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.

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 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.

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.

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.

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.

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.

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.

Multicentre retrospective cohort from 3 centres, March 2015 to May 2025. N=107: 39 dose-escalated vs 68 standard. Median follow-up 23 mo (range 3-104).

Curative-intent MIBC after TURBT, RT with or without concurrent chemo; node-positive allowed if M0. Metastatic or palliative-intent pts excluded. 51% received no chemo, mostly for poor PS or comorbidity.

Standard: 55Gy/20fx or 64Gy/32fx whole bladder. Escalation: SIB up to 60Gy/20fx or 70Gy/32fx to the primary lesion. Empty-bladder CT sim, daily CBCT, MRI/FDG PET fusion in select pts.

2-year local control for invasive and non-invasive disease, metastasis-free survival, OS, bladder preservation and toxicity. Invasive recurrence analysed by Fine-Gray competing-risk models.

Invasive recurrence was the only endpoint that separated (adjusted SHR 0.20, p=0.035); non-invasive recurrence, metastasis and OS did not differ. Full arm values in the table.

G2+ GU 17.9% vs 22.1% and G2+ GI 5.1% vs 7.4% (escalated vs standard), no difference (p=0.8, p=0.9). G3 toxicity only in 2 standard-dose pts; no early cessation.

BC2001 and BCON built modern TMT on radiosensitisation of whole-bladder RT, not on dose to the primary. RAIDER tested tumour-focused adaptive escalation prospectively; this series adds a routine-practice, CBCT-era hypofractionated experience in the same direction.

Asymmetric outcome ascertainment: 3 standard-arm recurrences were imaging-only and presumed invasive, while every escalated recurrence was cystoscopy-confirmed. Chemo use (56% vs 44%) and hypofractionation (97% vs 87%) also favoured the escalated cohort, and f/u starts at 3 mo, short for late bladder toxicity.

The in-field failure pattern in the standard cohort gives escalation a mechanistic rationale; the magnitude is not trustworthy given selection. Bladder preservation was high in both groups partly because relapsed pts were unfit for cystectomy, so it conflates control with fitness.

Retrospective, non-randomised; escalated cohort selected (all unifocal, less hydronephrosis). Few invasive events (2 vs 16), adjusted for T stage only, so dose cannot be separated from selection.

Secondary pathological analysis of the ProtecT randomized trial (active monitoring vs radical prostatectomy vs EBRT with neoadjuvant ADT). Central review of biopsy slides retrieved for 712 of 1,643 randomized pts, with both intention-to-treat and per-protocol analyses, the latter accounting for crossover to radical treatment.

PSA-screened men with clinically localized prostate cancer, the original ProtecT eligibility. Slides were regraded under 2019 ISUP criteria rather than the trial-era 2005 criteria; the presenter reports regrading did not change the picture. Age, PSA and revised Gleason score did not differ significantly across arms in the reviewed subset.

The RT arm was external-beam radiotherapy with 3 to 6 months of neoadjuvant ADT. No dose, fractionation or target volume is given in the source. The presenter notes cribriform-positive disease was more prevalent in this arm, attributed to chance since cribriform status was not a randomization characteristic.

Primary: metastases at 15-year median follow-up, analysed by cribriform status. Multivariable Cox modelling was used to compare metastasis risk across grade groups within the cribriform-negative stratum.

Roughly 13% of the reviewed cohort was cribriform-positive. Among the 87% cribriform-negative, early radical treatment produced no statistically significant reduction in 15-year metastases vs active monitoring, in both ITT and per-protocol analyses. Cribriform-negative grade group 2 carried metastasis risk equivalent to grade group 1.

Slides were available for under half the randomized cohort, so the analysis rests on whichever centres have so far returned material. The source excerpt is a video interview that stops mid-presentation and reports no HRs, CIs or event counts, so the size of the null in the cribriform-negative group cannot be judged from it.

The interest here is the inverse of the usual cribriform argument. Rather than showing cribriform-positive pts do badly on surveillance, the useful signal is that cribriform-negative grade group 2 behaves like grade group 1 over 15 years, which is a de-escalation read. Whether the cribriform-positive stratum shows the reciprocal benefit is not in the source excerpt.

Post-hoc subgroup of a non-stratified variable in 712 of 1,643 pts, with a non-significant negative result and no effect sizes in the source.

Retrospective, IRB-approved cohort from 2 centers within a single institution, Jan 2017 to Dec 2023. Hypothesis stated a priori: proton cohort would have higher CC. Median follow-up 42 mo proton, 47 mo photon.

Subpectoral 2-stage TE/I or DTI reconstruction with PMRT; N=175 (89 proton, 86 photon). Median age 49 (range 24-78), 63% Hispanic. Groups balanced except laterality and reconstruction type (both P<.001).

Pencil beam scanning proton vs IMRT photon PMRT; the TE was irradiated in all TE/I pts. Dose, fractionation, bolus and superficial dose constraints are not reported in source.

Capsular contracture by Kaplan-Meier; associated factors by Cox proportional hazards, verified with binary logistic regression.

Reconstruction type was the only factor that stayed associated on multivariable analysis; the proton effect did not reach significance after adjustment (see tables).

The source frames proton vs photon CC data as scarce and reports this as the largest PBS PMRT reconstruction cohort to date. RADCOMP compares proton vs photon breast RT on cardiac outcomes, not reconstruction complications, so it will not settle this question.

Photon DTI stratum is only n=15, so the within-DTI modality contrast is underpowered. CC grading scale and RT planning parameters are absent from the abstract, which blocks translation to a specific planning change.

Adjusted proton HR 1.76 with an interval of 0.93-3.32 excludes neither no effect nor a large one; P=.083 is not reassurance. The consistent direction within both reconstruction types is the stronger signal, and PBS plus DTI is where the risk concentrates.

Retrospective cohort with reconstruction type imbalanced between modalities (P<.001); proton effect lost significance on multivariable analysis, so the modality signal stays confounded.