onc brain

Multicenter, open-label, randomized phase 3 across 17 hospitals in China (NCT06507371). 1:1 allocation, n=77 per arm, stratified by clinical N stage (cN0 vs cN+). Pathologic response read by blinded independent central review.

Rectal adenocarcinoma with lower edge ≤10 cm from the anal verge, cT3-4 N0/+ M0, MSS/pMMR, age 18-75, ECOG PS 0-1. No positive lateral lymph node permitted, which excludes the population where lateral nodal management is itself contested.

Both arms received 5Gy x 5 days. The experimental arm's modification was target volume only: radiation to the tumor bed without tumor-draining lymph nodes, against conventional short-course fields in the control. Dose and fractionation were held constant, so the field is the only RT variable.

Experimental: tislelizumab 200 mg IV d1 plus oxaliplatin 130 mg/m² IV d1 and capecitabine 1000 mg/m² PO d1-14. Control: the same CAPOX backbone without tislelizumab. Both followed by TME, then adjuvant therapy and follow-up.

Primary: pCR rate in the ITT population. Secondary: MPR rate, TRG, organ preservation rate, EFS, OS and AEs. Only pCR and MPR are reported in the source; the time-to-event secondaries are not.

The presentation states the experimental approach reduced the incidence of severe gastrointestinal adverse events, consistent with a smaller irradiated volume, but no grade-specific rates are reported in source.

The control arm's 28.6% pCR sits above what short-course RT with consolidation chemotherapy has historically produced in pMMR disease, so the comparator is not obviously weak. The experimental result approaches the response depth usually reserved for dMMR/MSI-H disease, where checkpoint blockade already produces high complete-response rates; extending that to MSS is the claim being made.

Nodal recurrence is the outcome that decides whether sparing the tumor-draining nodes is safe, and no recurrence, EFS or OS data appear in the source. A pCR advantage at TME cannot answer it, and the cN+ stratum is where a nodal-omission failure would show first.

The trial's mechanistic premise, that irradiating draining nodes depletes the lymphocyte reservoir a PD-1 agent needs, is testable but not tested here: the field change and the checkpoint inhibitor were introduced together. A three-arm design (node-sparing RT + CAPOX, conventional RT + CAPOX + tislelizumab) would be needed to separate them.

Randomised phase 3, 1° EP met by central review, but confounds nodal-target omission with PD-1 addition and reports no recurrence or survival data.

Randomized phase III, 1:1, N=228 (115 TRT vs 113 control). Stratified by liver metastases and brain metastases. Primary: overall survival; key secondary ORR, PFS, toxicity.

Treatment-naive confirmed SCLC, stage IV or stage III ineligible for curative chemoradiation, ECOG PS 0-1, at least one measurable thoracic lesion. Asymptomatic or stable brain metastases allowed.

Both arms: 4 cycles durvalumab 1500 mg + carboplatin AUC=5 + etoposide 100 mg/m2 IV d1 with d2-3 IV or 200 mg/m2 PO d2-4, Q3W, then durvalumab 1500 mg Q4W until progression, toxicity, or patient choice.

30 Gy in 10 fractions starting day 21-28, so delivered concurrently with the later chemoimmunotherapy cycles rather than as post-chemo consolidation. PCI 25-30 Gy to responders and WBRT 20-30 Gy for brain metastases were optional per local routine in both arms. Target volume, technique, and dose constraints not reported in source.

Primary endpoint not met. PFS was likewise flat (5.1 vs 5.0 mo, HR 1.10, p=0.49), and neither landmark subgroup shifted the estimate below 1.0.

CREST (Slotman, Lancet 2015) established the same 30 Gy/10 fx schedule as consolidative TRT after chemotherapy alone and showed a 2-year OS gain. This trial asks the schedule against a durvalumab-containing backbone and finds nothing, which is the relevant question now that chemo-IO is standard first line.

Toxicity was a key secondary but no AE data appear in the source slides, so a harm-versus-local-benefit tradeoff cannot be assessed. No local control or pattern-of-failure endpoint is shown, and permitted PCI plus WBRT in both arms further blurs the RT contrast between arms.

The timing choice matters for how far the null generalizes: day 21-28 puts RT alongside active chemo-IO, not after it, so this tests concurrent thoracic RT rather than the CREST consolidation paradigm. What it does not settle is whether the null reflects absent local benefit or a benefit cancelled by added toxicity.

Randomised phase III, primary OS endpoint, prespecified stratification; result diverges from CREST-era practice of consolidative TRT. Design internally valid for the null claim.

International randomized trial (PREPEC / OPBC-02) of pre-pectoral versus sub-pectoral implant-based breast reconstruction after skin-sparing or nipple-sparing mastectomy. Follow-up to 24 months, with 6 post-randomization patient-reported timepoints.

Women undergoing nipple-sparing or skin-sparing mastectomy in either the therapeutic or risk-reduction setting. Primary analysis included 191 pre-pectoral and 189 sub-pectoral; safety was analysed by actual positioning (194 versus 186).

Primary: long-term patient-reported physical well-being (chest) on BREAST-Q, scored 0 to 100 with higher better. Main secondary safety endpoint: unplanned loss or replacement of expander or implant.

Primary endpoint met; the safety endpoint moved against pre-pectoral placement. See the endpoint tables above.

Unplanned implant or expander loss or replacement at 24 months was 21.1% (41/194) pre-pectoral versus 14.5% (27/186) sub-pectoral, adjusted difference 5.7% (-2.4 to 13.8), which the investigators call inconsistent with the non-inferiority hypothesis.

Longitudinal completion ranged 83-95% and the primary estimate rests on multiple imputation with imputed baseline values, so the 4.8-point difference carries missing-data assumptions on top of its confidence interval. Surgeon and patient blinding is not feasible for a positioning trial, which cuts directly at a patient-reported primary endpoint.

The trial answers the PRO question it asked and simultaneously undercuts the assumption that pre-pectoral placement is device-safe. Whether a 4.8-point BREAST-Q gain is worth a 5.7-point absolute rise in unplanned reoperation is a preference-sensitive decision, not one the trial resolves.

Randomised, prespecified PRO primary endpoint met, but the safety co-read failed its non-inferiority hypothesis, so the trade-off, not the win, is the finding.

Randomized trial of GammaTile brachytherapy vs post-op SRS after resection of a brain metastasis, N=230, reported as final results at ASCO 2026 (Weinberg). Randomization ratio, number of sites, and follow-up duration not reported in source.

Resected brain metastasis >2 cm, the size band where post-op cavity SRS control is weakest. Histology mix, number of brain metastases allowed, systemic disease status, and performance status not reported in source.

Experimental arm is GammaTile, a Cs-131 collagen tile implanted in the cavity at the time of resection, so dose starts without the post-op delay. SRS dose, fractionation, cavity margin, and time from surgery to SRS are not reported in source, and those are exactly the parameters that decide whether the control arm reflects the reader's own practice.

Primary I: time to surgical bed recurrence. Primary II: surgical bed recurrence-free survival. 2 yr OS is reported alongside them; the source does not state whether OS was a prespecified secondary.

Both primaries favor GammaTile with medians not reached vs 17 mo and 11 mo. No HR, confidence interval, or p-value appears in the source.

Radiation necrosis 7% SRS vs 8% GT, essentially flat. Leptomeningeal disease 3% SRS vs 10% GT is the signal that cuts against the arm winning on bed control; timing and denominators not reported in source.

Post-op cavity SRS became standard on N107C/CEC.3 and the MDACC randomized trial, both of which traded whole-brain neurocognitive toxicity for weaker bed control, with failure concentrated in larger cavities. ROADS attacks that residual failure directly rather than re-litigating whole-brain RT.

The 2 yr OS separation, 62% vs 36%, is far larger than bed recurrence alone (12% vs 1%) would mechanistically support, which points at arm imbalance, differential salvage, or systemic therapy that the source does not report. The trial is also inherently unblinded, and the LMD excess in the GammaTile arm has no reported timing to judge whether it is procedure-related seeding.

If the bed-control numbers hold in the full report, the cavity strategy for a large resected met becomes a surgical-planning decision made before the operation rather than a radiation-planning decision made after it. The OS claim should wait for the manuscript.

Randomized, both primaries reported, final analysis. Verdict held below practice-changing: conference-slide source with no HR, CI, or p-value, and unexplained LMD excess.

Randomised, multicenter, phase 3 trial, N=620 (310 per group), 13 referral hospitals in China, accrual 2013-2022. Follow-up on the DFS curve extends past 120 months.

High-risk locally advanced gastric or EGJ adenocarcinoma: cT3N2-3M0, cT4aN+M0, or cT4bNanyM0, Siewert II/III permitted. 225 (36.3%) had an EGJ primary, and every pt was intended for standardized D2 resection.

Both arms: 3 cycles preoperative XELOX (oxaliplatin 130 mg/m² D1, capecitabine 1000 mg/m² BID D1-14, Q3W) then D2 gastrectomy then 3 adjuvant XELOX cycles.

CRT arm added concurrent 45 Gy / 25 fractions after cycle 1 of preoperative chemo, with attenuated concurrent dosing (oxaliplatin 100 mg/m², capecitabine 825 mg/m²). Target volume not specified in source.

Primary: disease-free survival, from randomization to progression, relapse, or death. Secondary: overall survival, pCR, R0 resection, safety.

Primary endpoint met. The locoregional read is the one an RT reader needs: LRR 9.4% vs 18.3% among R0-resected pts.

G3+ haematologic toxicity 14.6% vs 10.3%, the expected cost of concurrent chemoRT. G3+ postoperative complications were comparable, 9.0% vs 7.6%, so preoperative RT did not measurably worsen D2 surgical morbidity.

CRITICS (postoperative chemoRT after D1+ surgery) and TOPGEAR (preoperative chemoRT with ECF/FLOT) both failed to show a survival gain for radiotherapy in this disease. Neo-CRAG differs on three axes at once: RT given preoperatively, D2 resection mandated, and enrolment restricted to node-heavy cT3N2+ or cT4 disease.

The 2013-2022 accrual window means the control arm reflects a doublet era; a 37.6 mo median OS in the control group is short against contemporary FLOT-treated series. Single-country enrolment with uniformly high-quality D2 surgery also caps generalisability to centres with variable nodal dissection.

The pCR, downstaging, ypN0 and LRR gradient forms a coherent mechanistic chain from RT to the DFS separation, which is what earlier negative trials lacked. What it does not settle is whether that chain survives a stronger systemic backbone, since much of FLOT's advantage over a doublet is itself locoregional.

Randomised ph3, prespecified DFS met with OS support, but the chemo backbone is XELOX not FLOT, so it contests RT omission without settling it.

Phase III open-label RCT, single-centre (Tata Memorial, Mumbai), N=208 randomised 1:1 to upfront (n=105) vs delayed cranial RT, both on TKI plus chemotherapy. Stratified by GPA (0-2 vs >2) and synchronous vs metachronous BM. Median follow-up 30.6 mo (28.7, 36).

Metastatic NSCLC with an EGFR or ALK alteration, ECOG PS 0-2, radiologically measurable brain metastases that were completely asymptomatic. Number, size, and location of lesions are not reported in source.

Upfront arm received cranial RT at diagnosis; the delayed arm received it at intracranial progression or patient's wish, so both arms are RT-exposed and the question is timing, not omission. Dose, fractionation, and technique (WBRT vs SRS) are not reported in source, which is the main barrier to transferring this result.

Primary: intracranial PFS. Secondary: OS, PFS, toxicity, ORR, neurocognition, PROM. Surveillance was MRI brain q3m for the first year, then q6m, which is what makes a delayed strategy safe to run.

Primary endpoint met. Survival ran the other way: 2y OS 48% upfront vs 60% delayed, OS HR 1.45, reported by attendees rather than captured in the slide OCR.

Radiation necrosis ~6% in the upfront arm and none in the delayed arm per attendee reports, and described as less severe when delayed. Full toxicity tables, neurocognition, and PROM were secondary endpoints not reported in the source.

The intracranial magnitude sits alongside the older WBRT-era data (QUARTZ, and the historic SRS-vs-WBRT trials) in showing that cranial RT controls the brain without buying survival. What is new is testing it where a CNS-penetrant TKI is the competing intracranial therapy, a setting those trials predate entirely.

Single-centre and open-label, and the RT prescription is absent from the source, so a reader cannot tell whether the necrosis signal reflects WBRT, SRS technique, or concurrent TKI exposure. Median follow-up of 30.6 mo is short relative to expected survival in this population, and the OS comparison was a secondary endpoint, not powered.

The result splits the two things RT is usually credited with: it clearly buys intracranial control, and it clearly does not buy time. Whether the OS direction is a real cost of upfront RT or noise in an underpowered secondary is the open question, and it decides whether deferral is merely non-inferior or actually preferred.

Randomised phase 3, prespecified intracranial PFS met, but the survival signal runs opposite the intracranial win. Directly contests reflex upfront cranial RT.