elective nodal recurrence 0%. 3-yr cumulative incidence: local 9.5%, regional 4.3%, distant 11%. 5-yr OS 87%, PFS 74%.

Mean composite MDADI 84.9 at 12 months, with no significant decline after treatment. No late G3+ toxicity, xerostomia, or feeding-tube rates reported in source.

Pooled single-arm data with no ENI control, so the 0% solitary elective recurrence carries no randomised contrast. Median follow-up 3.4 yrs underpins 5-yr estimates, and the AI nodal-selection step is not externally reproduced.

The dosimetric case for INRT rests on OAR sparing, but the only patient-reported outcome here is swallowing (MDADI 84.9), with no xerostomia or dysphagia comparison against ENI. Authors state randomized evidence is required before non-trial implementation.

Pooled single-arm prospective cohorts, N=117, no randomised ENI comparator; presenters explicitly require randomised evidence before non-trial use.

Phase III, open-label, randomized non-inferiority trial, Tata Memorial Centre and collaborating Indian centers. Accrual 2018-2023, completed at N~434, randomized 1:1 stratified by risk group and nodal status. Median follow-up is interim, 1-2 years.

High-risk, very high-risk and/or node-positive non-metastatic prostate cancer; ECOG 0-2; life expectancy 10 years. PSMA PET/CT staging permitted, which matters for how the node-positive stratum was defined relative to older conventionally-staged trials.

Arm A 36.25 Gy in 5 fractions (7.25 Gy/fx), every other day; Arm B ~68 Gy in 25 fractions (2.7 Gy/fx) over ~5 weeks. Both arms received prostate plus whole-pelvis elective nodal RT at 25 Gy / 5 fx (or equivalent), with SIB to positive nodes allowed in the SBRT arm. Delivered in the modern IMRT/VMAT with daily IGRT era.

Long-course ADT, ~2 years, in both arms. ADT is not a randomized variable here, so the trial isolates fractionation, not the systemic question.

Primary: biochemical failure-free survival (Phoenix, nadir + 2 ng/mL). Secondary: acute and late toxicity (RTOG/CTCAE v4.0/5.0), OS, MFS, clinical failure-free survival, QoL (QLQ-C30, QLQ-PR25, IPSS), cost-effectiveness.

Interim only. Source reports no signal of inferiority for the SBRT arm on BFFS and no difference in MFS or OS in early follow-up; no HR, CI, or non-inferiority margin is reported in source. OS data explicitly immature.

No significant difference in grade ≥2 toxicity between arms: acute GU ~5.4% vs ~4.0% (p=0.59), acute GI ~2.2% vs ~3.7% (p=0.20); late grade ≥2 GU ~10-12% vs ~9-11% and GI ~5-7% vs ~4-6%, both NS. Grade 3+ under 1% in both arms, acute and late. Urinary and bowel QoL domains stable and comparable.

HYPO-RT-PC established ultrahypofractionation non-inferiority (10y FFS 72% vs 65%, adjusted HR 0.84, 95% CI 0.69-1.03) but in node-negative disease, prostate plus proximal seminal vesicles only, no pelvic RT, no ADT, mostly 3D-CRT. PRIME is testing a different question: 5 fractions with elective nodal coverage on top of 2y ADT.

Interim analysis at 1-2 years against a BFFS primary read under 2 years of ADT, where testosterone suppression flattens both curves and early concordance is close to uninformative. Toxicity is reported as approximate ranges rather than point estimates with CIs. Open-label, though toxicity grading and PSA endpoints are only modestly susceptible to that.

Interim analysis at 1-2y of a BFFS primary that needs 4-5y maturity; safety-only read. Interim data cannot promote past early-signal regardless of clean design.

Phase 3 randomised, 1:1, multicentre. 1166 pts randomised against a target of 1128. This report is the prespecified acute toxicity analysis; the trial's primary endpoint, time to biochemical or clinical failure, is not yet mature.

High-risk localised prostate cancer: T3a-T4 and/or Gleason 8-10 and/or PSA >20 ng/ml. All planned for 12-36 months ADT.

Both arms 36.25Gy in 5f to prostate on alternate days. PPN-SBRT adds 25Gy in 5f to pelvic nodes. 11% of PPN-SBRT vs 4% of P-SBRT did not receive allocation, mostly because dose constraints were not met.

Co-primary for this analysis: CTCAE grade ≥2 GI and GU toxicity to 12 weeks. Patient-reported EPIC-26 domain scores collected at 4 weeks.

Grade ≥2 GI symptoms were more frequent with PPN-SBRT (28% vs 21%) across the 12-week window, with no difference at 12 weeks. No difference in acute GU toxicity by clinician or patient report. EPIC-26 bowel domain at 4 weeks mirrored the clinician-scored GI gap.

Acute window only, capped at 12 weeks; late GI/GU effects and cancer control are still accruing. Toxicity scoring is unblinded, which matters most for clinician-graded GI events. Effect sizes for the GI difference (CI, p) were not reported in source.

Randomised, but this is an acute-toxicity readout only; the primary biochemical/clinical failure endpoint is explicitly immature. Safety supports feasibility, not adoption.

Randomised trial (ARO-2021-09, NCT04495309) of systemic therapy alone vs systemic therapy plus local ablative radiotherapy to all metastatic lesions. Randomisation stratified by type of systemic therapy and treatment line. N=87 (43 experimental, 44 control).

Metastatic breast cancer, any treatment line, maximum 5 metastatic lesions, with the systemic regimen determined by multidisciplinary tumour board. Pts requiring palliative RT to all metastases were not eligible, though palliative RT to symptomatic sites was allowed. Median age 58 / 59; ECOG 0 in 76.7% of the experimental arm.

The intervention is local ablative radiotherapy to all metastatic lesions on top of the systemic backbone. Dose, fractionation, modality, and target-volume definition are not reported in the source slides, and 2/3 of treated lesions were bone metastases.

Co-primary: progression-free survival and quality of life (EORTC QLQ-C30) at 12 weeks post-randomisation. Secondary: overall survival, toxicity, compliance, QLQ-C30 and QLQ-BR23, and patient satisfaction with cancer care (EORTC PATSAT C33).

Both co-primaries read out in favour of adding MDT: PFS separated at HR 0.48 and the QoL summary score met non-inferiority against a -10 point margin. See the figure captions for the arm-level values.

Recruitment stopped early at <20% of the initial and <40% of the amended target, leaving N=87 and a wide HR CI (0.25-0.91). Open-label design with a patient-reported co-primary. No OS data reported in source, and the toxicity secondary endpoint is likewise absent from the presented slides.

The presenter frames this as the first RCT showing a PFS benefit from MDT in oligometastatic breast cancer, extending the STOMP / SABR-COMET line of evidence into a histology where systemic control is comparatively good. Eight further randomised trials are accruing, so the magnitude here should be read as provisional.

Randomised but stopped early at <20% of initial accrual target; N=87 with wide HR CI (0.25-0.91). Underpowered for a durable PFS estimate.