onc brain

Paired dosimetric replanning study at 2 institutions (TJU, UAB). 15 previously treated pts from each site were replanned by the other site with its own technique. Comparison by paired 2-tailed Wilcoxon signed-rank, prespecified α .05.

30 pts with 4 to 10 brain metastases, 217 targets, median 7.5 per case. Individual target volume 0.014 to 17.73 cm3; total PTV 0.49 to 27.32 cm3, median 7.05 cm3.

14 to 24 Gy single fraction, prescriptions unchanged between plans and largely RTOG 9508-based. RA used 2 to 4 noncoplanar VMAT arcs at 10 MV FFF with 3 ring tuning structures. MME used automated noncoplanar DCAs at 6 MV FFF with up to 1 mm MLC margin and island-blocking avoidance.

Per target: RTOG CI, Paddick CI, coverage. Per plan: V12Gy, V8Gy, V5Gy, mean brain dose, plus arc, MU, and beam-on estimates.

RA favored conformity and the V12Gy/V8Gy band; MME favored V5Gy and Dmean. The brain DVHs cross near 6 Gy, and below 2.1 cc total PTV MME was favorable on most metrics.

Gevaert et al (10 cases, 40 mets) found higher V12Gy and V5Gy for RA. Its Paddick CI of 0.65 ± 0.08 (MME) and 0.67 ± 0.16 (RA) sits below this study's 0.70 and 0.77, which the authors read as plans that were not fully optimized. Narayanasamy et al (8 pts, 40 targets) found the platforms comparable but was likely underpowered.

Different beam energies and dose algorithms (pencil beam vs AAA) per platform, so platform effects cannot be cleanly separated from energy and algorithm. Each platform had one expert institution, so planner skill is part of the RA result. Hotspots and homogeneity were not compared, and text and Table 1 medians disagree for V12.

Both platforms met clinical goals, and the differences are small and dose-band specific. Moderate isodose spill has retrospective links to radionecrosis, while low-dose spill has no toxicity correlation yet. It may matter more as pts survive to repeat SRS or WBRT.

Dosimetric planning study with no clinical endpoints; 6 vs 10 MV energy and two dose algorithms confound the platform comparison. Platform and planner effects not separable.

Dosimetric planning study: three plans (DCAT, CoVMAT, NcVMAT) per pt for 15 pts treated April 2016 to October 2017, single institution. Two-way ANOVA with Bonferroni post-hoc for PTV/GTV indices; repeated-measures ANOVA with Holm for normal brain.

Single brain metastasis, longest diameter 2-3 cm, chosen because local control and radionecrosis are worse than for smaller lesions. Median PTV 6.4 cm3 (range 3.7-16.2).

20 Gy/1 fx to PTV (GTV + 1 mm), normalized to D99.5%, 6 MV on TrueBeam STx, AcurosXB. PTV D2% held near 142% of Rx across techniques so the comparison is at matched heterogeneity.

NcVMAT gave the best conformity (RTOG-CI and Paddick CI vs DCAT) and lowest normal-brain V20 to V5Gy vs both comparators. CoVMAT had the largest V15Gy through V5Gy and the fewest MU; both VMAT techniques ran longer beam-on than DCAT.

Vogelbaum et al. showed higher local recurrence and radionecrosis for mets >2.0 cm, which is the population chosen here. Molinier et al. compared the same three techniques but across mixed intracranial targets and with different TPS and algorithms, which this study removes as a confounder.

V12Gy is a planning surrogate for necrosis; no clinical outcomes were measured. Plan quality for inverse-optimized techniques is operator- and optimizer-dependent, and DCAT plans used manual MLC shaping, so the margin between techniques may not transfer across centers.

The useful finding is that coplanar-only VMAT is not an adequate substitute for non-coplanar DCAT on low-dose spill, while non-coplanar VMAT beats both. The cost is beam-on time, relevant for intrafraction motion in frameless SRS.

Planning study in 15 pts; dosimetric V12Gy surrogate stands in for radionecrosis, with no clinical outcomes, single TPS and single institution.

Single-institution retrospective review of consecutive pts treated 1966-1997. 468 pts, 531 lesions; median f/u 5.8 yr (range 2-24).

Biopsy-proven epithelial skin cancer: 389 BCC, 142 SCC; 364 previously untreated, 167 recurrent. Median age 73 (BCC) and 72 (SCC).

Superficial x-rays 60%, electrons 19%, electrons + superficial 20%, megavoltage photons <2%. Volume was tumor plus microscopic extension, with an additional 1 cm margin depending on size; lead eye shields when near the eye, and bolus use evolved over time.

Local control (relapse-free from RT start), cosmesis (telangiectasia, pigment change, fibrosis) and complications.

Overall LC 89%; untreated 93% vs recurrent 80%. On multivariate analysis, fraction size (p=0.01), lesion diameter and histology (p<0.01) predicted local failure; modality did not (p=0.345).

Complications 5.8% overall (13% for lesions >5 cm), mainly soft-tissue necrosis: 9% of SCC vs 2% of BCC. Fair/poor cosmesis was 4% with superficial RT vs 12% electrons and 19% combination.

The same institution's 1986 series (Lovett et al.) found electrons worse on multivariate analysis. Here that association disappears, which the authors attribute to wider electron margins in later years. The <2 Gy/fx failure signal matches Silva et al. in pinna lesions.

Treatment spans three decades with evolving bolus and margin policy. The cosmesis data are missing for 15-25% of untreated lesions, and the SCC dose cells are small, so the absent SCC dose response may reflect low power.

The data support RT as definitive therapy for early BCC/SCC and put the main lever on fraction size and lesion size, not beam type. Recurrent SCC carries the poorest control and the most cosmetic cost, so failure at first treatment is expensive.

Retrospective single-institution series spanning three decades; modality chosen by lesion size, not randomized, so dose and modality associations are confounded. No surgical comparator.

Retrospective single-centre series, 434 tumours in 333 pts treated January 2001 to December 2006. Analysis per tumour; LRF and MFS as one minus cumulative incidence with death as competing risk.

Biopsy-proven BCC (n=332) or SCC (n=102), primary RT (n=386) or postop for residual disease (n=48). Median age 74.8y BCC, 78.3y SCC; 59.4% face, 22.4% elsewhere on head.

Electrons, 54 Gy/18 fx of 3 Gy (n=159) or 44 Gy/10 fx of 4.4 Gy (n=275), four fx per week. 4-12 MeV by tumour depth, tumour + 1 cm margin, copper foil to offset skin sparing.

No significant LRF difference between schedules in BCC (p=0.67) or SCC (p=0.46). T stage was the only factor associated with local recurrence (p=0.036); gender, age, histology, indication, site, dose and lesion number were not.

Toxicity not reported beyond cosmesis. In a 14-pt pilot, pt-scored good/fair cosmesis was 75% (54 Gy) and 100% (44 Gy), observer-scored 87% and 83%, no significant difference.

The authors cite RT local control of 87-97% for BCC and 56-91% for SCC in prior series, placing these rates at or above that range. They describe them as comparable to surgical series.

Frail pts were moved to 44 Gy before it became standard, which may bias toward fewer recurrences being seen (competing deaths) rather than toward better control. SCC CIs are wide (54 Gy lower bound 79.1%), so equivalence for SCC is not shown.

The authors argue follow-up was adequate because recurrences came early (median 10.4 mo BCC, 3.3 mo SCC). They conclude 44 Gy/10 fx is optimal for T1-T2 disease. The data support non-inferior-looking control at small size, not a formal non-inferiority claim.

Single-centre retrospective; schedule assigned by era and frailty, older 44 Gy cohort with shorter follow-up; univariate only, 15 events total. Cosmesis from 14 pts.

Single-centre analysis of a prospectively maintained database, RT delivered 2007-2011. Recurrence was assessed clinically. Univariate then backwards logistic regression, per tumour, with no correction for multiple lesions per pt.

389 pts, 448 BCC/SCC lesions, median age 78 (41-99). 67.9% <2 cm; 9% in immunosuppressed pts. Primary 53.3%, recurrent 29.7%, postoperative 16.7%.

Orthovoltage 100-300 kV, electrons 6-18 MeV with bolus, or 1-2 field photons (IMRT selectively). Most common schedules 50 Gy/20 fx and 40 Gy/10 fx. GTV by clinical mark-up plus a 1-2 cm margin; CT planning for deep tumours.

LC 84.2% at median f/u 18.4 mo; median time to recurrence 11.4 mo. Independent predictors were age, size ≥2 cm, immunosuppression and modality; EQD2 and indication (primary vs recurrent vs postop) were not.

LC sits below the ranges the authors cite (BCC 87%-98%, SCC 56%-97%). The van Hezewijk series used higher-EQD2 schedules (44/10 vs 54/18) with 3y LC 96.1% and 96.9%, but the populations are not comparable.

Logistic regression treats a time-to-event outcome as binary, so pts with 0-mo follow-up count as controlled. The 3-category modality variable cannot separate technique from tumour depth. Recurrence was not split into in-field vs marginal.

The independent risk factors are patient and tumour features, not dose, which points to selection and target coverage rather than prescription as the lever. The modality OR reflects case mix per the authors and should not drive technique choice.

Single-centre retrospective analysis; logistic model ignores censoring, modality effect confounded by indication, and 18.4-mo median f/u undercounts late BCC recurrence.

Retrospective treatment-planning comparison at one institution. 26 pts, 76 lesions, each GK plan replanned with SmartArc and HyperArc. ROC analysis on RTOG CI and NT V12Gy set the threshold volumes.

Pts treated with GK SRS for brain metastases in 2018-2019 who had two or three targets (26 selected from 121). Targets with a prescription below 12 Gy were excluded from the V12Gy analysis.

Linac plans used HD-120 MLC with FFF beams, with one or two isocenters per pt. Example prescriptions ranged from 13 Gy to 24 Gy single fraction.

The ROC thresholds were 0.4 cc for SmartArc (CI and V12Gy), 0.2 cc for HyperArc CI and 0.5 cc for HyperArc V12Gy. Averaged, they give the proposed 0.4 cc cutoff: GK is favored at or below it and VMAT above it. Median beam-on time was 56.25 min for GK vs 8.33 and 13.58 min for VMAT.

This is consistent with Liu et al, where VMAT matched or beat GK at a median volume of 0.5 cc. Potrebko et al and Vergalasova et al split targets by mean volume or diameter bins and planned more targets per pt (median eight and seven), so their cutoffs are not directly comparable.

The cutoff is an average of four ROC thresholds, not tested in a validation set. For ≤0.4 cc, Table 4 shows HyperArc CI 1.46 vs GK 1.68 (p=0.032), which conflicts with the text's 'comparable conformity'. Closely adjacent targets were dropped, and these are exactly the cases where MLC dose bridging matters most.

The useful signal is that the threshold depends on the platform: HyperArc stays competitive with GK on small-target V12Gy where SmartArc does not. No clinical endpoint links these dosimetric differences to radionecrosis or local control.

Single-institution retrospective replanning with dosimetric surrogates only. The threshold is an unvalidated average of ROC cutoffs, with no clinical toxicity or control endpoint.

Retrospective real-world analysis of commercial and Medicare claims databases, indexed at the date ADT was prescribed. Data cutoff May 2024. Presented at ASCO GU 2026 and discussed in a UroToday interview, not a full paper.

~17,000 pts with prostate cancer receiving ADT. ~90% GnRH agonist, ~10% GnRH antagonist (degarelix ~two-thirds, relugolix ~a third). Agonist pts were older, more likely on Medicare, and had longer median f/u.

Primary: two- and three-point MACE. Secondary: MACE before vs after 2021, the year HERO and PRONOUNCE reported.

Overall MACE ~four per 100 person-yrs. Antagonist pts had ~37% numerically lower MACE than agonist pts. Preexisting CVD carried ~11 per 100 person-yrs, about threefold. Post-2021 showed a modest reduction vs pre-2021.

Direction matches HERO, which the presenter cited for lower MACE with relugolix vs agonist. PRONOUNCE was cited for the value of cardiologist involvement, which frames the preexisting-CVD finding as a referral question, not only a drug-choice question.

Baseline age, payer and f/u imbalances bias the crude class comparison. MACE misses earlier cardiometabolic harm (diabetes, metabolic syndrome, renal dysfunction), as the interviewer pointed out. The pre/post-2021 shift is a secular trend with no causal link to the trials.

The more robust signal is the preexisting-CVD rate, which identifies who needs cardiovascular co-management whatever the ADT class. A PCF consensus statement on risk-tiered cardiology referral is described as forthcoming.

Retrospective claims comparison, 'numerically lower' with no CI or adjustment reported; agonist group older, more Medicare, longer f/u. Antagonist group mostly degarelix.

Prospective single-centre observational cohort following STROBE. Pts were resected between 1990 and 2001, follow-up closed Dec 2005, median f/u 43 mo. Cox models used forward selection, with a 200/415 learning-validation split for internal validation only.

615 assessable white pts with primary cutaneous SCC at any body site, median age 73, 5% immunosuppressed. Excluded: SCC in situ, keratoacanthoma, collision tumours, and recurrent SCC treated elsewhere.

No pt received adjuvant RT. Every resection reached tumour-free margins by 3D-histology, with re-excision as needed, so outcomes reflect surgery alone.

The source states the primary endpoints as time to metastasis and time to local recurrence, each measured from diagnosis of the primary. Seven candidate predictors were chosen a priori.

26 (4%) metastases and 20 (3%) local recurrences. No tumour ≤2.0 mm metastasized. The thinnest tumour that metastasized was 2.8 mm thick.

Clayman and colleagues reported LR in 12% (15 of 130) of primary SCC. Margin-controlled resection here gave 3% (20 of 615). The authors cite an Australian series of 266 pts with nodal disease that also supports tumour thickness over horizontal size.

Follow-up after the early period relied partly on mailed questionnaires to treating physicians. New field-cancerization SCC can mimic local recurrence. University referral may have enriched for poorly differentiated tumours.

Thickness, immunosuppression and desmoplasia outperformed Broders' grade and horizontal size as prognostic factors. The authors propose thickness-based T1-T3 cutoffs (≤2.0, 2.1-6.0, >6.0 mm) with "d" and "i" modifiers. The study does not test whether any treatment changes the high-risk course.

Single-centre prognostic cohort, model selected by forward selection with events per predictor below 5. Validated only internally; no external cohort.

Retrospective single-institution series of 671 lesions treated 1972-2007. Mean follow-up 38.016 mo (range 1-351). Actuarial cure rate by life-table method; chi-squared for dose and size associations.

Basal and squamous cell carcinomas of the skin overlying the nasal cartilages. Histology split of the full cohort not given in the source excerpt. Relapses included 10 lesions already recurrent after prior non-radiological treatment.

CRT in 668 lesions: 55-60 kV, HVD 2-12 mm, 5 Gy/fx twice weekly, total 30-75 Gy (median 55 Gy). Margin 0.5-1 cm, 1.5 cm for morpheaform BCC. Septal cartilage shielded with 1 mm Pb nostril inserts at the alae.

CR 98.80% at 1 mo; 5-yr cure 88.09%, 10-yr 86.51%. Recurrence 38 lesions (13 central, 25 marginal), onset 3-96 mo. No relationship between relapse and dose or size.

Cosmesis good or acceptable in 96.84%; 16 lesions not acceptable. Authors report no complications or sequelae, and flag the 7 newly not-acceptable cases for continued follow-up.

No contemporaneous comparator. The authors cite randomised facial BCC data comparing RT with surgery: cosmesis was similar on nasal skin but control favoured surgery, in tumors under 4 cm treated with mixed RT techniques. Mohs surgery, the usual comparator for nasal BCC today, is not addressed.

Toxicity is clinician-rated cosmesis without a named scale, and a mean follow-up near 3 years is short for late cartilage effects. The null dose-relapse finding is likely confounded by dose being chosen by lesion size.

The data support kV RT as an effective, cartilage-sparing option for nasal skin carcinoma, where tight adherence of skin to cartilage complicates excision. They do not establish superiority over surgery, and the marginal-failure pattern raises the question of whether margins were adequate.

Single-institution retrospective series, 1972-2007, no surgical comparator; the authors' claim of superiority over other modalities rests on cross-literature comparison this design cannot support.

Retrospective single-institution series, 114 pts and 134 lesions treated Nov 2006 to Dec 2011. Analysis per lesion; median follow-up 33 mo.

92 BCC and 42 SCC, all clinically N0. 77.3% definitive, 22.7% adjuvant after excision with positive or close margins.

Ir-192 HDR plesiotherapy, 3 Gy/fx, 3 fx/wk; mean 48.79 Gy (45-54) for BCC and 50.55 Gy (45-57) for SCC, prescribed 3-5 mm below the surface with a 0.5-1 cm margin. Leipzig 2 or 3 cm applicators for flat lesions ≤2 cm (75.4%); customized molds for raised or larger lesions.

Overall 3y/5y DFS 95.12%/93.36%, CR 98%. Recurrent lesions did worse than primary (85.9% vs 95.6% at 5y, p=0.003); applicator and definitive vs adjuvant did not separate DFS.

Acute RTOG G3 40.3%, G4 2.2%; toxicity higher with definitive intent (OR 2.928, p=0.013) and borderline with molds (p=0.067). Late G0-1 95.2%; cosmesis excellent/good 82%.

Authors place results alongside the Kohler Leipzig series (91% complete remission) and Guix's mold series (5y DFS 98%). They cite one randomized surgery vs RT trial as the only head-to-head data, with no numbers given in source.

Molds treated larger lesions, so mold vs Leipzig DFS and toxicity differences cannot be separated from size. Reported recurrence counts do not add up, and the acute toxicity figure differs between abstract and results.

Supports surface HDR as a definitive alternative to excision for small primary NMSC. It does not settle optimal fraction size, and the high acute G3 rate argues for weighing applicator and dose per fraction for larger lesions.

Retrospective single-institution series, no comparator arm; applicator comparison confounded by lesion size and location; DFS per lesion with 33-mo median f/u.

Phase 3, randomized 1:1, N=231 (113 vs 118), accrued July 2021 to March 2023. Median follow-up 36.8 vs 35.6 mo at the October 1, 2025 cutoff.

cT3-4 or N+ rectal adenocarcinoma, tumor ≤10 cm from the anal verge. MMR/MSI composition of the enrolled cohort is not reported in source.

Experimental: SCRT 25 Gy/5f. Control: 50.4 Gy/28f with concurrent capecitabine 825 mg/m2 BID. Target volumes are not reported in source.

Both arms: 2 neoadjuvant + 6 adjuvant cycles of CAPOX. Experimental adds camrelizumab 200 mg d1 given alongside CAPOX for up to 17 cycles.

Primary: BIRC-assessed pCR rate (result not in source). Key secondary endpoints with prespecified α: investigator-assessed EFS and OS.

G≥3 TRAE over the whole treatment period 51.3% (59/115) vs 48.2% (54/112). The RT-attributable split is not reported.

RAPIDO set SCRT followed by consolidation chemo as a TNT option, and PRODIGE 23 did the same for an LCCRT-based approach. UNION is the first phase 3 to layer a PD-1 inhibitor onto SCRT in LARC, building on earlier SCRT + IO phase 2 signals such as TORCH.

The safety population (115 vs 112) does not match randomization (113 vs 118), so some pts received the other arm's treatment. Neoadjuvant CAPOX was only 2 cycles in the control arm, lighter than full TNT backbones. OS and surgical or organ-preservation outcomes are absent.

The EFS effect is large and was tested under alpha control, but it comes from a two-variable comparison. It supports the whole package and does not establish what SCRT or camrelizumab contributes individually.

Randomized phase 3, but the primary pCR result is not in source and EFS is secondary. SCRT and camrelizumab change together, so the benefit cannot be attributed to either.

Phase III, randomised 1:1, 25 centres in 9 countries, accrual 2018-2024. Powered (80%, alpha 10% two-sided) for a 10-point MDADI difference; 54 evaluable needed, 84 planned for 35% attrition, 86 randomised.

T1/T2 N0-1 OPSCC/SGSCC or T1 N0 HPSCC suitable for either TOS or DO-IMRT. Median age 64, 86% OPSCC, 49% HPV-positive; arms balanced.

Dysphagia-optimized IMRT (DO-IMRT). Dose, fractionation and target volumes not reported in source. 7/44 (16%) allocated to DO-IMRT declined treatment.

Primary: MDADI total score at 12 months (ANCOVA). Secondary: MDADI at 4.5, 6 and 9 months, PSS-HN, oncological outcomes, toxicity.

12-mo MDADI adjusted difference +3.9 points (90%CI -2.7 to +10.5; p=0.326), consistent across sensitivity analyses. Arm-level secondary outcomes are in the table.

G≥3 treatment-related AEs 21% in each arm. TOS: hemorrhage 5%, fistula 2%. DO-IMRT vs TOS: mucositis 39% vs 10%, dry mouth 49% vs 14%, dysgeusia 46% vs 17%.

ORATOR randomised TORS against RT in OPSCC and also found comparable function with different toxicity profiles. Best-of extends the comparison to supraglottic and hypopharyngeal primaries and to a phase III frame, but still with a small N.

The EFS HR CI (0.77-3.50) is wide and follow-up reaches only 2 years. A 49% HPV-positive mix limits transfer to HPV-positive de-escalation. RT technique is unreported, so the DO-IMRT arm cannot be audited.

With swallowing function apparently similar, toxicity profile and patient preference become the deciding factors. The numerically lower CR and EFS in the DO-IMRT arm (98% vs 82%; 84% vs 72%) are not significant and may partly reflect pts who declined RT, so they need longer follow-up before they carry weight.

Phase III, but differential 12-mo MDADI evaluability (86% vs 64%) and 16% refusal of DO-IMRT; CI does not exclude the 10-point margin, so equivalence is not shown.

30-question electronic survey sent to ~400 American Brachytherapy Society clinician members. 16 fully completed surveys analyzed; one incomplete survey excluded. Nearly all US respondents, one from Spain.

Radiation oncologists using skin surface brachytherapy for cSCC and BCC. Practice settings spanned academic, hospital-based and private; aggregate experience ranged 8 to 1800 cases.

Hypofractionation preferred; clinical-scenario doses ranged 30 Gy in 5 fractions to 64 Gy in 32 fractions (EQD2 40 Gy-65 Gy). Median max prescription depth 5 mm; shielded applicators most common, custom molds for large or curved areas. Respondents avoided daily schedules when hypofractionating.

Margin on gross disease 3-15mm, median 5mm. Max skin dose 125-150% (median 135%) of prescription; CTV coverage 90-100% (median 95%). No consensus on dosimetric constraints.

Eight respondents described severe acute and late toxicity on the lower extremity, especially pretibial skin. Three referred non-healing in-field ulcers for hyperbaric oxygen.

The cited prior literature (Guix custom-mold HDR, Paravati electronic brachytherapy, van Hezewijk hypofractionated electrons) reports single-series outcomes. This survey adds no outcomes; it documents how widely dose, margin and constraints vary across practices using the technique.

Several key tables carry ambiguous row-value pairing in the source, and the scenario table (Table 4) was not captured. Toxicity is anecdotal recall with no denominators.

The useful output is the spread itself: margins, skin-dose ceilings and the lesion-size threshold for gentler fractionation all vary several-fold. Prospective trials and expert consensus are what the authors call for, and this survey cannot substitute for either.

Practice survey of 16 self-selected respondents; no efficacy or toxicity endpoints measured, so the authors' 'convenient and safe' conclusion is not testable from this design.

Systematic review and meta-analysis (PRISMA/MOOSE) of 27 studies, 1183 pts, published 2010-2022; random-effects pooling with meta-regression. All retrospective except HILUS (prospective phase II); none randomized. Median f/u ranged 7.6-44.5 mo.

Ultra-central lung tumors treated with SBRT (≥5 Gy/fx, photons), ≥5 eligible lesions per study. Excluded reirradiation and hilar/mediastinal nodal targets. Histology mixed; 9 studies (33%) were entirely primary NSCLC.

Dose 30-70 Gy in 3-10 fx, most often 50 Gy/5, 60 Gy/8, 60 Gy/12. Motion management in 96% of studies, mostly 4DCT. OAR dosimetry reporting was variable.

1-yr LC 92% (95% CI 86-96), 2-yr LC 89% (82-94); primary NSCLC subset 95% at both timepoints. Higher BED tracked with 1-yr LC (HR 2.14, p=0.03), not 2-yr (p=0.66).

Any G3-4 6% (3-10), any G5 4% (2-6), G5 hemoptysis 1% (0-3). G5 ≥10% in 7 studies; HILUS 15%. Risk factors: endobronchial tumor, antiplatelet/anticoagulant use, VEGF inhibitor within 30 days (HR 16.9), ILD.

Pooled 2-yr LC sits beside RTOG 0813 (89.4% in central/UC tumors). A prior 250-pt systematic review reported higher toxicity (treatment-related mortality 5%, G≥3 10%); the authors attribute the lower rates here to more contemporary, conformal series.

Fig 3 dose-event mapping drew on only 37 events from 9 studies, and PBT substructure dosimetry was rarely reported, so constraints beyond HILUS's could not be derived. Toxicity attribution in retrospective series is open to misclassification.

Efficacy is not the question; airway dose is. The ISRS constraint (PBT Dmax <133-150 Gy BED3) is built from cross-series convergence of fatal-hemoptysis doses, not a modeled threshold, and is pending SUNSET and LUNGTECH.

Pooled retrospective series (one prospective, none randomized) with I² >90% for LC, publication bias on every endpoint, and inconsistent ultra-central definitions. Guideline layer is expert opinion.

A treatment-planning study with no patients. Plato BPS 14.2.4 plans were built on Nucletron radiographic cylinders (tip space ~0.5 cm) and CT/MR-compatible cylinders (tip space 0.6-0.8 cm). Dose uniformity at each depth was measured as the mean dose (MD) and SD across dose points spaced evenly around the dome and along the cylinder.

Cylinders were 2.0, 2.5, 3.0, 3.5 and 4.0 cm in diameter, with active lengths of 3 to 8 cm (upper third to the whole vagina). Prescription was to the surface (P0) or to 0.5-cm depth (P5), with or without optimization points on the curved end (NEP). The worked illustration used 7 Gy × 3 fractions.

Primary measures: MD and SD at the surface and at 0.5-cm depth. Dose fall-off was the ratio of MD at 0.75 cm to MD at 0.5 cm.

Surface prescription gave surface SD 6% vs 18% with P5 (2-cm cylinder, 0.8-cm tip), with almost the same fall-off beyond 0.5 cm. NEP plans produced hot spots >150% and cold spots <60%. A shorter tip space raised dosimetric uncertainty >30%.

The paper frames its result against the ABS 2000 guidance (dome optimization points, report doses at both surface and 0.5 cm) and an ABS survey in which >90% prescribe to 0.5 cm. It also cites Sorbe's randomized 2.5 vs 5.0 Gy × 6 trial, in which higher dose increased atrophy, bleeding and shortening.

The M regression was fit on only two lengths × two diameters, using one vendor's applicators and TPS. The claim that a lower surface dose reduces atrophy and shortening is extrapolated from other trials, not measured.

A 0.5-cm depth prescription delivers its intended depth dose only when dome points are included, and the surface dose it gives varies with cylinder size and tip space. Prescribing to the surface with a geometry-scaled dose fixes the surface number. Whether that changes toxicity remains open.

Planning-system dosimetry with no patients or outcomes. 'Surface prescription is optimal' rests on mucosal dose uniformity, a surrogate never tied to toxicity or vaginal control here.

Retrospective NCDB cohort, dx 2010-2013, analyzed 2018-2019. Univariate + multivariate Cox for OS; points assigned to features in proportion to effect size, then the composite was selected on C-index, AIC and clinical judgement.

Upfront surgery + adequate neck dissection (LN yield ≥15), non-metastatic T1-4 N0-3 M0 (AJCC 7th). HPV+ OPSCC n=2302 vs HPV-unassociated HNSCC n=13 022; OPSCC without HPV testing and surgery + chemo alone excluded.

5-y OS (KM, log-rank) and discrimination by C-index. Multivariate models adjusted for age, sex, race, comorbidity, insurance, adjuvant RT and/or CRT, and hospital type.

In HPV+ OPSCC only T stage, LVI, number of LN mets and ENE tracked with mortality; margins, LN size, level IV-V and bilateral nodes did not. Composite C-index 0.67 (3 tiers) vs 0.58 traditional.

The traditional tiers being tested come from NCCN, ASCO, ECOG 3311 and PATHOS definitions, the de-escalation trials that use pathology to allocate adjuvant RT vs CRT. ICON-S refined clinical staging for HPV+ disease but was built on definitive CRT with only 2% surgical pts, so it could not weigh pathologic features.

Points include margins despite no multivariate association, a judgement call that inflates their weight. The source states the traditional high-risk share inconsistently (46.1% and 45.1%), and HPV testing method is not described.

Traditional HNSCC pathologic tiers are weakly prognostic in HPV+ OPSCC, and nodal burden plus T4 matter more than ENE or margins. Whether the reclassified majority can safely receive less adjuvant therapy is untested here and belongs to the next deintensification trials.

Registry retrospective, OS-only, model scored in its own derivation cohort without external validation; cannot show reclassified pts tolerate less adjuvant RT/CRT.

Secondary dose-volume analysis of the HRT arm of the multicenter NRG/RTOG 0415 trial, N=521. Cohort split 70%/30% into training and validation with preserved toxicity rates; univariate and multivariate logistic regression on bootstrapping.

Low-risk prostate cancer treated on the HRT arm. Median follow-up 5.9 yr.

70 Gy at 2.5 Gy/fraction, 3DCRT/IMRT N=108/413. Doses converted to EQD2 with rectum α/β 3 Gy and bladder 6 Gy; trial rectal constraint EQD2 74 Gy ≤15%.

Late ≥G2 GI and GU toxicity, plus proctitis and pollakiuria (the symptoms with rates ≥10%). Generalizability required validation AUC within training AUC ± SD, p≤0.05, and pHL >0.05.

Rectal D5% was the dominant GI predictor; with or without acute GI toxicity it generalized (AUCvalidation 0.64, 0.65). Modeled late GI falls from 20% to 10% at D5% ≤62 Gy. No GU dose-response was found, including at α/β 0.8 Gy.

PROFIT, CHHiP, HYPRO and RTOG 0415 established moderate HRT with similar biochemical control to CFRT but a tendency to more late toxicity. The late GI rate here was 19% vs 2% in a cited high-dose CFRT IMRT series planned with a strict high-dose rectal constraint.

Validation is an internal random split of the same cohort, not an external dataset. The IMRT-heavy mix (79% vs 21%) left a technique interaction untestable, and constraint adherence was incomplete, so part of the signal may reflect plan quality rather than tolerance.

Results point to small rectal hotspots as the modifiable driver of excess late GI toxicity after moderate HRT, with authors also advocating rectal spacers. GU toxicity likely needs a substructure (not whole-bladder) approach.

Post-hoc NTCP modeling within one arm of a phase III; modest AUC 0.64-0.65, internal split validation only, no prospective test of the proposed D5% constraint.

Single-institution retrospective cohort at MSKCC, mastectomies January 2006 to December 2011. Median follow-up 5.6y. LRR defined as biopsy-proven ipsilateral chest wall or axillary, internal mammary or supraclavicular recurrence.

T1-T2N0 invasive breast cancer with ≥1 high-risk feature (age <40y, multifocal/multicentric, LVI, medial/central location, high nuclear grade). N0 meant no tumor in the SLNs, including ITCs and micrometastases. Neoadjuvant chemo, bilateral and recurrent disease excluded; 15 PMRT pts excluded, leaving 657.

98% had SLNB alone. 86% received adjuvant systemic therapy: 41% chemo plus endocrine, 14% chemo alone, 32% endocrine alone. 70% of HER2+ pts got trastuzumab.

No PMRT in the analyzed cohort. Only 15 of 672 (2%) received PMRT over the study period, so no RT comparator exists.

LRR 4.7% (31 pts), local and regional each 2.6%. Tumor size HR 1.70 (95% CI 1.26-2.29); systemic therapy HR 0.40 (95% CI 0.17-0.92). Number of risk factors not associated with LRR (P=.54).

EORTC 22922 and MA.20 showed DFS benefit from regional nodal RT in populations that included high-risk N0 disease; per the source, N0 made up 10% of MA.20 and 44% of EORTC. The regional recurrence here without RT (2.6%) sits below the EORTC 22922 control arm (4.2%). SUPREMO, which includes high-risk N0 pts, is the randomized test of this question.

Only 32 pts had 4-5 features (Fig 1), so the null risk-count finding is underpowered where it matters most. Surgery was done by high-volume breast surgeons, and axilla-only failures after SLNB suggest a false-negative contribution not addressed by PMRT decisions alone.

Authors attribute the low LRR to contemporary systemic therapy and argue conventional features do not by themselves mandate PMRT. The data establish baseline risk without RT, not the size of any PMRT benefit, so the question for T2 tumors carrying several features stays open.

Single-institution retrospective series with no PMRT comparator; describes baseline LRR risk, cannot estimate PMRT benefit. Small ≥4-feature subgroup limits the null risk-factor finding.

Retrospective translational cohort within phase 3 SWOG S8814, which enrolled 1989-1995. RT use was not randomized: it was expected after BCS and left to physician discretion after mastectomy. Reported under REMARK guidelines.

Postmenopausal, ER/PR+, node-positive women from the tamoxifen-only and CAF-T arms who had RS assayed. Final N=316: BCS + RT or mastectomy without RT. Pts who received PMRT were excluded, so the mastectomy cohort is the group whose physicians judged RT unnecessary.

Tamoxifen 20 mg daily for 5 y, alone or after 6 cycles of CAF (CAF-T). The concurrent CAF + tamoxifen arm was excluded.

Primary: LRR (breast, chest wall, axillary, infraclavicular, supraclavicular or IMN), censored at distant recurrence or death. The primary analysis used continuous RS; the secondary analysis compared RS <18 vs ≥18.

The continuous-RS primary analysis was not significant (P=.11). The categorical split and the subset tables carry the signal.

Direction agrees with NSABP B-28, where RS also independently predicted LRR. Absolute LRR at 1-3 nodes was higher here than in B-28, which treated every pt with chemo and allowed no PMRT. MA.20 and EORTC 22922 show a nodal RT DFS benefit even where LRR is low, so LRR alone may underestimate what RT buys.

Treatment era: CAF and tamoxifen only, with no taxanes or AIs, both of which may lower baseline LRR. LRR was censored at distant recurrence, which can undercount local failures. The ≥4-node mastectomy subset had no n reported.

RS looks prognostic for LRR beyond nodal count, but it cannot yet select pN1 pts for PMRT omission. That question belongs to TailorRT (MA.39), which randomizes only low-RS pN1 pts. Nodal burden still dominates the risk at ≥4 nodes.

Retrospective correlative of a chemo trial with nonrandomized RT. Prespecified continuous-RS analysis null (P=.11); the cut at 18 was confirmed post hoc; nodal subsets exploratory with few events.

Retrospective population-based cohort from the BCCA Breast Cancer Outcomes Unit database. N=821 of 1117 identified, after excluding 296 who received RT. Cox multivariable modeling, then a classification model built from the significant factors. Median follow-up 7.7y.

pT1-T2, 1-3 positive axillary nodes, diagnosed 1989-1997, all treated with modified radical mastectomy and axillary dissection. Excluded pT3-T4, ≥4 N+, M1 and unknown pTN. Median age 62.

Adjuvant systemic therapy in 94% per BCCA guidelines: chemo alone 21.7%, hormonal alone 57.1%, both 15.1%. Chemo was AC, CMF or FAC; hormonal therapy was mostly tamoxifen.

No pt received locoregional RT; the study defines baseline no-PMRT risk to inform selection, not RT efficacy. Authors anchor benefit estimates on an RT relative LRR reduction of approximately two-thirds.

Primary: isolated LRR (chest wall, axillary, infraclavicular, IMN as first site) and LRR±simultaneous distant recurrence. Secondary: BCSS and OS.

Overall 10y LRR±SDR 15.9%. Each of age <45, T2, grade 3, ER-negative, medial location, >1 N+ or >25% N+ alone conferred >20% 10y LRR on univariate analysis. Age was the first model split (29.3% vs 13.7%, p<0.0001).

No-PMRT LRR here (13-16% at 10y) sits well below the ~30% in DBCG 82b/82c and nearer the BCCA randomized trial (16% at 10y) and systemic-therapy trial cohorts (12-20%). Authors attribute the gap to axillary staging, systemic therapy and selection differences.

Excluding the 296 PMRT recipients likely removed higher-risk pts, biasing baseline risk downward. The >25% nodes positive ratio depends on ALND node yield, and its ILRR HR CI (0.99-4.05) touches 1. The ER status row in Table 1 shows a transposition in the source.

Authors propose <10% 10y LRR as a low-risk group that may be spared PMRT, >30% as justifying it, and 15-20% as the threshold for discussion. The model supports considering PMRT in all women <45 and recommending it when >25% of nodes are positive.

Retrospective single-province no-RT cohort; excluded PMRT recipients; data-driven breakpoints, no validation set; pre-taxane, ALND-era systemic therapy limits transfer to modern pts.

Retrospective analysis of two MD Anderson cohorts used to build (932 pts, 1997 to 2003) and validate (804 pts, 2004 to 2005) CPS+EG; 39 excluded, N=1697. Median f/u 51 mo.

All pts received neoadjuvant anthracycline and/or taxane chemotherapy; median age 50. Neoadjuvant trastuzumab and preoperative RT excluded; 20 pts missing ER or grade also excluded.

Local therapy: BCT 656 (39%), mastectomy alone 297 (17%), mastectomy + PMRT 744 (44%). Institutional PMRT indications were clinical stage III, ypN+, or select cT1/T2N1 with high-risk features. Dose, fractionation and fields not reported in source.

LRR = invasive cancer in ipsilateral breast, chest wall or regional nodes, counted regardless of distant timing. Objectives: CPS+EG vs stage for LRR stratification, and whether a score threshold could identify pts safely omitting PMRT.

5-yr freedom from LRR 71% to 99% by CPS+EG vs 86% to 97% by clinical or pathologic stage. In the PMRT-indicated cohort with CPS+EG ≤2, local therapy type made no difference (P=0.73).

NSABP B-18/B-27 (cited) reported 10-yr LRR of 10.3% with BCT and 12.3% with mastectomy but gave no PMRT, so cannot address it. The MD Anderson Prognostic Index omitted ER and grade. NSABP B-51 later randomized regional nodal RT in cN+ → ypN0, a different population from the ypN+ pts here.

Prose direction for the CPS+EG ≥3 subgroup (mastectomy alone favored) contradicts the MVA; overall LRR is reported as both 6.5% and 6.1%. Median f/u of 51 mo is short for ER-positive disease, the biology driving the favorable scores.

The stratification claim is sound and adds biology to anatomic staging for LRR. The omission claim is a null comparison in a small, selected subgroup with no equivalence margin, so it frames a trial question rather than settling one.

Retrospective single-institution cohort; the PMRT-omission claim rests on a non-randomized subgroup with confounding by indication and only 72 mastectomy-alone pts.

Single-institution retrospective cohort, N=1289, 1989-2007. Median follow-up 10.2 yrs after definitive surgery. LRR and DR by cumulative incidence with competing risks; Cox multicovariate models.

Stage II-III breast cancer with cytologically confirmed axillary metastases, NAT, then BCS or mastectomy with ALND. Axillary pCR in 368 (28.5%).

RNI defined as RT purposely directed to at least one regional nodal basin, at physician discretion, given to 1080 (83.8%). Median breast/chest wall 50 Gy/25 fx, median boost 10 Gy/5 fx; institutional standard covered undissected axilla, SCV and IMN, with variable field design. Of 209 without RNI, 142 had no RT at all.

LRR (breast or regional nodes) and DR (LRR or DM, first event), plus DSS and OS.

Univariate RNI effect null for LRR and DR. Adjusted, RNI reduced LRR (HR 0.497) and DR (HR 0.731), with the largest DR effect in HER2+ pts on trastuzumab (HR 0.237). No DSS or OS effect.

Authors read the benefit as carrying over the LRR and DM reductions seen in EORTC 22922 and MA.20 after adjuvant chemo into the NAT setting. They contrast prior HER2+ series (Danish 82b/c, SweBCG91-RT) suggesting relative radioresistance, and the ALTTO subset showing no RNI effect.

RNI pts had more adverse baseline features, so adjustment does heavy lifting. 'No RNI' may include unrecorded high tangents. Half the HER2+ cohort predated trastuzumab and was excluded from MVA, shrinking the subgroup behind the HR 0.237 estimate.

Supports RNI after NAT when nodal disease persists. Does not settle omission after axillary pCR; the authors defer that to B-51.

Retrospective, discretionary RNI with marked baseline imbalance; benefit appears only after covariate adjustment, univariate null. HER2+ trastuzumab DR signal is a subgroup estimate.

Retrospective single-institution cohort (Massachusetts General Hospital), 1980-2000, identified via tumor registry and breast center databases. Median f/u 100 mo. LRR estimated by cumulative incidence (CIF); KM results reported as slightly higher, not substantially different.

877 node-negative invasive cases (870 pts) after mastectomy + axillary dissection, no PMRT; T4 excluded. Median age 64, median 15 nodes examined. Systemic therapy in 276 cases (148 hormones alone, 74 chemo alone, 54 both).

Total LRR (first event, with or without simultaneous distant mets) and isolated LRR (no distant mets for ≥4 mo). Only total LRR reported for prognostic factors.

10y total LRR 6.0%. Size >2 cm, deep margin <2 mm, premenopausal status and LVI independent on MVA with similar HRs (range 2.6 to 3.8). 3 factors: 10y LRR 40.6%; only 1 pt had all 4.

No RT delivered. Chest wall was the site in 87.5% of isolated and 80.4% of total failures, so the authors propose chest wall-only PMRT without regional nodes for high-risk N0 to limit toxicity.

Converges with the IBCSG analysis of 1,275 N0 women on size, LVI and menopausal status, and adds margin status, which IBCSG could not assess. The M. D. Anderson series (141 N0 pts) did not report absolute LRR for its N0 subset.

Most cases (601/877) had no systemic therapy, so absolute risks likely overstate the modern setting. Receptor subtype not reported. LVI not recorded was pooled with absent, and the risk count assumes equal weights.

Authors suggest considering PMRT for postmenopausal pts with all 3 of T2+, close/positive margin and LVI, and premenopausal pts with any 2. Benefit of PMRT in these strata is inferred from risk level, never tested.

Retrospective single-institution 1980-2000 cohort with no PMRT arm; stepwise risk model unvalidated, high-risk strata small with wide SEs. Defines who might benefit, not benefit itself.

Pooled secondary analysis of 5 NSABP node-positive adjuvant trials (B-15, B-16, B-18, B-22, B-25). Cumulative incidence for IBTR and oLRR; IBTR and oLRR entered Cox models as time-varying covariates. Median time on study 13.3 yrs.

Of 10,010 women entered, 2,669 had breast-conserving surgery and were eligible. Negative margins were required; about two thirds had 1-3 positive nodes. B-18 contributed only its postoperative chemotherapy arm.

AC, CMF, PF/PAF and tamoxifen-based adjuvant regimens from 1984-1994, including AC cyclophosphamide intensification in B-22 and B-25. Pts aged >50 received tamoxifen in several protocols; premenopausal women did not receive tamoxifen irrespective of ER status.

All pts received whole-breast irradiation after lumpectomy. Dose, fractionation, boost and any regional nodal coverage are not reported in source.

Cumulative incidence of IBTR and oLRR; DDFS and OS after each event; mortality modeled with clinical factors plus IBTR or oLRR.

oLRR carried roughly double the mortality hazard of IBTR (HR 5.85 vs 2.58), and supraclavicular recurrence had the poorest DDFS. Arm-level values are in the detail table.

Consistent with the NSABP B-06 IBTR literature the authors cite and with the EBCTCG overview linking local failure to breast cancer mortality. The supraclavicular-dominant oLRR pattern is the population later addressed by randomized RNI trials such as MA.20 and EORTC 22922.

Lumpectomy was not the randomized variable, so the 2,669-pt subset is self-selected. Site-specific DDFS estimates rest on small numbers with wide CIs, and no HER2 or RT technique data are available.

oLRR clusters with nodal burden and receptor negativity, the same drivers of distant failure, so it may flag disseminated disease rather than cause it. Later IBTRs fared better, consistent with the authors' view that many are new primaries. The role of chemotherapy at recurrence was unresolved at publication.

Post-hoc pooled analysis of a non-randomized lumpectomy subset; LRR is a prognostic marker here, not a tested intervention target. Pre-taxane, pre-HER2 era therapy.

Single-institution retrospective cohort from a prospectively maintained database, mastectomy 1995-2006. PMRT given at physician discretion. Median follow-up 10.8 yr.

T1-2N1 (1-3 positive nodes), N=1087. Excluded T3/T4, neoadjuvant chemotherapy, and isolated tumor cells. Median age 51, median tumor 1.8 cm; 58% had one positive node.

All PMRT pts received chest wall RT; supraclavicular field in 137/163 (84%), axilla 7 (4%), IMN 6 (4%). Dose and fractionation not reported in source.

Systemic therapy in 98%; chemo 88%, mostly anthracycline and/or taxane. All ER+ pts received hormone therapy; trastuzumab in 51/123 HER2-amplified.

Without PMRT, age <40 (HR 4.15) and LVI (HR 3.47) independently predicted LRR. Chest wall (51%) and supraclavicular nodes (27%) dominated failure sites.

The EBCTCG 1-3 node subset showed 20.3% 10-yr LRR without PMRT, versus 7.0% here, a gap the authors attribute to modern systemic therapy and thorough ALND (median 18 nodes). EORTC 22922 included lumpectomy and stage I-III pts, limiting direct comparison.

Dose and target-volume data absent, so the 4.0% PMRT LRR cannot be tied to a technique. Pathology not re-reviewed, and HER2-directed therapy was incomplete in the cohort. The 10-yr LRR 28% subgroup CI as printed (11.0-22.1) excludes its own estimate.

The useful product is a risk filter for omission, not a PMRT efficacy estimate. It shows age and LVI separating a 2% from a 28% 10-yr LRR in unirradiated pts, which is the decision a T1-2N1 consult turns on.

Retrospective, non-randomized; PMRT selected for higher-risk pts, so null LRR/RFS/OS difference cannot estimate PMRT effect. Risk-stratification value lies in the no-PMRT cohort only.

Retrospective single-institution review of 789 mastectomy pts at Fox Chase; 136 (17%) had tumor within 1cm of the deep margin. 34 pts met criteria and received no postoperative RT. Median f/u 59 mo (range 7-143).

Invasive breast cancer, clinical T ≤5cm, 0-3 positive nodes, microscopic deep margin ≤1cm, MRM in all. Median age 43 (29-76); 65% node-negative, 35% 1-3 positive nodes; no deep muscle involvement.

Chemo ± tamoxifen in 23 pts (CMF 12, CAF 10, AC 1); tamoxifen alone in 7. Systemic therapy tracked age: 91% of women ≤50 got chemo vs 25% of women >50.

5 chest wall recurrences, median interval 26 mo. Cumulative incidence 9% at 5yr, 18% at 8yr. Age ≤50 vs >50: 28% vs 0% at 8yr (p=0.04); margin ≤2mm vs 2.1-6mm 24% vs 7% (p=0.36). 5yr OS 82%, DFS 74%.

The source cites Ahlborn (margin ≤4mm 5.7% vs >4mm 3%) and Mentzer (≤5mm 11% vs >5mm 3%), neither significant and both crude rates at short f/u. This series adds the age interaction those did not report.

Age band estimates rest on 11-12 pts per group. 19 of 34 margins were not centrally re-reviewed. Systemic therapy is pre-taxane, pre-HER2-targeted, so absolute risks likely overstate contemporary failure rates.

The title's claim is really two claims: margin alone does not drive risk, and young age does. The first rests on a non-significant comparison in 34 pts, which is absence of evidence rather than evidence of no effect.

Retrospective single-institution series, 5 events; age subgroup confounded with chemo use (91% vs 25%); no RT comparator arm, so PMRT benefit inferred not measured.

Single-institution retrospective review, Mallinckrodt Institute and affiliates, 1964-1986, N=224 irradiated with curative intent. Median follow-up 46 mo (range 24-241); actuarial life-table method.

First isolated local-regional recurrence after radical (34%), modified radical (61%) or total (5%) mastectomy. Excluded prior postmastectomy RT, pts failing salvage elsewhere, and clinical or radiographic distant mets. Chest wall alone in 134 (60%).

Entire chest wall via tangents, 1.5-6.0 MV to 4500-5000 cGy with bolus and a 6-12 MeV electron boost to gross disease; SCV AP field to 4500-5000 cGy at 3 cm. About 90% treated at 180-200 cGy/d; small 1-2 cm-margin fields used early in the series.

At recurrence, 49 pts received chemotherapy (most often CMF or CAF) and 69 hormonal therapy, usually tamoxifen. Combined-modality vs RT-alone analysis deferred to a later report.

5-yr LRC 57%; whole-CW fields gave 75% vs 36% 5-yr freedom from CW re-recurrence vs small fields (p=0.0001). For <3 cm lesions, 100% controlled at ≥6000 cGy vs 76% lower; larger lesions about 50% even at 7000 cGy.

Grade 2 sequelae 9%, grade 3 1%, none fatal. Arm edema 11% vs 1% with vs without elective axillary RT; pneumonitis higher with a parasternal field (8% vs 2% tangents alone).

Toonkel and co-workers, cited here, found a survival advantage with comprehensive nodal RT, while Deutsch reported the opposite, with that elective-nodal group carrying more extensive disease. Chen saw 27% failure in an uninvolved site after involved-field RT, consistent with this series' case for elective CW and SCV coverage.

Small-field group was only 14 pts and clustered in the early era, so the field-size effect also captures changes in staging workup and systemic therapy. The elective CW p-value is printed as both .32 and .33, and dose was set by physician preference.

The pattern of failure argues the whole chest wall carries subclinical disease, which favors comprehensive fields over excision alone or small portals. Large, diffuse or combined CW-plus-nodal recurrences stay poorly controlled at any dose, and the authors point to hyperthermia, altered fractionation or systemic combinations in prospective trials.

Single-institution retrospective spanning 22 years; field size, dose and elective coverage chosen by era and physician preference, so selection and era effects confound every comparison.

Retrospective single-institution cohort of 1141 consecutive pts treated 2001-2012. Nomogram from Fine and Gray competing-risks regression in 623 unirradiated pts; risk tiers by decision tree (CHAID); internal bootstrap validation only. Median follow-up 74.9 mo.

T1-2, 1-3 positive axillary nodes, mastectomy with negative margin plus ALND (median 17 nodes dissected). Excluded neoadjuvant therapy, synchronous metastases, other malignancy. All received adjuvant chemotherapy, 90.5% anthracycline- or taxane-based; median age 47.

46-50 Gy in 23-25 fx, CT-based planning. Fields: ipsilateral chest wall, infraclavicular and supraclavicular; IMN only for central tumors, axilla only with ECE.

LRR as first event (chest wall or regional nodes), DR and BCM, all as cumulative incidence with death as a competing risk.

Nomogram C index 0.73. Risk tiers by score: low ≤10 (n=412), intermediate (n=385), high >18 (n=344). PMRT associated with lower LRR, DR and BCM only in the high-risk tier.

EBCTCG showed PMRT benefit in 1-3 node pts, but its control 10-yr LRR of 21% is well above this cohort's 6.0% 5-yr unirradiated rate, which is the gap a risk model tries to exploit. SUPREMO (NCT00966888) is the prospective test of selective PMRT in this setting.

PMRT recipients skewed to adverse features, so within-tier comparisons carry residual confounding. Era of low trastuzumab use (26.2%) and no capture of nodal size or margin width; a prior 242-pt nomogram (Wadasadawala) used different factors.

The model mostly formalizes features clinicians already weigh (T stage, node count, ER, grade, LVI) into a score. Its value is the low-risk tier's very low baseline LRR, which supports omission, but the benefit estimates need external validation before they guide individual decisions.

Retrospective, clinician-allocated PMRT; risk cutoffs data-derived and tested on the same cohort without external validation. Low-risk null rests on 2 events.

Single-institution retrospective chart review of pts seen for CWR at MD Anderson 1988-1998. Kaplan-Meier, log-rank and Cox regression; time 0 = CWR diagnosis. Median f/u 41.4 mo from CWR.

N=96 post-mastectomy pts with pathologically confirmed CWR, no prior PMRT, no distant mets at CWR. Groups: T1-T2N0 (n=41), T1-T2 with 1-3 N+ (n=20), T3-T4 or >4 N+ (n=35). Group 3 had more LVI (62.9%) and neoadjuvant therapy (40.0%).

XRT was part of CWR salvage in 70.7% / 75.0% / 68.6% (p=0.879). Of the 29 not irradiated, reasons included refusal (6), progression on systemic therapy (6), no referral (3) and unknown (10). Dose, fractionation and target volume are not reported.

OS and DMFS from the date of CWR.

5-yr OS 79.9% vs 41.9% vs 29.1% (p=0.0001); 5-yr DMFS 75.2% vs 33.6% vs 25.9%. Group 1 beat Groups 2 and 3, and Group 2 vs 3 did not differ (MVA OR 1.544, p=0.330). No XRT for CWR independently predicted worse OS (OR 4.524) and DMFS (OR 4.024).

The PMRT trials the authors cite showed ~30% → ~10% 10-yr LRR and a 9% absolute OS gain in high-risk populations, which supports PMRT for T3-T4 or ≥4 N+. This series adds the salvage half of the argument for 1-3 N+, where the authors describe the LRR risk without RT as ~10-15%.

Cox estimates are labeled 'OR'. Group 3 5-yr OS differs between abstract (29.1%) and Table 2 (21.8%), and the DMFS pairwise ORs duplicate the OS values. The benefit of salvage XRT is confounded by indication: pts progressing on systemic therapy were not irradiated.

If salvage of a CWR in 1-3 N+ disease is as poor as in advanced stage, then the PMRT decision has to rest on prevention, which means the absolute LRR reduction becomes the deciding number. The series cannot say what that reduction is worth in OS. The authors defer that to the randomized Intergroup trial.

Single-institution retrospective, n=20 in the key 1-3 N+ group, non-uniform salvage, internal table/text discrepancies; PMRT benefit inferred from salvage outcomes, never tested.

PACE is a phase III open-label multiple-cohort RCT; PACE-A randomised 1:1 to SBRT or prostatectomy. 123 randomised (60 prostatectomy, 63 SBRT) between August 2012 and February 2022. Sexual outcomes analysed by treatment received.

Early localised prostate cancer, cT1-T2, Gleason ≤3+4, PSA ≤20 ng/mL, and suitable for prostatectomy. Baseline median EPIC-26 sexual domain score was 62 in the prostatectomy group and 79 in the SBRT group.

36.25Gy/5 fractions delivered in 1-2 weeks. ADT not permitted. Platform, margins and target volume not stated in source.

Comparator was prostatectomy by open, laparoscopic or robot-assisted approach. Nerve-sparing status not stated in source.

Co-primary (previously reported): 2-year bowel and urinary symptoms. Secondary, reported here through 5 years: EPIC-26 sexual domain score, proportion with MCID (≥11-point reduction), IIEF-5, clinician-reported CTCAE grade ≥2 erectile dysfunction. Significance threshold p<0.01.

All patient-reported measures favoured SBRT in direction; only IIEF-5 met the prespecified p<0.01 threshold. Clinician-graded erectile dysfunction was similar between groups.

ProtecT randomised prostatectomy against external beam RT given with ADT, so its sexual-function comparison carried a hormonal confound that PACE-A avoids. PACE-A is described by its authors as the first randomised comparison of SBRT and prostatectomy with long-term sexual outcomes.

Baseline sexual scores were unbalanced (median 62 vs 79), and the MCID analysis rests on 22 and 35 men. Surgical approach was mixed and nerve-sparing use is not reported. Accrual ran from 2012 to 2022, so technique on both sides spans a decade.

The direction is consistent across three patient-reported measures, which carries more weight than any single p-value here. SBRT still produced a decline (median change -17), so the result is a relative advantage, not preserved function. Cancer control is not reported in this abstract.

Secondary PRO endpoint, open-label, analysed as treated; EPIC-26 and MCID p-values miss the trial's own p<0.01 threshold. PRO return 60% and 63% at 5y.

Secondary analysis of NRG/RTOG 9601, a phase 3 trial of sRT ± high-dose bicalutamide, using GC scores (Veracyte) from a prior translational project. GC-available cohort n=352, median follow-up 18.2 years. Multivariable Cox or Fine-Gray models, adjusted (s)HR with 95% CI.

Pts treated with sRT on NRG/RTOG 9601 who had a GC score. Median GC 0.59 (Q1-Q3 0.42-0.76); 29%, 23%, 38% and 11% were low, intermediate, high and very high risk. Other baseline features not reported in source.

sRT with or without high-dose bicalutamide (AAT). Bicalutamide dose and duration not reported in source.

Salvage RT in both arms. Dose, fractionation and target volume not reported in source.

Primary objective: prognostic impact of GC (per 0.1) on PCSM. Secondary: OS, MFS, DM. Additional: PCSM and OS by pre-defined GC strata, and PCSM benefit of AAT by GC (<0.6 vs ≥0.6) within pre-sRT PSA subgroup (<0.7 vs ≥0.7).

GC was independently prognostic for every profiled endpoint (tables above). The AAT-by-GC estimates are absolute 15-year PCSM differences with no significant interaction in either PSA stratum.

Extends the earlier GC validation in this same trial with final outcomes, and layers GC onto the prior 9601 finding that pre-sRT PSA predicts AAT benefit. GETUG-AFU 16, NRG/RTOG 0534 (SPPORT) and RADICALS-HD tested ADT with post-prostatectomy RT; none is addressed in this source.

AAT benefit by GC is given as point estimates only: no CIs, no cell sizes. PCSM was chosen as primary for this secondary analysis because of suspected other-cause mortality with bicalutamide, which sets aside the endpoint where AAT harm would show. Whether the GC-available subset matches the full trial is not reported.

The prognostic claim is well supported at long follow-up. The predictive claim is not: the GC gradient runs in opposite directions in the two PSA strata. The authors frame GC-guided selection for modern ADT in early sRT as a hypothesis, which is the right ceiling.

Secondary biomarker analysis of a GC-available subset; predictive claim rests on non-significant interactions, and the hormone agent was high-dose bicalutamide, not contemporary ADT.

Biomarker evaluation in two prospective post-op SBRT cohorts (SCIMITAR, EXCALIBUR). Risk scores came from the original intact-prostate model without refitting. Discrimination assessed as continuous AUC and as dichotomized performance at the prespecified 0.50 threshold, then exploratory threshold recalibration; AUCs bootstrapped (1,000 iterations) and pooled by fixed-effects meta-analysis.

Post-prostatectomy pts receiving SBRT to the prostate fossa. SCIMITAR: 100 enrolled, 89 evaluable. EXCALIBUR: 74 evaluable. Adjuvant vs salvage mix, PSA at RT and ADT use not reported in source.

SCIMITAR: 30-34 Gy in 5 fractions to the prostate fossa ± pelvic nodes. EXCALIBUR: 5-fraction SBRT to the prostate bed ± nodes, dose not reported in source. Toxicity by nodal coverage not reported in source.

Outcome: late grade 2+ GU adverse events. Predictor: PROSTOX Ultra score, continuous and dichotomized. Toxicity scale and follow-up duration not reported in source.

Per-cohort discrimination is in the table. Pooled AUC at 0.25 was 0.748. Clinical covariates (age, baseline pad use, IPSS, time from RP to SBRT) were not associated with toxicity (all p>0.2).

The signature was built and thresholded for late GU AEs after intact-prostate SBRT, where 0.50 was prespecified. Post-op, risk ordering held (continuous AUC 0.814 and 0.824) but the 0.50 cutoff did not transfer: EXCALIBUR binary AUC was <0.50.

Sensitivity and specificity at 0.25 are not reported in the source text, only AUC. EXCALIBUR's event count and both cohorts' follow-up duration are missing, so the stability of the EXCALIBUR estimates cannot be judged. Source is a trade-press account of a talk, not a full report.

The read is a stable germline signal with a downward-shifted trigger after prostatectomy. That supports the biology and leaves the clinical tool unfinished: a cutoff tuned on these cohorts needs an independent post-op set before it gates fractionation or counseling.

Prespecified 0.50 threshold failed in EXCALIBUR; the 0.25 cutoff is exploratory, chosen and scored on the same two cohorts with no external validation.

Retrospective chart review across multiple sites of a single institution, VS treated 2008-2017; N=85 (36 GKRS, 49 LINAC). Platform set by provider preference, as GKRS and LINAC sit at different centers. Median follow-up 27 mo.

Vestibular schwannoma, 95.3% solid, intracanalicular (45.9%) or intra- plus extracanalicular (43.5%); Koos II majority with no Koos difference between cohorts (p=0.65). Pre-SRS symptoms were common: tinnitus 62.4%, gait disturbance 48.2%, vertigo 30.6%.

All single-fraction SRS. GKRS: 12.5 Gy to the 50% IDL, stereotactic head frame. LINAC: 12 Gy to the 80-99% IDL with no CTV/PTV margin, then from May 2017 frameless, 12 Gy to the 100% IDL with a 5 mm PTV margin by VMAT.

No primary endpoint stated in source. Outcomes were new tinnitus, vertigo, gait disturbance and facial palsy (HB grade 3 or higher) in pts free of each at baseline, plus volumetric MRI tumor control. Hearing not reported; trigeminal dysfunction excluded for inconsistent documentation.

Local control 98.8%, with 1/85 pts needing salvage (surgery, LINAC arm). No difference in direction of tumor size change (p=0.199).

Both new LINAC facial palsies resolved (2/2); none occurred after GKRS. New gait disturbance resolved in 3/4 GKRS and 2/4 LINAC pts, and the single new GKRS tinnitus persisted.

Authors position this against prior series reporting favorable local control with GKRS or LINAC individually, where direct symptom and QOL comparisons were lacking. The source names no randomized GK vs LINAC comparison; the authors call for prospective data.

The 'QOL' outcomes are chart-abstracted symptoms, with HB grade assigned by the reviewing author when not documented. Mean follow-up differs (24 vs 36 mo), and the tinnitus p=0.0007 on multivariable analysis rests on 1 event per arm. Methods and results disagree on pre-2017 LINAC immobilization.

Median follow-up of 27 mo sits inside the 3-year window in which the authors cite 20-30% pseudoprogression, so the enlargements in both arms are not yet resolved as benign. The data show no signal of platform-specific vestibular or facial harm; they do not show parity.

Retrospective, provider-preference allocation, N=85; symptom comparisons use difference tests on single-digit event counts, so the 'interchangeable' conclusion is not something this design can establish.

Retrospective SEER-Medicare claims analysis of localized prostate cancer diagnosed 2010-2017. 797 focal therapy patients Mahalanobis matched 2:1 to 1,594 IMRT patients on demographics, Medicaid eligibility, comorbidity, flu vaccination, primary care access, year, cancer characteristics and ADT. Logistic regression at 6, 12 and 24 months.

Fee-for-service Medicare beneficiaries with localized PCa as first and only cancer, continuously enrolled parts A and B from 12 months pre-diagnosis through 24 months post-treatment. New York, Idaho and Massachusetts registries excluded for missing AJCC staging. Patients who died within 24 months of treatment were excluded.

IMRT defined as external beam with no surgery plus ≥20 IMRT fractions and an IMRT planning code; a gap of ≥30 days between radiation dates counted as a separate course. SBRT and proton patients were excluded, as were patients with rectal hydrogel spacer, so the IMRT arm is conventional fractionation without a rectal spacer.

Presence of claims indicative of a GI or GU complication within 6, 12 and 24 months of treatment, assessed both as combined diagnosis and procedure codes and as procedure codes only. No patient-reported outcomes and no graded toxicity scale.

Direction reversed by organ system: GI favored focal therapy from 12 months onward, GU favored IMRT at every window measured. The 0-6 month GI comparison was null (OR 1.06, P=.81).

GU excess with focal therapy was driven by incontinence therapy (17.4% vs 7.5%) and erectile dysfunction (18.2% vs 13.1%), both P<.01. GI events with IMRT were predominantly rectal bleeding and colitis; the authors note related procedures were rare and not significantly different.

Focal therapy patients were disproportionately rural (6.4% vs 1.9%) and lower-income (51.5% vs 38.7% in the lowest two quintiles) before matching, so claim-generating behavior may differ by arm independent of toxicity. Baseline continence and erectile function were unmeasured, which matters most for the two endpoints driving the GU result.

The GI result is fragile in a specific way the abstract does not foreground: it collapses to one diagnosis subcategory and disappears in the procedure-only analysis. The GU result is the more robust half, and it runs against the premise that ablation is the lower-toxicity option.

Claims-based retrospective matching, not randomised; toxicity defined by diagnosis codes, and the GI difference vanished when restricted to procedure codes. No PROs, no baseline function.

Cross-sectional cohort of 4908 breast cancer pts treated with 3D-CRT or IMRT from 2008 to 2018 at one Canadian tertiary center, 2223 left-sided in the primary analysis. Median follow-up 10.8 years (IQR 8.4-13.1). Dosimetry auto-segmented from planning CT, converted to EQD2; competing-risks (Fine and Gray) regression adjusted for cardiovascular risk factors.

Breast cancer treated with 3-dimensional conformal or intensity-modulated RT, 2008 to 2018, with the primary analysis restricted to left-sided disease. Systemic cardiotoxic exposure (anthracycline, trastuzumab) is not reported in source.

3D-CRT or IMRT across the heart-sparing era; LAD and heart automatically segmented and dose converted to EQD2. The threshold is a max point dose to the LAD, not a mean, and the reference schedules are moderate hypofractionation (42.5 Gy in 16 fx) and ultrahypofractionation (26 Gy in 5 fx).

Adverse cardiac events: MI, or admission / ED visit for unstable angina, arrhythmia, heart failure, pericarditis, myocarditis. Coronary angiography and revascularization captured separately as CAD. Discrimination compared by ROC C index, adjusted association by competing-risks regression.

10-year cumulative incidence of cardiac event or CAD was 5.0% (95% CI 4.1-6.0). Metric-by-metric comparison is in the table above.

Current whole-heart constraints descend from population dose-response work on cohorts irradiated when incidental cardiac exposure was far higher (Darby, NEJM 2013), the era in which mean heart dose had usable spread. This is the modern counterpart of those series, and the reversal it reports is what you would expect if heart-sparing planning compressed mean heart dose below its discriminating range. The referenced schedules, 42.5 Gy in 16 fractions and 26 Gy in 5 fractions (FAST-Forward), are current practice, so the dosimetric translation transfers.

The mean heart dose null is hard to separate from restricted range: a 2 Gy dichotomy inside a heart-sparing cohort may not span enough exposure for a gradient to show. The endpoint counts coronary angiography and revascularization, which track ascertainment and access as well as biology. Systemic cardiotoxic exposure is not reported in source, leaving an obvious confounder unaddressed.

The asymmetry that matters is cost: an LAD max objective plus breath-hold usually costs optimization time, not target coverage, so a weak association is enough to justify it, while it would not justify trading away chest wall or nodal coverage. The measurement problem cuts the other way, since a max point dose to a small mobile auto-segmented vessel is among the least reproducible quantities to write into a protocol. Motion management carries the least methodological baggage of the two recommendations: it lowers LAD dose and heart dose together.

Cross-sectional single-center cohort with a cut point derived in the same data; C index 0.58 barely above chance and its interval overlaps mean heart dose's.

Observational AS cohort inside the GÖTEBORG-1 PSA screening trial (1995 to 2014 diagnoses, follow-up to Dec 31, 2023). Data were collected prospectively, but AS was not randomized and followed no predefined protocol. Kaplan-Meier estimates plus a multivariable Cox model for failure.

Of 1052 screen-detected PCs, 494 (47%) were on AS and 488 were included: 251 very-low, 129 low, 108 intermediate risk. High-risk excluded. Median age 66, PSA 4.1 ng/ml, PSA density 0.12.

Treatment-free, failure-free (noncurative PSA relapse, starting HT, metastasis, or PC death), PC-specific, and overall survival, all measured from diagnosis.