Real-world evidence
ADT Class and Cardiovascular Risk (Hahn, ASCO GU 2026)
ForProstate cancer pts starting GnRH agonist or antagonist ADT
TL;DRMACE ~four per 100 person-yrs overall; ~37% numerically lower with GnRH antagonist vs agonist; 11 per 100 person-yrs with preexisting CVD.
Reported via UroToday →
In men with preexisting cardiovascular disease starting ADT, this supports flagging them for cardiology or primary care input given ~11 MACE per 100 person-yrs; it does not establish antagonist superiority over agonist, which rests on an unadjusted, degarelix-dominated comparison. The longer read
10 details 1 trial watching
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.
- Does the antagonist MACE difference persist after adjustment for age and payer?
- Relugolix vs degarelix cardiovascular risk
- Does risk-tiered cardiology referral lower MACE on ADT? recruiting High Cardiovascular Risk Intervention With Cardio-Oncology Consultation for Prostate Cancer Following Androgen Receptor Pathway Inhibitor (ARPI) Therapy (Heart-Safe) Phase 2n=80 · primary completion 2030-08 · cardio-oncology referral vs PCP notice, high CV risk
📚 Sources · 📄 1 paper
Abstract
PROTEUS
ForHigh-risk prostate cancer, perioperative setting
TL;DR5-yr BCR-FS 44%, MFS 71%, CSS 92% at 60-mo median f/u in a real-world high-risk prostate cancer benchmark cohort.
7 details 1 trial watching
Design not stated in source; described as a real-world benchmark. Median follow-up 60 mo.
Reported: 5-yr BCR-FS, 5-yr MFS, 5-yr CSS. No primary endpoint or effect size stated.
Framed as a reference point for perioperative treatment strategies in high-risk disease, not a test of one. Useful only once the cohort definition and treatments received are known, since those determine which trial populations it can benchmark.
| Endpoint | 5-yr estimate |
|---|---|
| BCR-FS | 44% |
| MFS | 71% |
| CSS | 92% |
Descriptive benchmark with no comparator, N, eligibility, or treatment details in source; cannot classify impact on any perioperative decision.
- Which perioperative strategies improve on this BCR-FS benchmark? active COACTION Trial - COmbination Androgen bloCkade in inTermediate to hIgh-risk prOstate caNcer Phase 4n=144 · primary completion 2026-03 · RCT neoadjuvant leuprorelin+darolutamide pre-RP, pCR EP
- Cohort high-risk definition and treatments received
📚 Sources · 🐦 1 tweet
🔹 Median follow-up: 60 mo
— Can Aydogdu (@CanDAydogdu) August 28, 2026
🔹 5-yr BCR-FS: 44%
🔹 5-yr MFS: 71%
🔹 5-yr CSS: 92%
Providing a real-world benchmark to contextualize perioperative treatment strategies in this high-risk population.
📄 https://t.co/NyszMg9uCA#ProstateCancer #PROTEUS #Urology
Focal Ablation vs IMRT Toxicity (SEER-Medicare)
ForLocalized prostate cancer, fee-for-service Medicare, mean age ~73
TL;DRGI toxicity favored focal therapy at 24mo (11.0% vs 21.5%, OR 0.45) but GU toxicity favored IMRT (41.7% vs 29.3%, OR 1.69).
The GI advantage rests on diagnosis claims alone: procedure-code-only GI events were too few to report and not significantly different, while the GU excess with FT was concrete (incontinence therapy 17.4% vs 7.5%). For an RT reader counseling an older man weighing ablation, that asymmetry is the point.
In an older man with localized prostate cancer choosing between focal ablation and IMRT, this supports counseling that the tradeoff runs GU-for-GI rather than uniformly lower toxicity with ablation; it does not extend to SBRT or proton patients, who were excluded. The longer read
The IMRT comparator is a 2010-2017, ≥20-fraction cohort with SBRT, protons and rectal hydrogel excluded, so the GI toxicity attributed to radiation predates spacer-era rectal sparing. That caps how much of this GI gap should carry into a current consent conversation, while the GU result (incontinence therapy 17.4% vs 7.5% favoring IMRT) transfers intact.
For ablation, the toxicity cost is concrete and periurethral: incontinence therapy 17.4% vs 7.5% and erectile dysfunction 18.2% vs 13.1%, both P<.01. The offsetting GI advantage collapsed in the procedure-only analysis, so the low-morbidity premise for cryotherapy and laser ablation in older men is weaker than the headline suggests.
10 details 5 trials watching
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).
| Toxicity / window | FT | IMRT | OR (95% CI) |
|---|---|---|---|
| GI 0-6 mo | 3.6% | 3.5% | 1.06 (0.67-1.67), P=.81 |
| GI 0-12 mo | 6.2% | 9.5% | 0.63 (0.45-0.88) |
| GI 0-24 mo | 11.0% | 21.5% | 0.45 (0.35-0.58) |
| GU 0-12 mo | 34.6% | 15.8% | 2.69 (2.21-3.28) |
| GU 0-24 mo | 41.7% | 29.3% | 1.69 (1.42-2.01) |
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.
- Does the tradeoff hold vs SBRT or spacer-era IMRT? n=184 · primary completion 2027-06 · IRE vs prostatectomy or RT, side-effect endpointn=356 · primary completion 2029-08 · focal therapy vs usual care RCT, ISUP 2/3
- Do patient-reported outcomes track the claims-based GU signal? n=300 · primary completion 2030-12 · prospective validated urinary/sexual PROs after HIFUn=200 · primary completion 2032-03 · questionnaire outcomes across HIFU, cryo, laser, IRE
- Do HIFU and RFA carry the same GU profile as cryo/laser? n=354 · primary completion 2028-12 · HIFU hemi-ablation, continence + toxicity endpoints
📚 Sources · 📄 1 paper
Abstract
PSMA PET Natural History Study in PSMA-Positive BCR
ForBiochemically recurrent prostate ca, post-definitive + salvage RT, PSA ≥ 0.5
TL;DRBaseline data on first 130 pts: most BCR men with PSADT >9-12mo still have PSMA PET findings once PSA exceeds 5.
Reported via UroToday →
The RT-relevant point is where the disease sits: prostate bed recurrence and nodal disease are the dominant baseline patterns, all in men who already had or declined salvage RT. If most slow-PSADT pts light up above PSA 5, PET positivity alone cannot gate metastasis-directed SBRT, and the trigger has to come from kinetics or serial change.
In post-salvage-RT BCR with PSADT over 9mo and a PSMA PET showing a few nodal or bed lesions, this supports serial imaging over reflex systemic therapy; it says nothing about pts with rapid PSADT or conventional-imaging metastases. The longer read
Nodal disease and prostate bed recurrence dominate the baseline patterns in men already past salvage RT, so this is the population MDT gets offered to. If most slow-PSADT pts are PET-positive above PSA 5, lesion count reflects scan timing more than biology, which weakens PET positivity as the gate for SBRT.
Only about a third of the cohort has started any therapy, and only 5 of the first ~150 progressed on conventional imaging at ~1.5yr. That is the counterweight to reflex mCSPC-style doublet therapy triggered by PSMA PET findings in men whose PSA kinetics are slow.
11 details
Prospective observational natural history cohort at the NCI, presented at GU-ASCO 2026. Baseline data on the first 130 pts; the cohort is ongoing at a median follow-up of about 2 years with interim outcome data pending.
Men with biochemical recurrence after definitive therapy, all of whom had already received salvage radiation or declined it. PSA ≥ 0.5 required for a baseline PET. Deliberately framed as PSMA-positive BCR, a state that would not have been detectable in the historical trials these pts map onto and that excluded them from metastatic trials.
The presented analysis is cross-sectional: PSMA PET findings at baseline against PSA doubling time, the field's working predictor of metastasis in BCR. Imaging cadence is protocolized at annual if the baseline PET is negative, every 6 months if anything is seen, including equivocal findings.
Among pts with slow kinetics (PSADT > 9mo and > 12mo), the majority still had PSMA PET findings once PSA was above 5: nodal disease, prostate bed recurrence, and small equivocal bone lesions. Only about a third have started any therapy. A companion poster found 5 of the first ~150 pts progressed on conventional imaging at roughly 1.5yr, and over 95% showed no abrupt PET change out of step with PSA.
The counts are reported conversationally in an interview ("about 130", "the first 150 or so", "that number's five"), with no stratum denominators and no CIs, so the PSADT-by-PET relationship cannot be quantified from this source. Allowing any therapy under 6 months, including SBRT and intermittent ADT, means the observed group is not an untreated comparator.
The claim being staked is that PSMA PET positivity in BCR is near-ubiquitous above PSA 5 and therefore weakly discriminating, so it should not by itself trigger treatment. What the cohort has not yet shown is whether PET burden or its change over time adds anything to PSA doubling time for predicting the outcomes that matter.
Baseline cross-sectional read of an ongoing single-institution cohort, median f/u ~2yr, no outcome analysis yet. Numbers reported conversationally, not tabulated.
- Does PET burden or its change add to PSA doubling time for predicting progression?
- Which PSMA-positive BCR pts can safely be observed off therapy?
- Are small equivocal bone lesions on PSMA PET true metastases?
📚 Sources · 📄 1 paper
Abstract
MROQC ADT Practice Patterns
ForIntact high-risk M0, N0-1 prostate cancer, definitive RT
TL;DRGuideline-concordant ≥18mo ADT intended in 67.0% of high-risk M0/N0-1 pts receiving definitive RT; ARPI recommended in 23.2% of STAMPEDE-eligible pts post-publication.
Facility-level variability in ≥18mo ADT recommendations persisted after adjusting for cN1, grade group and PSA (P<.0001), so treating site, not only tumor features, shapes duration. Among STAMPEDE M0-eligible pts, ARPI recommendations reached only 23.2% after publication, a gap a department can audit directly in its own high-risk RT cohort. The longer read
Grade group drove concordant ADT recommendations most (GG5 OR 9.45, GG4 OR 6.23), and site-level variability survived adjustment (P<.0001). For an RT department the benchmark is concrete: 67.0% intended ≥18mo ADT and 23.2% ARPI uptake in STAMPEDE M0-eligible pts after publication.
9 details
Prospective statewide quality-consortium data (MROQC), N=553 across 26 centers, June 2020 to November 2024. Multivariable analysis of predictors, a mixed-effects model with treatment site as random intercept, and ARPI adoption compared before vs after STAMPEDE M0 publication.
Intact high-risk M0, N0-1 prostate cancer treated with definitive RT: cT3/4 13.3%, cN1 19.9%, GG 4-5 75.0%, PSA ≥20 ng/mL 40.0%. 27.9% met STAMPEDE M0 criteria (≥2 of cT3/T4, GG 4-5, PSA ≥40 ng/mL, or cN1).
Primary: intended guideline-concordant ADT (GC-ADT, ≥18 months) per 2022 AUA/ASTRO. Also assessed: ARPI recommendation in STAMPEDE-eligible pts and facility-level variability.
91.3% recommended any ADT, 67.0% guideline-concordant. ARPI recommendations in STAMPEDE-eligible pts rose from 0% to 23.2% after publication; facility variability persisted on MVA (P<.0001).
| Factor | OR (95% CI) |
|---|---|
| cN1 | 2.94 (1.44-5.99) |
| GG4 | 6.23 (2.85-13.62) |
| GG5 | 9.45 (4.46-20.06) |
| PSA ≥40 ng/mL | 3.64 (1.22-10.87) |
Benchmarks practice against the 2022 AUA/ASTRO 18-36 month recommendation and STAMPEDE M0 ARPI intensification criteria. Single-state data, and the source offers no comparison with other practice settings.
The abstract gives no reasons for sub-18mo recommendations (comorbidity, pt preference, toxicity), so non-concordance is not necessarily poor care. The ARPI comparison is an uncontrolled before-after design, and no OR is reported for cT3/4.
The strongest predictors of a concordant recommendation were grade group (GG5 OR 9.45) and cN1, consistent with shorter courses being offered when high-risk status rests on other features. Residual site variability points to local norms beyond the modelled case mix, though unmeasured covariates could contribute.
Practice-patterns study of intended ADT recommendations; no efficacy or outcome endpoint, so nothing here confirms or challenges SOC.
- Delivered vs intended ADT duration in routine definitive RT practice
- Drivers of facility-level variation in ADT duration recommendations
- Barriers to ARPI intensification in STAMPEDE M0-eligible pts
📚 Sources · 📄 1 paper
Abstract
OCEANUS
ForAdvanced NSCLC receiving RT with ICI, newly diagnosed or ICI-refractory
TL;DRSequential RT+ICI mOS 20.3 vs 16.0 mo for concurrent, aHR 0.68 (0.47-0.99), in newly diagnosed advanced NSCLC; retrospective registry.
The RT-relevant gap is the exposure itself: the source text neither defines the sequential window nor reports dose, fractionation or target, so the timing signal cannot yet guide SBRT versus palliative-course scheduling around ICI. In refractory disease, continuing ICI after RT gave 11.2 vs 6.7 mo rwOS (P=.20), limited to 90-day survivors.
In newly diagnosed advanced NSCLC starting ICI with an RT indication, this adds observational support for sequencing RT rather than overlapping it; it does not extend to unresectable locally advanced disease, and in ICI-refractory disease the maintenance signal is non-significant. The longer read
Timing is the RT variable: sequencing RT around ICI rather than overlapping it tracked with longer rwOS in newly diagnosed advanced disease. Dose, fractionation, target and the sequential window are not reported in source text, so the signal cannot yet separate SBRT from palliative-course scheduling.
In ICI-refractory NSCLC, ICI maintenance after RT gave 11.2 vs 6.7 mo rwOS (P=.20), non-significant and limited to 90-day survivors. Chemotherapy tracked with longer rwOS only in newly diagnosed disease, magnitude not reported in source, so the systemic partner question stays open.
9 details 2 trials watching
Territory-wide retrospective cohort from the Hong Kong Hospital Authority CDARS database (more than 90% population coverage), NSCLC diagnosed 2010 to 2021. Overlap weighting was the primary propensity method, IPTW the sensitivity analysis; RMST was specified where proportional hazards failed.
Of 3522 ICI-treated pts, 335 received RT: 155 newly diagnosed advanced and 180 refractory NSCLC. 247 (73.7%) male, median age 64 (range 34-90).
RT dose, fractionation, modality, target site and the interval separating sequential from concurrent delivery are not reported in source text.
Primary: real-world OS after landmark, via weighted Kaplan-Meier and Cox models. Exposures: sequential vs concurrent RT+ICI (newly diagnosed), RT with vs without ICI maintenance (refractory), and receipt of chemotherapy.
Chemotherapy tracked with longer rwOS in newly diagnosed disease but not in refractory disease; no chemotherapy effect size in source text. IPTW estimates were similar to the primary analysis.
| Cohort | Exposure arm | Reference arm | Effect |
|---|---|---|---|
| Newly diagnosed advanced (n=155) | Sequential RT+ICI: 20.3 mo (13.3-NR) | Concurrent RT+ICI: 16.0 mo (8.3-30.0) | aHR 0.68 (0.47-0.99), P=.045 |
| Refractory (n=180) | RT + ICI maintenance: 11.2 mo (7.9-20.6) | RT without ICI maintenance: 6.7 mo (4.4-17.4) | P=.20 |
The source notes randomized data on RT+ICI sequencing are limited. PEMBRO-RT tested SBRT before pembrolizumab in advanced NSCLC, and PACIFIC placed ICI after concurrent chemoRT in unresectable locally advanced disease; neither randomized timing as this cohort compares it.
Undefined timing window and unreported RT parameters make the exposure heterogeneous, possibly mixing consolidative and palliative courses. The 2010 to 2021 window spans shifting first-line ICI practice, and any RMST estimates are not reported in source text.
A sequential advantage cuts against the common assumption that overlap maximises RT-ICI interaction, but urgent symptomatic RT given during ICI could explain it equally well. Whether continuing ICI after RT helps refractory disease remains open.
Retrospective propensity-weighted registry cohort; residual confounding by indication likely, upper CI bound 0.99 in n=155, and authors frame it as hypothesis generating.
- Does sequential vs concurrent RT+ICI timing change OS when randomized?
- Does continuing ICI after RT benefit refractory NSCLC? recruiting A Study Evaluating The Combination of Immunotherapy With Radiotherapy in Non-Small Cell Lung Cancer Phase 2n=39 · primary completion 2030-06 · post-IO progression, ICI + ablative hypofractionated RT
- Which RT dose and target drive any timing effect? n=366 · primary completion 2027-06 · abscopal control across RT fractionation arms + ICI
📚 Sources · 📄 1 paper
Abstract
Tumour bed boost after BCS+WBRT (Dutch cohort)
ForPost-BCS invasive breast cancer receiving WBRT, boost decision pending
TL;DR10yr IBTR 1.2% with 0-2 risk factors regardless of boost, supporting boost omission in the modern systemic era.
The decision this moves is boost omission, and the number that moves it is 10yr IBTR 1.2% in the 0-2 risk-factor group whether or not a boost was given, on 15,085 vs 13,845 pts. Note the ≥3 group ran higher WITH boost (3.3% vs 2.7%), which is allocation bias, not boost harm. Boost dose and fractionation are not in the source.
In a post-BCS patient over 40 with grade 1-2, hormone-receptor-positive disease receiving guideline-concordant systemic therapy, this supports omitting the tumour bed boost; it does not resolve the boost question for pts carrying three or more risk factors. The longer read
The omission decision rests on 10yr IBTR of 1.2% in the 0-2 risk-factor group with and without boost (15,085 vs 13,845 pts). The ≥3 stratum ran higher WITH boost (3.3% vs 2.7%), a signature of risk-based allocation rather than boost harm. Boost dose and fractionation are absent from the source.
| Risk factors | N no boost | N boost | 5yr no boost | 5yr boost | 10yr no boost | 10yr boost |
|---|---|---|---|---|---|---|
| 0-2 | 15,085 | 13,845 | 0.6% | 0.7% | 1.2% | 1.2% |
| ≥ 3 | 149 | 733 | 1.3% | 2.9% | 2.7% | 3.3% |
| Uncertain | 592 | 944 | 0.8% | 3.3% | 1.4% | 3.6% |
+2 more figures
9 details
Population-based Dutch cohort from the Netherlands Cancer Registry linked to pathology, on behalf of the DBRT group. Treatment years 2012-2016, follow-up to 10 years. Observational, no randomisation and no adjusted comparison reported in source.
Breast-conserving treatment with or without an RT boost, N=31,348 across the three risk strata. Stratification is by a count of five risk factors: age ≤40, grade 3, triple-negative, guideline-indicated systemic therapy not adequately given, and no pCR after neoadjuvant chemo in TNBC or HER2+.
Whole-breast RT with or without a tumour bed boost. Boost dose, fractionation, technique (photon vs electron vs SIB) and the WBRT schedule are not reported in the source slides, which limits transfer to a specific departmental protocol.
Primary: ipsilateral breast tumour recurrence (IBTR), histologically confirmed, identified by an algorithm over pathology report codes and free text. Reported as cumulative incidence at 5 and 10 years by risk-factor count. Benchmarked against the Assisi thresholds: omission acceptable at <3% 10yr IBTR with boost, <6% without.
IBTR was low in every stratum. The only cell crossing an Assisi threshold was ≥3 risk factors treated with a boost at 10 years, and even there the no-boost value in the same stratum was lower.
EORTC 22881-10882 established that a boost roughly halves IBTR, and that trial's control-arm event rates were an order of magnitude above these. IMPORT HIGH and the 2024 Assisi think tank both moved the field toward de-escalating or restricting the boost; this cohort supplies the contemporary absolute rates those recommendations assumed but could not show.
Boost was allocated by guideline-based risk, so the boost groups are adversely selected and the raw contrast understates any boost effect; the higher rate in the ≥3 boost group is the visible signature of that confounding. The ≥3 no-boost cell holds only 149 pts, and the 'uncertain' stratum (592 / 944) shows a boost-no-boost gap wide enough to suggest unmeasured risk is driving allocation there too.
The finding is about absolute rather than relative benefit: a preserved 50% relative reduction applied to a 1.2% 10-year event rate is not worth five extra fractions and a fibrosis penalty. What the cohort cannot say is whether the boost is the reason those low-risk rates are low, since roughly half the low-risk group received one.
Registry cohort, no randomisation and no adjusted effect estimate; boost allocation confounded by risk. Supports the direction already set by IMPORT HIGH and Assisi thresholds.
- Which ≥3 risk-factor subgroups actually benefit from a boost
- Whether boost omission holds under randomised testing in low-risk pts
- Boost dose and technique used across this cohort
📚 Sources · 🐦 1 tweet
Day TWO of #ESTRO26 Coverage by OncoAlert 🚨
— OncoAlert (@OncoAlert) May 16, 2026
Is a boost to the tumour bed still indicated after breast-conserving surgery and whole-breast radiotherapy in the era of modern systemic therapy? Presented by Femke Froklage 🇳🇱 #RadOnc ☢️
We aimed to identify a subgroup of breast… pic.twitter.com/RqK5r9XPqW
OligoCare
ForOligometastatic solid tumors treated with SABR, mixed primaries and lesion sites
TL;DRReal-world SABR local failure 5.0% at 1yr, 11.4% at 3yr across 2447 pts / 3533 lesions; CRC worst at 19.6%.
The actionable RT signal is minimum PTV dose, called the single most critical technical factor, and the de novo vs repeat OMD gap the authors attribute to higher delivered dose. CRC failed most (19.6% at 3yr) despite the highest median dose per fraction, which argues for escalation or combination rather than coverage alone. No dose thresholds are reported in source.
For a prostate or NSCLC oligomet being planned for SABR, this real-world cohort supports expecting durable in-field control (8.1% and 9.8% failure at 3yr); it does not support the same expectation for a colorectal met, where 3yr failure reached 19.6%. The longer read
Minimum PTV dose is named the most critical technical factor, so coverage of the low-dose region, not the prescription isodose, is where the planning attention goes. CRC failed worst (19.6% at 3yr) despite the highest median dose per fraction, so escalation alone may not close that gap. No dose thresholds reported in source.
SABR delivers 88.6% in-field control at 3yr in routine practice, so local failure is not the dominant driver of progression in most oligometastatic primaries. The exception is colorectal, at 19.6% failure by 3yr, where the authors suggest combination systemic approaches alongside local therapy rather than dose escalation alone.
| Primary | Total | 1 year | 3 years |
|---|---|---|---|
| Colorectal | 518 | 9.3% | 19.6% |
| Breast | 378 | 4.1% | 11.3% |
| NSCLC | 530 | 6.0% | 9.8% |
| Prostate | 1021 | 2.7% | 8.1% |
+2 more figures
10 details 4 trials watching
Prospective EORTC OligoCare registry cohort, interim analysis. 57 institutions, enrolment July 2019 to July 2025. No randomisation and no comparator arm; technique and dose were chosen by the treating institution.
2447 eligible pts with 3533 lesions. Median age 69 (range 28-94), 69% male. Primaries reported for the local-control breakdown were prostate (1021), NSCLC (530), colorectal (518) and breast (378).
SABR to oligometastatic lesions across bone (869 non-vertebral, 515 spine), lung (807), non-regional nodes (558), liver (306), brain (231) and other (247) sites. Minimum PTV dose was the technical factor most associated with outcome; specific dose and fractionation schedules are not reported in source.
Local in-field progression, reported as cumulative incidence with 99% CI, at 1 and 3 years. Median follow-up 31 months, minimum 6 months.
Overall local in-field progression 5.0% at 1yr and 11.4% at 3yr, ie 88.6% local control at 3yr. By primary, colorectal was the outlier and prostate the best.
Randomised oligometastatic SABR trials (SABR-COMET, STOMP, ORIOLE) were built on much smaller, more selected cohorts and reported survival or progression endpoints rather than lesion-level in-field control at this scale. This registry does not test the SABR question those trials asked; it reports what in-field control looks like once SABR is delivered in routine multi-institutional practice.
Dose and fractionation were institution-chosen, so the minimum-PTV-dose association is confounded by target site, prior irradiation and case selection. No PTV dose threshold, no per-primary dose data and no toxicity are reported in source, so the technical conclusion cannot be translated into a planning constraint.
The CRC finding is the one that changes a plan: worst local control despite the highest median dose per fraction points at intrinsic radioresistance rather than underdosing, and the authors call for escalation or combination strategies. The de novo versus repeat OMD gap is reported as a dose effect, which is plausible but is exactly the kind of comparison a registry cannot separate from the reasons a lesion is being re-treated.
Prospective multi-site registry, no randomised comparator, institution-chosen technique. Large real-world cohort supports existing SABR practice in OMD rather than testing it.
- Minimum PTV dose threshold that predicts local control
- Combination or dose-escalation strategies for colorectal oligomets recruiting Fruquintinib Combined With Sintilimab ± Radiotherapy for Third-line Treatment of Colorectal Cancer With Liver Metastases Phase 2n=62 · primary completion 2026-10 · SBRT+LDRT with sintilimab/fruquintinib, MSS CRC liverrecruiting Low and Intermediate Risk OliGometastatic ColoREctal CancEr PatieNts Treated with Stereotactic ABlative Radiotherapy Phase NAn=204 · primary completion 2031-04 · randomised SABR + chemo in 1-3 CRC oligomets
- Whether repeat OMD failure reflects dose or disease biology active Bony M - Stereotactic Ablative Radiotherapy (SABR) of Bony Metastases in Patients With Oligometastatic Disease Phase NAn=67 · primary completion 2023-01 · SABR in de novo vs recurrent OMD bone lesionsn=397 · primary completion 2028-06 · MR-guided adaptive SBRT, tumor control by site
📚 Sources · 🐦 1 tweet
📣 #ESTRO26 - @UmbertoRicardo e2irradiate @EORTC prospective OLIGOCARE registry of SABR for oligomets. ~2500 patients, ~3500 mets.
— Shankar Siva (@_ShankarSiva) May 17, 2026
➡️ local failure 5% at 1 year and 11% at 3 years
➡️ Colorectal cancer has higher risk of progression
➡️ minimum PTV dose correlated with outcome… pic.twitter.com/cx4zERqHhK