onc brain

Single-institution retrospective comparison of 693 single-isocenter VMAT SRS plans: HyperArc (23-pt pilot + 350 pts) vs 320 consecutive prior mVMAT pts as historical control. Clinical outcomes evaluated only in the HyperArc cohort.

Plan cohort mixed metastatic and benign/vascular targets; 59.9% single-target, 12.0% with 6 to 22 targets. Clinical cohort: 107 pts with 377 brain mets, median age 58, mostly NSCLC, breast and melanoma.

No margin on GTV. 18-20 Gy in 1 fx, or 30 Gy/5 fx when any target exceeded 2-3 cm or involved deep structures. 10 MV FFF, HD120 MLC, CBCT with 6DOF correction.

Per-target conformity, gradient and falloff indices, mean brain dose, film PSQA against TG-218, planning and delivery times. Clinical: lesion-level LC (no 25% diameter increase) and grade 3+ CTCAE v5 toxicity.

Conformity equivalent; gradient and falloff favor HyperArc; mean brain dose 4.6% vs 5.1%. 1-yr LC 90.1%, 3 grade 3 seizures, no grade 4/5.

Builds on the Clark 2012 class solution and the Thomas 2014 low-dose-spill penalty that matched Gamma Knife plans. Here the automated tool reaches that expert-solution level without nested tuning structures.

Software version differs between eras (Eclipse 15.5 vs 13.6). Planning time measured from structure-set timestamps as a surrogate. LC depends on 47 tumors at risk at 1 year.

The case for automation is standardization, not a dosimetric leap: an expert manual program already sits near the ceiling. What remains unsettled is rotational-error underdosing of off-isocenter targets with zero margin, and which plan-quality metric actually tracks clinical outcome.

Retrospective historical-control dosimetric comparison; clinical outcomes single-arm HyperArc only with 5-mo median imaging f/u and toxicity scored by chart review.

Prospective single-arm trial, N=40, enrolled Feb 2017 to Aug 2019, registered NCT02886572. Median follow-up 15.2 mo. Funded by Varian Medical Systems.

4 to 10 untreated brain mets, age ≥18, KPS ≥70, life expectancy >3 mo, DS-GPA ≥0.5, largest lesion ≤4 cm, >2 mm from optic apparatus; brainstem lesions allowed. Excluded SCLC, germ-cell, lymphoma, leukemia, myeloma, leptomeningeal disease. Median age 61, KPS 90, 6 mets; NSCLC 50%, breast 27.5%; 11 had prior SRS/WBRT.

Single-isocenter VMAT, 1 mm PTV margin. 20 Gy for PTV <2 cm, 18 Gy for 2.0 to <3.0 cm; 5 Gy x5 to all lesions if any PTV >3 cm, any brainstem lesion, or brain V12Gy >20 mL. 24 pts (125 lesions) got 1 fraction, 16 pts (79 lesions) got 5; median beam-on 8 min.

Primary: OS, judged non-inferior if ≥17 of 40 pts outlived DS-GPA-predicted survival. Secondary: local recurrence, distant brain recurrence, neurologic death, AEs, QOL, steroid use.

22 pts outlived prediction; mOS 8.1 mo, 1-yr OS 35.7%. 1-yr local failure 5% (10 of 204 lesions); distant brain recurrence 35.8% at 12 mo. Neurologic death 20% of deaths.

AEs in 73%, all G1-2, mostly headache and fatigue; no G3-5 treatment-related AEs. Radionecrosis in 5 lesions in 4 pts; 2 pts needed surgery. MMSE, Trail Making, HVLT and FACT-Br unchanged at 3 mo.

mOS of 8.1 mo sits inside the range of prior multi-met SRS series summarized in the paper's Table 4 (medians 5.8 to 14.1 mo), most of them retrospective. The randomized SRS vs WBRT trials for 4 to 20 mets (NCT03550391, NCT03075072, NCT01592968) are the comparators this cannot replace.

The DS-GPA benchmark uses the original formulation, measures from first brain-met diagnosis, and was applied here from protocol SRS in a cohort where 11 had prior brain RT. LC and DBF exclude the 8 pts who died before first MRI, and the paper's own Discussion gives a 6-mo distant failure figure (58%) that conflicts with its Results (20%).

The OS endpoint mostly shows the technique does not shorten life against a prognostic index; it cannot show SRS beats WBRT. The more usable signal is the per-lesion one: 5-fraction plans held 98% LC with low necrosis despite larger volumes, which supports hypofractionating high-volume multi-met plans.

Single-arm, N=40, single institution; OS benchmarked against a DS-GPA prediction, not a randomized WBRT or multi-isocenter comparator. Too few events for LC or necrosis modeling.

Retrospective two-center series (Rome, Negrar), 31 consecutive pts, 204 BM. Outcomes by Kaplan-Meier from SRS; dosimetric accuracy from offline CBCT fused to planning CT with residual shifts applied.

Age ≥18, 4-10 BM <3 cm. Median age 60; lung 14, melanoma 8, breast 5. Concurrent systemic therapy in 9 pts (IO 4, targeted 5).

Single-isocenter DCA via Brainlab Elements, 10 noncoplanar arcs at 5 couch positions. 20-22 Gy for <2 cm, 16-18 Gy for ≥2 cm or near critical structures; PTV = GTV + 1 mm (176 lesions) or 2 mm (28).

1y/2y LC 89%/77% per pt, 94%/86% per lesion; mOS 16.1 mo. Coverage loss (V95 <95%) in 28 targets, driven by distance ≥39 mm (P=.0001) and volume <0.40 cm3 (P=.015).

No G3-4 toxicity. Necrosis in 5 (16.1%) pts, 11% per lesion at 12 mo, 2 with G2 motor deficit; individual V12Gy >10 cm3 predicted it (P=.01).

Roper et al showed coverage held at 0.5° simulated rotation but failed in over one-third of plans at 2°; here measured residuals stayed within 0.5 mm / 0.5° tolerance, which is why 1 mm sufficed. Necrosis tracking V12Gy matches the Korytko gamma knife series the authors cite.

The paper reports pt counts inconsistently (4-6/7-10 vs 4-7/8-10; 10 vs 12 pts with coverage loss). LC is not stratified by margin or by distance from isocenter, so the clinical consequence of the dosimetric miss is untested.

The case for 1 mm is a trade-off: the margin rescues small distal targets while Table 4 shows each added millimetre inflates a 1 cm lesion's volume steeply, feeding V12Gy. That trade-off only holds if intrafraction drift is caught and corrected.

Retrospective 31-pt series, median f/u 11 mo, no comparator arm; margin conclusion rests on dosimetric re-computation, not lesion-level clinical failure by margin.

Retrospective chart review of 100 pts treated at Princess Margaret 1982-1993; 94 analyzed after 6 lost to follow-up. Median follow-up 2.9y (range 0.2-10.4) in the 45 survivors.

Histologically confirmed SCC of the nasal skin; nasal vestibule SCC excluded. T1 60, T2 11, T4 7, TX 16; only 1 pt N1 at presentation.

35 Gy/5 for lesions <2 cm, 45 Gy/10 for 2-5 cm, 50 Gy/20 for >5 cm or bone/cartilage invasion. Orthovoltage in 81%, energy chosen by lesion thickness (75-100 keV <2 mm, 125 keV 2-4 mm, 250 keV >4 mm); 1-cm field-edge margin; no elective nodal coverage.

Primary: local failure-free rate. Secondary: nodal failure-free rate, OS, cause-specific survival, late toxicity.

No RTOG G4 late toxicity and no cartilage or bone necrosis. Skin pallor, atrophy and telangiectasia common 1-5y post-RT, progressive but usually asymptomatic.

The Mazeron nose and vestibule series cited by the authors reported 11% local failure for SCC, in line with the 10% 2y local failure here. A cited vestibule series reported 5y local relapse-free 80%, consistent with the authors' point that vestibule disease does worse and was rightly excluded.

Treatment-era orthovoltage technique and no formal cosmetic assessment, so the optimal schedule cannot be derived. Dose was chosen by size and frailty, confounding any dose-response read.

Authors now prefer 50 Gy/20 or 60 Gy/30 for large infiltrative lesions, since schedules under 4 weeks usually leave a visible cosmetic defect after 1-2y. Many elderly pts still accept 1-2 week courses and the cosmetic trade-off.

Retrospective single-institution series without a surgical comparator; toxicity and cosmesis not formally scored; short survivor follow-up in an elderly cohort.

Retrospective single-institution series, 51 lesions in 48 pts referred 1999-2005. Median follow-up 45 mo (range 4-102); LC by Kaplan-Meier.

Facial BCC (82.4%) and SCC (17.6%), mean diameter 1.5 cm (0.5-4 cm), thickness ≤3 mm in all; thicker lesions went to electrons. Median age 78; 95% radical, 5% adjuvant after lateral-margin-positive excision.

Ir-192 HDR contact BT via custom wax nasal molds (CT-planned) or bolus applicators on flat skin, 1 cm margin, prescribed at 3 mm depth. Standard 48 Gy in 12 fx of 4 Gy, 3 fx/wk, over 4 wk; 3 Gy x 17-18 and 7 Gy x 5 schedules also used.

5 relapses (9.8%) at 6-32 mo, all on the nose and all with three-tube applicators. Nasal tip LC 73% vs 95% on pyramid/wing; all salvaged surgically.

Acute G4 dermatitis in 11 pts (21%), healed within 3 wk; no late complications including chondritis. Cosmesis good or very good in all cases.

Source cites Guix et al. contact HDR-BT with 5-yr LC 98% at 60-65 Gy/1.8 Gy fx, and Rio et al. LDR interstitial BT with 92.5% radical LC. This series sits below those on the nose, driven by the tip.

Only 9 SCC, so no histology-specific read. Cosmesis was physician-graded and the G4 dermatitis rate differs between Results (21%) and Discussion (12%).

Authors attribute nasal-tip failure to undersized three-tube molds and poor catheter bending at the tip's lower surface, and now add catheters. A deeper prescription point was not excluded as a cause.

Retrospective single-arm series, 51 lesions, one institution; no comparator vs Mohs, electrons or orthovoltage. Nasal-tip failures tied to an early three-tube applicator.

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.

International, placebo-controlled, randomised 1:1 phase III, N=1,106 accrued 30APR20 to 09AUG23. Single prespecified interim after 87 MFS-CI events, disclosed only if 2-sided p<0.012. Median follow-up 3.8 yr (IQR 3.3-4.5).

Very high-risk localised prostate cancer, or biochemically persistent/recurrent disease within 1 yr after RP. Median age 71, Gleason 9-10 in 73%, pelvic nodal involvement on CT in 29%, prior RP in 15%.

Darolutamide 600 mg BID vs placebo for 96 wk, both arms on an LHRH analog for 96 wk.

Definitive or salvage RT to prostate or prostate bed plus pelvic nodes in both arms. Dose and fractionation not reported in source.

Primary: MFS on conventional imaging (CT and/or Tc bone scan), chosen per ICECaP surrogacy for OS. Secondary: PSA-PFS, PCSS, OS.

Primary met at interim (table above). OncLive reports MFS benefit consistent across primary vs salvage RT and N+ vs N0, and castration resistance and subsequent hormonal therapy endpoints favouring darolutamide; no numbers given for those.

Any G≥3 AE 43% vs 36%. G≥2 fatigue/asthenia 14% vs 10%; hypertension, fractures and cardiac events not higher with darolutamide.

Tests the same ARSI-added-to-ADT-plus-RT question as ENZARAD (enzalutamide) and ATLAS (apalutamide), and sits against the STAMPEDE abiraterone data that currently anchor intensification in high-risk nonmetastatic disease. DASL-HiCaP differs by mandating pelvic nodal RT and including early post-RP salvage pts.

Staging and progression on conventional imaging in a PSMA-era practice; salvage pts are only 15%. Backbone was 96 wk ADT plus pelvic RT in everyone, so benefit with shorter ADT or prostate-only fields is untested.

The MFS-CI gain is large but OS events are few (21 vs 24) and PCSS is 99% in both arms at 4 yr. Whether this becomes a darolutamide option alongside abiraterone in this setting depends on surrogacy holding at final analysis.

Prespecified interim analysis, not the final primary analysis; MFS-CI surrogate with PCSS and OS immature (OS HR 0.88, CI crosses 1). Randomised, placebo-controlled design is otherwise clean.

Prospective, multicenter, observational, single-arm cohort; N=792 of 800 planned (80% power to exclude a 10% 5-yr LR). Median f/u 5.1y; cumulative incidence with death as competing event.

Women ≥70y, ER ≥50%, HER2-negative, ≤1cm grade 1/2 or ≤2cm grade 1, free margins, after BCS with no RT and no ET. Median age 73.6y.

Primary: 5-yr LR, a histologically confirmed invasive ipsilateral event. Secondary: contralateral BC, OS, BC-specific survival.

5-yr LR 14.8% (95% CI 12.3-17.5), exceeding the prespecified 10% threshold. 2 of 81 deaths BC-related.

PRIME II and CALGB 9343 supported RT omission in older women who received ET; TOP-1 tests the population that skips both. The trial's own benchmark is a national registry LR of 1.3% with RT, not a randomized arm.

Only invasive ipsilateral events counted, so DCIS recurrence is excluded from the primary. Registry comparator differs in era and selection, and ER+ low-grade recurrences accrue well beyond 5y.

Dropping both adjuvant therapies failed the study's own safety bar, while salvage remained mostly breast-conserving. The authors keep RT omission as a shared-decision option, but the result does not show which omitted therapy drove the excess.

Single-arm observational cohort against a historical registry benchmark; no concurrent RT or ET arm, and 5.1y f/u is short for low-grade ER+ recurrence kinetics.

Randomized 2:1, chemo + SBRT vs chemo alone, 75 enrolled and 74 eligible across 14 centers. Phase not stated in source.

Potentially operable (n=48): borderline resectable, or operable with tumor >4 cm, extrapancreatic extension, or nodal involvement. Inoperable (n=26): locally advanced or medically inoperable.

Three months of mFOLFIRINOX or gemcitabine + nab-paclitaxel by clinician choice, then reassessment for surgery. Resected pts received 3 more months adjuvant; unresected pts 3 more months systemic chemo.

SBRT 40 Gy in 5 fractions with fiducial marker guidance and real-time RT quality assurance. 39 of 49 (80%) assigned to SBRT initiated it.

Primary: locoregional recurrence at 12 months. Secondary: PFS, OS, surgical outcomes, toxicity.

Primary endpoint met; benefit significant in the potentially operable stratum, not significant in inoperable disease (P=0.16). Resection and R0 rates numerically higher with SBRT, both non-significant.

G3+ toxicity 70.2% vs 64.0% (P=0.27), no significant increase with SBRT. RT-specific and late toxicity not broken out in source.

Randomized evidence for adding RT to chemo in pancreatic cancer has been inconsistent: LAP07 tested conventional chemoRT in locally advanced disease, and PREOPANC tested preoperative chemoRT in resectable and borderline disease. MASTERPLAN differs by pairing short-course SBRT with modern multiagent chemo and by powering on local control rather than OS.

Incomplete SBRT uptake (80%) and clinician-chosen chemo add noise to a small trial. The OS gain sits on a secondary endpoint with no HR reported in the source, and late GI toxicity is not described.

A local control benefit of this size, carried into PFS and OS, makes a larger confirmatory trial a priority. It does not yet settle which stratum benefits, whether the OS signal is real, or how SBRT should be sequenced with surgery.

Randomized with primary endpoint met, but N=74 across heterogeneous strata, 80% SBRT uptake, and OS/PFS secondary; phase not stated, conference trade-press source only.

Prospective single-institution series, 136 consecutive pts treated 1992-1997 in Barcelona. Minimum follow-up 12 mo; median follow-up not reported.

Pathologically confirmed facial BCC (102) or SCC (34), 73 primary and 63 recurrent after prior local therapy. Gross tumor left in place in most; margins positive in 128. No nodal or distant disease on CT head/neck and chest X-ray.

HDR Ir-192 via 117 custom PMMA molds (3-7 parallel catheters, 5 mm bolus layer) or 19 Brock applicators. 6000-6500 cGy in 33-36 fx of 180 cGy at 5 mm depth; lesions ≥4 cm boosted 1800 cGy/10 fx after a 3-wk rest to 7500-8000 cGy. Eye shielded with a 5 mm lead sheet in the mold.

All pts complete responders; 3 local recurrences (1/73 primary, 2/63 recurrent). 5y actuarial LC 98% overall, 99% primary, 87% recurrent; no regional or distant failure.

Erythema G1 in 117 and G2 in 19; 14 (10%) had G1 ulceration at 6 wk, all healed by 4 mo. Good/excellent cosmesis 98% at 6 mo; no severe late complications.

Primary-tumor LC of 99% sits alongside the 95% superficial X-ray result in the Lovett EBRT series and above Lovett's 77% with electrons. Daly's Ir-192 interstitial implants reached 96% LC but with 18% severe late effects, the toxicity gap the mold approach is designed to close.

Dose per fraction (180 cGy) far from modern short-course skin brachy, so the late-effect profile may not transfer. Recurrent-tumor LC timepoint reported inconsistently (5y vs 4y), and cosmesis was graded by the treating team.

The contribution is technical: a reproducible, afterloaded surface applicator that conforms to non-flat facial anatomy with a sharp edge gradient. It shows high control with conventional fractionation but does not settle how it compares head-to-head with superficial X-ray, electrons, or Mohs.

Single-arm single-institution series without a comparator; follow-up minimum only 12 mo with median unreported; comparisons rest on historic EBRT and implant series.

Retrospective single-institution series of 13 pts treated at the Christie Hospital up to July 1996. Technique description with three illustrative cases.

9 BCC, 3 SCC, 1 intraepidermal carcinoma. Lesion confined to pinna skin; dermal ultrasound confirmed cartilage not invaded in all but one.

HDR microselectron with single stepping iridium source via custom vacuum-formed mould. 45 Gy in 8 fx over 5 days prescribed to the surface, mould height set so tumour depth lies within the 80% isodose. Sandwich mould case reduced to 42.5 Gy.

Complete tumour resolution in all pts, barely perceptible scar. No recurrences and no late complications over minimum 18 mo f/u.

Moderate cutaneous erythema limited to the high-dose area, settled by the 6 wk visit. No discernible reaction on the contralateral pinna skin.

Authors position moulds against electrons (poor fall-off for thin lesions, cartilage necrosis risk), 30 kVp X-rays (dose inhomogeneity on curved surfaces, limited availability) and surgery (amputation or excision with graft). No head-to-head data.

Outcomes reported as a blanket statement without per-pt f/u, actuarial LC, or a validated cosmesis scale. Late cartilage toxicity can emerge beyond 18 mo, and the LQ-based BED rationale assumes complete repair between fractions.

The contribution is technique, not efficacy: ultrasound depth measurement plus tunable source height makes the plan conformal to sub-millimetre tumour thickness. Whether a higher late-tissue BED is tolerated because of the small volume is asserted, not shown.

Single-institution case series of 13 selected pts, no comparator, 18 mo minimum f/u too short for late cartilage effects; outcomes descriptive only.

Single-institution retrospective review, January 2007 to December 2018. 50 pts, 53 lesions, minimum 6 mo follow-up, median follow-up 15 mo (range 6-27). LC by Kaplan-Meier.

Histologically confirmed BCC or SCC, AJCC 8th T1, all NCCN high-risk by area H or area M location. Median age 80; selected by a multidisciplinary dermatology clinic, mostly for inability to tolerate or refusal of surgery.

40 Gy in 8 fractions twice weekly (BED 60 Gy, α/β 10) via Ir-192 HDR catheter flap, CT-planned in BrachyVision. CTV = visible tumor + 5 mm, PTV = CTV with no margin; 5 mm spacers protected the nasal mucosa, globe and gingiva.

1-yr LC 92%, 4 local recurrences, 3 in nose/eyelid/lip. 49 lesions (92%) had good/excellent cosmesis with complete remission.

Acute G1 60%, G2 35%, G3 5%, all after fraction 5. Chronic G2 telangiectasia in 2 pts (4%) at 12 mo, no chronic G≥3, no toxicity-related hospitalization.

Local control falls inside the 87%-100% range of prior retrospective HDR surface-mold series. The only randomized surgery-vs-RT trial in facial BCC cited by the authors found 4-yr failure 7.5% vs 0.7% favoring surgery, though RT there was mostly interstitial brachy, not surface HDR.

Median V100 85% falls short of the ≥95% PTV coverage goal, and depth was assessed mostly by palpation. Abstract and body disagree on acute toxicity grade, and the Discussion understates chronic G2 events.

The flap's value is conformity on irregular surfaces where surface molds and electrons struggle, yet recurrences clustered in exactly those sites. BCC and SCC got identical dose and margins, consistent with NCCN, the 2020 ASTRO guideline and the 2019 ABS consensus, so histology-specific dosing is still untested.

Single-arm retrospective series, surgery-unfit/refusing pts, 15-mo median f/u; no comparator vs Mohs or EBRT. Consistent with prior HDR surface-mold series.

Retrospective review of all Ir-192 HDR surface mould cases at one BC Cancer center, 2010-2017, 65 lesions in 59 pts. Median follow-up 8 months.

Median age 82 (45-97). BCC 54%, SCC 31%, plus melanoma, lentigo maligna, Merkel cell, cutaneous NHL and one keloid. Mostly head and neck (forehead/temple, nose, scalp, cheek/lip); 7 lesions palliative-intent.

Individualized Aquaplast + superflab mould, catheters ~1 cm apart, CT-based planning in BrachyVision. Most common 40 Gy/10 fx (48.2%); range 15 Gy/3 to 60 Gy/30 fx. Prescribed at 0.5 cm depth, CTV from clinical wire with no PTV expansion.

2-yr LC 84.9%, 2-yr PFS 71.5%, 2-yr OS 77.6%; CR 96.8% at 2-4 mo. Of 20 deaths, only two were from the skin malignancy. No dosimetric or histologic factor reached significance on univariate analysis.

No G3-5 acute or late toxicity. Acute G2 dermatitis 32% and ulceration 8%; one late G2 necrosis (2%) appearing around 10 months.

The authors place their LC within the brachytherapy literature range of 83.3% to 100% and against EBRT LC of 87-100% and Mohs at 95-99%. Gauden et al. reported LC 98% with 36 Gy/12 fx, but at similarly short follow-up and largely in a post-resection margin-positive setting. GEC-ESTRO grades the technique B.

Histology and intent are pooled (keloid, lymphoma, melanoma, palliative lesions). Toxicity was graded retrospectively from records and photographs, and cosmesis was not scored. Internal inconsistencies (median age 82 vs 83, follow-up 8 vs 9 mo, sex counts summing to 65 of 59 pts) lower confidence in the tabulated data.

The series shows the technique is deliverable and tolerable in a very old cohort, which is the realistic use case. It does not settle the durability of control, the right prescription depth or margin, or whether coverage metrics predict recurrence.

Retrospective single-institution series, n=59, mixed histology and intent; 2-yr estimates drawn from a median 8 mo follow-up with no comparator arm.

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.

Single-centre series of 94 pts treated with Axxent eBT, Sept 2015 to Oct 2017. Each eBT plan was replanned a posteriori for Ir-192 and Co-60 (282 plans); toxicity scored by RTOG. Mean follow-up 14 mo (4 to 25).

Postoperative endometrial cancer, mean age 65.9 (33 to 84), FIGO IA through IVA. 33 pts (35%) received chemo before RT.

eBT alone 25 Gy/5 fx (n=37, stage IA plus seven IB1) or pelvic EBRT 23 × 2 Gy then eBT 15 Gy/3 fx (n=57), twice weekly. Dose prescribed at 5 mm from a 2.5 to 3.5 cm cylinder; 50 kVp source, TG-43 planning, no RBE correction.

Only one G2 acute event. At 1 month, vaginal G1 5.3%, rectal G1 1.1%, urinary G1 2.1%, no G2.

PORTEC-2 established vaginal brachytherapy as adjuvant RT for high-intermediate risk disease using conventional HDR; this series does not test eBT against that clinical benchmark. A cited multicentre eBT series reported bladder V50% 11.5 ± 9.7% and rectum 17.4 ± 10.9%, in the same range as here.

Higher V150/V200 places hotter dose at the vaginal mucosa, where late stenosis would show and 14 mo cannot capture it. TG-43 without heterogeneity correction may misstate low-energy dose in tissue.

The OAR advantage comes from rapid dose fall-off at low energy, the same property that concentrates dose near the applicator surface. Whether uncorrected RBE translates into more late mucosal toxicity, or whether RBE-based de-escalation would cost control, remains open.

Single-centre uncontrolled series, 14 mo mean f/u; HDR comparison is replanning, not a treated arm; no late toxicity or local control data at meaningful follow-up.

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).

Retrospective multicenter imaging review, 4 academic centers, staging scans read by a single abdominal radiologist. Each node transferred to a CT template by its relation to the aorta and renal arteries, with craniocaudal scaling for height.

90 pts, CS IIA/B or recurrent CS I seminoma after orchiectomy, nodes ≤5cm. 40 (44%) relapsed on CS I surveillance at a median 8.5 mo (range 3.2-50.4); 50 (56%) node-positive within 3 mo of diagnosis. 48 (53%) left-sided, 41 (46%) right-sided primaries.

Proposed CTV: 2.5cm lateral/posterior and 2.1cm anterior expansion of arterial vasculature, superior border 1cm above the right or 1.5cm above the left renal artery. Classen acetabular inferior border retained; NCCN 2cm GTV boost and setup margins added on top.

145 nodes, average 1.6 per pt, median size 18 mm. 99% of nodes fell inside the proposed expansion; nodal region was unrelated to CS at presentation (P = 0.16) or primary laterality (P = 0.15).

Classen extended fields (prospective phase II, 2003) are the NCCN- and European consensus-endorsed standard; this map supports Classen's acetabular inferior border but argues the T10/T11 superior border overtreats. MRC TE10 linked smaller fields to less acute GI toxicity and leukopenia. Martin et al. used a 1.4cm aorta/IVC expansion from non-enlarged nodal anatomy.

Single-timepoint CT in many pts, so original nodal position before reaching size criteria was estimated, not observed. Two atypical nodes (1.4%) were excluded from the expansion analysis. Relapses that would emerge outside the reduced field after treatment are unmeasured.

The case for smaller fields rests on second-malignancy risk in a young cohort, with extended fields linked to up to 50% more SMNs than PA strip fields in cited data. The trade the authors accept is a small out-of-field relapse risk, judged salvageable, against lower SMN risk.

Retrospective imaging-defined node map; proposed CTV never tested for relapse or toxicity. Authors themselves limit it to research use pending validation.

Prospective multicentre observational study, 30 German centres, enrolment April 1991 to March 1994. 94 enrolled, 87 assessable, median follow-up 70 mo. Analysed ITT, including 22 pts with major protocol violations.

Histologically confirmed pure testicular seminoma, Royal Marsden stage IIA (<2 cm) or IIB (2-5 cm) after high inguinal orchiectomy. Elevated AFP excluded; βHCG up to 200 IU/L allowed after year 1. 66 IIA, 21 IIB; median age 32.5 and 32.

AP/PA hockey-stick to para-aortic/paracaval and ipsilateral high iliac nodes, gross disease plus 2 cm margin, T11 to acetabular rim. 2.0 Gy/fx: 30 Gy for IIA, 36 Gy for IIB, no boost; 5 pts treated bilateral iliac.

Primary: relapse-free survival at 5 years. Secondary: disease-specific survival (expected at least 95% at 5 yr) and acute/late GI and skin toxicity.

Acute toxicity dominated by grade 1 nausea (53% IIA, 52% IIB); no grade 4. No late GI toxicity, no peptic ulceration, no second malignancy to date; one pt with G1 skin hyperpigmentation.

Prior stage II series used larger portals covering the entire ipsilateral iliac/inguinal chain and contralateral pelvis; this cohort shows the reduced field loses no pelvic control. The source places modified EP (9% relapse, 33% G3/4 leukopenia) and carboplatin alone (15% failure) as no better on control with more toxicity.

Study was not designed to test reduced vs extended portals, so the toxicity advantage is inferred against historic series. Seven pts lost to follow-up were excluded rather than censored, and the IIB cohort is too small for its own protocol-violation analysis.

Failures were all extra-field (mediastinal or lung) except one lateral para-aortic field-edge relapse, and all were salvaged, so DSS was 100%. The authors suggest room for dose reduction below 30 Gy in IIA, though no dose-response relationship was established.

Single-arm observational cohort with no randomised comparator vs chemo; IIB subset small (n=21). Single-arm gate caps the verdict despite 70-mo follow-up.

Multi-institutional phase I/II, single-arm, N = 62. Median follow-up 39.4 mo.

Intraprostatic radiorecurrence (IPR) after any form of RT for localized prostate cancer. GC results available in 31 pts.

Dose-escalated focal salvage HDR, up to 30 Gy in 1-2 fractions. 24 pts received one fraction and 38 received two.

Primary: acute RT-related G3+ GU and GI toxicity (CTCAE v4.03). Secondary: all-grade toxicity, QoL (EPIC-26, IPSS), bPFS, rPFS, LRFS, MFS and survival.

No acute G3 toxicity. Late G3 toxicity in 2 pts (3.2%); QoL changes did not meet MCID criteria.

Prospective salvage brachytherapy data after EBRT are sparse, with RTOG 0526 testing whole-gland salvage LDR in this setting. F-SHARP adds a focal, dose-escalated HDR approach and a genomic risk layer that prior salvage series lacked.

The GC analysis is restricted to 31 of 62 pts and the >0.85 cutpoint rests on n = 4, so it is a descriptive tail, not a validated threshold. The 1 vs 2 fraction comparison was not randomized and is underpowered for equivalence.

Toxicity is the settled part: focal dose escalation to 30 Gy in the re-irradiated gland produced no acute G3 events. Durability is the open part, since bPFS at 3 yr is 62.7% and the efficacy endpoints carry no comparator.

Single-arm phase I/II, N=62, toxicity primary objective; efficacy endpoints secondary and uncontrolled. GC signal from half the cohort.

Retrospective single-centre audit of 97 pre/post-treatment CBCT pairs from 20 pts. Margins were calculated from IFPM alone and with the updated BIR geometric uncertainty guidelines.

36.25 Gy in 5 fractions SBRT without intra-fraction tracking, with fiducial-based daily online CBCT IGRT. Current margins were 6 mm isotropic, 3 mm posterior. Mean pre- to post-imaging interval was 9 min.

magnitude and direction of IFPM and coverage by current margins. Secondary: margins derived from IFPM alone and from the BIR guidelines.

Averaged 3D RMS IFPM was 2.5 mm (4.2 mm), mostly posterior (70%) and inferior (63%). Current margins covered 92% of fractions, and 8 of 97 exceeded them, six posteriorly.

The authors report RL motion above comparable CBCT series, with AP and SI comparable. A larger cited margin study (n=205) found smaller systematic errors and similar random errors.

Delineation error, the dominant component, came from an MRI-only study and is probably smaller than real CT or fused MR/CT error. Deformation was set to 0, match error was assumed rather than measured, and AP and SI were not split by direction.

The guideline-derived numbers suggest lateral margins could shrink while the inferior margin grows, but the inferior increase rests heavily on one outlier contour. The authors advise checking outcomes in current trials before changing practice, given favourable control and toxicity with existing margins.

Single-centre retrospective geometric audit, n=20, no clinical outcome endpoint; proposed margin changes are untested against toxicity or biochemical control.

Single-institution consecutive series from a prospectively maintained registry, 854 pts treated 1998-2012. Median follow-up 11.3 yr (max 19). Not randomized; no comparator arm.

Biopsy-proven, clinically localized prostate adenocarcinoma across all NCCN risk groups: 266 LR, 238 FIR, 106 UIR, 244 HR. Median age 68, median PSA 8.6 ng/mL. ADT in 61%, mostly 1-6 mo.

70 Gy/28 fx at 2.5 Gy/fx, IMRT with daily IGRT (BAT ultrasound 94.8%). CTV prostate alone for LR, plus proximal SV for IR/HR; PTV margin 4-10 mm. Elective pelvic nodes in only 5 of 244 HR pts.

Whole-cohort 10-yr bRFS 71%, cRFS 86%, OS 69%, PCSM 6.8%. Of 125 clinical failures, 117 were distant and 8 local-only.

10-yr late G≥3 GU 2% (mostly urethral stricture) and G≥3 GI 1% (mostly rectal bleeding). One grade 5 event each in GU and GI. 119 pts (14%) developed a new cancer, lung most common.

Authors place this alongside RTOG 0415, CHHiP, PROFIT, HYPRO and the MDACC series, none with 10-yr outcomes at publication. RTOG 0415 used the same 70 Gy/28 fx with G3 toxicity 3% to 4% at 5 yr, under looser dose-volume constraints and without mandatory IMRT.

Toxicity was physician-reported from retrospective chart review, likely underreporting events. Institutional constraints (rectal/bladder V70 5%, up to 10%) are far tighter than NRG-GU005 allows, so the toxicity rates may not hold under trial or community constraints.

The schedule controls the prostate well over 10+ yr; the risk-group gradient is driven by distant failure. What is left open is whether HR outcomes improve with longer ADT and nodal coverage at this fractionation.

Single-institution nonrandomized cohort without a comparator arm; long follow-up adds durability to randomized hypofractionation data but cannot establish equivalence on its own.

Retrospective development (training n=756, RP genomic data) and validation (n=235, biopsy genomic data) with competing-risks DM estimates; training median follow-up 8 years. Two prospective cohorts (n=4,960 RP; n=977 biopsy) used for reclassification only.

Localized prostate cancer across NCCN low to high/very-high risk. Training cohort second-line therapy included adjuvant RT 7%, salvage RT 13%, salvage ADT 18%.

Outcome: distant metastasis at 10 years; PCSM secondary. Discrimination by time-dependent c-index; reclassification vs NCCN three-, four- and six-tier systems.

Clinical-genomic tiers separated DM where NCCN fav-int and unfav-int did not split from their neighbors; c-index 0.77 vs 0.68 for NCCN four-tier in training.

Benchmarked against NCCN risk groups and CAPRA (continuous score 0.68, groups 0.64 in training), both outperformed on DM discrimination. The authors frame NCCN as built to predict biochemical recurrence, which ICECaP found is not a surrogate for survival.

Adjusting for ADT and RT cuts clinical-genomic HRs from 9.3 and 21.9 to 3.5 and 6.1, so part of the gradient tracks treatment received. Training specimens date from 1997-2004, and many authors are GenomeDx employees.

The system turns a continuous classifier score into categories that fit existing NCCN-based decision rules, which is its practical value. It does not answer whether treatment intensification or de-intensification by the new tier changes outcomes.

Retrospective development with a 235-pt biopsy validation set and sparse low-risk events; prognostic only, no evidence that reclassification-driven treatment changes outcomes.

Retrospective two-center review (MGH n=248, BWH n=154), N=402. Univariate and multivariate logistic regression, forward stepwise selection. External validation in a separate, previously published community-hospital set of 206 pts.

Clinically node-negative invasive breast cancer with 1-3 H&E-positive SLNs and completion ALND, defined as ≥6 nodes examined. No neoadjuvant systemic therapy. Mastectomy 46%, breast conservation 53%.

Outcome modeled: ≥4 involved axillary nodes (SLN plus non-SLN). Model performance was assessed by AUC, Hosmer-Lemeshow, sensitivity and NPV.

Seven independent factors: tumor size, lobular histology, LVSI, ENE, number of positive SLNs, macrometastasis, and number of negative SLNs. AUC 0.83 in derivation, 0.81 in validation. At a 5% cutoff, NPV 94.7% and sensitivity 97.5%.

The authors' hypothesis is that pts below 5% predicted risk could be treated with modified high tangents instead of comprehensive nodal RT to the SCV fossa and axillary apex. That would have spared 34% (derivation) and 37% (validation).

Similar in aim to the MD Anderson mastectomy series, where pts without three risk features had <2% risk of ≥4 nodes, and to Chagpar et al's 1,133-pt model. This model adds LVSI and SLN metastasis size. It predates the Z0011 and AMAROS axillary-management era.

The ≥6-node ALND definition may include axillary samplings. The abstract and results disagree on the count of ≥4-node pts (87 vs 81). Validation underestimated observed cases, and the validation set was chosen for availability.

The tool estimates nodal burden, a surrogate for the risk of regional failure. Whether tangent-only RT is safe in the low-risk group needs outcome data the paper doesn't have.

Retrospective model built on dissected pts with one small external validation. It predicts nodal burden, not regional recurrence after RT field reduction; the omission hypothesis was never tested.

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.

Multicenter, randomized, phase 2/3 trial. 658 screened and 588 randomized from August 2022 to August 2025 (296 iTNT, 292 TNT). Data as of February 6, 2026; blinding not stated in source.

Mid-to-low pMMR LARC. Median age 59, 71.1% male. T3-4 94.9%, node-positive 92.9%, lower tumors 71.3%, MRF+ 48.8%, EMVI 45.4%.

SCRT followed by 4 cycles of CAPOX with sintilimab (iTNT) or the same regimen without sintilimab (TNT). After evaluation, resection or W&W, then 2 additional cycles of the same prior regimen.

SCRT 5 Gy x5 in both arms, delivered first. All pts completed SCRT. Technique, target volumes and the interval to surgery are not reported in source.

Primary: CR rate for phase 2 and 3-year DFS for phase 3. This report covers short-term efficacy and safety only.

Arm-level CR, pCR, toxicity and compliance are in the table above. 92 pts (15.6%) adopted W&W after cCR, and 458 had undergone surgery with 8 awaiting.

Grade 3-4 toxicities 27.7% (iTNT) vs 19.9% (TNT). Grade 3-5 immune-related AEs in 3.4% of pts. Chemotherapy completion was similar (92.9% vs 94.1%); surgical morbidity is not reported.

Per the source, several phase II studies suggested that adding immunotherapy to TNT raises CR, but phase 3 comparisons of TNT with vs without immunotherapy were lacking. RAPIDO and the original STELLAR trial established SCRT-based TNT, while UNION and TORCH tested SCRT plus checkpoint blockade without an otherwise-identical immunotherapy-free TNT control.

Overall CR pools pathological and clinical response, and whether cCR assessment was blinded is not stated. pCR is computed on operated pts only, with unequal denominators (211 vs 247). The per-arm W&W split is not reported.

The randomized variable is sintilimab alone, so the trial isolates the drug and says nothing about SCRT vs long-course CRT as its partner. A higher CR opens an organ-preservation route, but whether it converts to DFS in pMMR disease is unsettled until the phase 3 primary reads out.

Randomized and fully accrued, but this is a short-term CR readout; the phase 3 primary (3-year DFS) and W&W regrowth data are not yet reported.

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.

Phase III randomized trial, 1:1 protons vs photons, stratified by planned fractions (5 vs 15) and tumor vascular thrombosis. 117 screened June 2017 to January 2026, 116 randomized, 115 eligible/analyzed (protons 57, photons 58). Powered for HR 0.58 with 112 eligible pts and 88 OS events (80% power, 1-sided alpha 0.05), with 1 interim at 63 OS events.

Unresectable or locally recurrent HCC, pathologically or radiographically proven, Zubrod PS 0-1, Child-Pugh A or B7, 1-3 HCCs with size limits of 15, 10 and 6 cm for 1, 2 and 3 lesions; TVT allowed with a single lesion. Median age 72, 93% CP A, 75% no prior treatment, 57% single tumor, 23% TVT.

Protons or photons in 5 fx (30-50 Gy) or 15 fx (37.5-67.5 Gy), dose individualized on liver-GTV mean dose in both arms. Delivered dose by arm, proton delivery technique and motion management are not reported in source.

Primary: overall survival (Kaplan-Meier, log-rank). Secondary: PFS, local progression, adverse events (CTCAEv4).

Trial released at the planned interim after the futility boundary was crossed (HR>1), median follow-up 20 months. No endpoint favored protons with statistical support; arm-level figures are in the table.

Treatment-related grade 3+ AEs were 11% with protons vs 24% with photons (p=0.09), numerically lower but not statistically different. AE type, hepatic decompensation and late effects are not broken out in source.

Retrospective proton vs photon comparisons in HCC had suggested a survival advantage attributed to liver sparing, and that hypothesis set the effect size this trial was powered for. Under randomization the OS estimate sits on the other side of unity. The source cites no comparator trial.

Cause of death is not reported, so an OS gap alongside PFS HR 1.02 and similar LP cannot be attributed to liver toxicity, competing mortality at median age 72, or chance. Subsequent systemic therapy by arm is unreported across an accrual period running June 2017 to January 2026. No subgroup data by Child-Pugh class, tumor size or fraction schedule in the abstract.

The trial rules against the large OS benefit it was designed to find; with a 90% CI of 0.83-2.04 it does not establish harm. The only signal in the hypothesized direction is the G3+ AE rate, which is underpowered. What stays open is whether protons help where liver reserve is the binding constraint, a group this cohort (93% CP A) barely samples.

Reported at planned interim after futility boundary crossed, abstract only, 115 pts with wide CIs. Negative for proton superiority, not evidence of harm; photons remain the default.

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.

Open-label, randomised phase 2/3 at 37 sites in five European countries. Phase 2 randomised 1:1:1 to LCCRT-OP, SCRT-OP or primary TME (N=120); phase 3 used a partially randomised patient-preference design, with OP choosers randomised 1:1. Bayesian framework; this 12-month analysis covers 426 pts recruited before Aug 8, 2023 (409 mITT).

Rectal adenocarcinoma ≤40 mm, mrT1-T3bN0 on MRI, ECOG 0-1, with primary TME judged reasonable. Excluded: MRI nodal involvement or EMVI, tumour within 1 mm of the mesorectal fascia, anterior tumours above the peritoneal reflection, predominantly mucinous histology, metastases. mrT2 in 242 (73%) OP pts; 266 (80%) below the peritoneal reflection.

LCCRT-OP: 50 Gy in 25 fractions with oral capecitabine 825 mg/m² twice daily. SCRT-OP: 25 Gy in five fractions. Response assessed at 16-20 weeks with TAE for near-complete response; target volume not in source text.

Phase 2 primary: feasibility, recruitment at months 12 and 24 against thresholds of ≥4 and ≥6 randomisations/month (achieved 3 and 6). Phase 3 primary: organ preservation at 30 months (no TME, stoma or local recurrence), not yet reported. This analysis reports 12-month TME-free survival, response and safety.

Phase 2 alone gave HR 3.7 (95% CI 1.7-8.0), with median TME-free survival 7.6 mo after SCRT-OP vs not reached after LCCRT-OP; pooling phase 3 pulled the estimate toward the null.

Primary TME: G≥3 SAEs in 14 (18%) of 78, intraperitoneal perforation from anastomotic leak in 12 (15%), and one postoperative death from sepsis. After TAE, perineal fistulation occurred in two (1%) OP pts. Capecitabine dose modification in 18 (11%) of 161.

At design, primary TME without neoadjuvant therapy was standard for this population. OPRA addressed watch-and-wait after neoadjuvant therapy in locally advanced disease; STAR-TREC is a randomised test of which radiation schedule best supports response-adapted organ preservation in smaller, node-negative tumours.

The shrinking HR from phase 2 to the pooled cohort suggests early overestimation, and phase-difference analyses are exploratory post-hoc. Occult nodes in 17 (22%) TME specimens imply MRI N0 misses nodal disease that organ-preserving arms never sample. Median follow-up was 34 and 35 mo, but outcomes were censored at 12 mo.

At 12 months, a longer RT course with capecitabine buys more complete responses and fewer TMEs than SCRT, at the cost of more acute SAEs. What it does not settle is durable organ preservation, local regrowth and function, all tied to the 30-month endpoint.

Governance-led interim at 12 mo; prespecified 30-mo organ-preservation endpoint not yet reached. Open-label, TME-free survival only, TME comparison non-randomised in phase 3.

Retrospective review of a departmental re-RT database, single institution (Porto), treated 2017-2021. Thirteen identified, two excluded (different fractionation; T4 treated with WBI), leaving N = 11. Median follow-up 41 months (27-62), Kaplan-Meier estimates with two-sided log-rank comparisons.

Isolated ipsilateral breast tumor recurrence after BCS plus whole-breast irradiation, all T1-2, clinically node negative, no metastatic disease before second BCS. Inclusion required age ≥ 50, unifocal disease on ultrasound, mammography and MRI, size < 2-3 cm, and an interval of ≥ 48 months from primary treatment. Median age at recurrence 63 (41-81), ECOG 0-1 in all.

Initial course was whole-breast irradiation at 2 Gy/fraction in all 11, with a 10 Gy / 5 fraction boost in 2. Re-RT was partial breast, 40 Gy at 2.67 Gy daily, direct-planning IMRT, supine, without DIBH. Median interval between courses 107 months (27-239).

No registered primary. LR-FS, DR-FS and OS by Kaplan-Meier from the day of re-RT completion, with adverse events graded by CTCAE v5.0 (acute < 90 days, late > 90 days) and cosmesis by the Harris scale.

At 3 years, 9/11 free from local recurrence, 10/11 from distant recurrence, 9/11 alive, each 86%. Two local recurrences, at 11 and 15 months. TAM-stratified LR-FS was 100% low risk, 80% intermediate, 100% in the single high-risk patient; the OS difference between low and intermediate risk was not significant (p = 0.75).

No grade 3 or higher late reactions. Acute events were skin-limited, most commonly grade 1-2 dermatitis (8 grade 1 erythema, 2 grade 1 pigmentation, 1 pruritus). At 1 year, grade 1 fibrosis in 9 and grade 1-2 oedema in 5, breast pain grade 1 in 2. No cardiopulmonary events, no rib fractures. Cosmesis good in 6, fair in 2, poor in 3.

RTOG 1014 (45 Gy / 1.5 Gy BID, 3D-CRT, n = 66) reported 7% late grade 3 and no grade 4-5 at 5.5 years; Janssen 2018 (n = 83, 45 Gy / 1.8 Gy daily) reported a 15% LR rate at 35 months. Brachytherapy series sit at 94-100% third-IBTR-free survival with 8-11% grade 3-4 complications. This cohort's toxicity is at or below all of them, on a fraction of the patient numbers and follow-up.

The first course's dose distribution was unavailable, so no composite plan sum could be produced and cumulative OAR dose stays uncharacterized, which is the number that actually gates re-RT safety. Cosmesis was scored unblinded by the treating radiation oncologist, and the reported confidence intervals (46-62%, 52-65%, 47-63%) do not contain their own 86% point estimates as printed.

The contribution is schedule feasibility, not efficacy: a once-daily 15-fraction re-RT plan met every published constraint with wide margin, which is what a department needs before abandoning BID. Whether 40 Gy in 15 fractions matches 45 Gy BID for in-breast control remains untested; two events in 11 patients cannot answer it.

Retrospective single-arm series, N=11, 2 events, median f/u 41 months. No comparator vs mastectomy or vs the established BID re-RT schedules.

Prospective observational natural history cohort at the NCI, presented at GU-ASCO 2026. Baseline data on the first 130 pts; the cohort is ongoing at a median follow-up of about 2 years with interim outcome data pending.

Men with biochemical recurrence after definitive therapy, all of whom had already received salvage radiation or declined it. PSA ≥ 0.5 required for a baseline PET. Deliberately framed as PSMA-positive BCR, a state that would not have been detectable in the historical trials these pts map onto and that excluded them from metastatic trials.

The presented analysis is cross-sectional: PSMA PET findings at baseline against PSA doubling time, the field's working predictor of metastasis in BCR. Imaging cadence is protocolized at annual if the baseline PET is negative, every 6 months if anything is seen, including equivocal findings.

Among pts with slow kinetics (PSADT > 9mo and > 12mo), the majority still had PSMA PET findings once PSA was above 5: nodal disease, prostate bed recurrence, and small equivocal bone lesions. Only about a third have started any therapy. A companion poster found 5 of the first ~150 pts progressed on conventional imaging at roughly 1.5yr, and over 95% showed no abrupt PET change out of step with PSA.

The counts are reported conversationally in an interview ("about 130", "the first 150 or so", "that number's five"), with no stratum denominators and no CIs, so the PSADT-by-PET relationship cannot be quantified from this source. Allowing any therapy under 6 months, including SBRT and intermittent ADT, means the observed group is not an untreated comparator.

The claim being staked is that PSMA PET positivity in BCR is near-ubiquitous above PSA 5 and therefore weakly discriminating, so it should not by itself trigger treatment. What the cohort has not yet shown is whether PET burden or its change over time adds anything to PSA doubling time for predicting the outcomes that matter.

Baseline cross-sectional read of an ongoing single-institution cohort, median f/u ~2yr, no outcome analysis yet. Numbers reported conversationally, not tabulated.

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.