onc brain

About · curated by Nick Boehling, MD · @nb2276

2026-06-10

Challenges SOC

RTOG 0848 NCT01013649

ForResected pancreatic head adenocarcinoma, post 6 cycles adjuvant gemcitabine-based chemo

Overall survival

HR 0.96

90% CI 0.79-1.18, 1-sided P=.38; did not meet OS

TL;DRAdjuvant CXRT after 6 cycles gemcitabine-based chemo missed OS (HR 0.96), but node-negative pts gained: 5yr OS 48.1% vs 28.6%.

Why it mattersRadiation oncology

The whole RT read sits in 91 node-negative pts: 5yr OS 48.1% vs 28.6%, median OS 3.9 vs 3.0 yr, with interaction P=.022. Delivery was standard and QA'd (50.4 Gy/28 fx, tumor bed plus pancreatojejunostomy plus regional nodes, 81% IMRT), so the technique transfers directly. G4-5 toxicity was unchanged (6% v 5%).

Monday clinic

In a resected pancreatic head adenocarcinoma pt who is node-negative and progression-free after adjuvant chemotherapy, this supports discussing CXRT; it does not extend to node-positive disease, where no treatment effect was seen, or to margin-positive pts (only 10 node-negative/margin-positive across both arms).

The longer read
10 details 2 trials watching

Prospective randomized phase IIR/III, two-step, multicenter (RTOG then NRG). Step 2 opened November 2009, closed October 2018, analyzed December 2023. Randomization 1:1, unmasked, stratified by nodal status, CA19-9, margins and adjuvant systemic treatment.

Curative-intent gross total resection of pancreatic head adenocarcinoma with documented microscopic margin status; body/tail excluded. Only pts without recurrence after five cycles of chemotherapy entered step 2: 546 entered step 1, 354 randomized (174 chemo, 180 chemo+CXRT). 74% node-positive, 17% margin-positive, 81% T3.

Step 1 was gemcitabine (67%), gemcitabine plus erlotinib (28%) or non-oxaliplatin gemcitabine combinations (5%); no pt received FOLFIRINOX. Both arms then took a sixth cycle; the experimental arm followed with CXRT within 21 days, sensitized by capecitabine (83%) or infusional 5-FU (15%).

50.4 Gy in 28 fractions to the postoperative tumor bed, pancreatojejunostomy and regional nodes; median delivered dose 50.4 Gy over 28 fractions and 38 days. 81% IMRT, 19% 3D conformal, 79% with no interruptions, 88% received ≥50 Gy. Centers were IROC-credentialed and every plan underwent real-time central review before start.

Primary: overall survival from second-step randomization. Secondary: DFS and adverse events (CTCAE v4.0). Final analysis triggered at the earlier of 316 OS events or 5 years of potential follow-up for all pts; it fired on the latter with 270 events, cutting power to 72%.

Grade 4 or 5 AEs were not increased (6% v 5%, P=.68), with one grade 5 in each arm (hepatic failure, sepsis). Grade 3 rose to 38% v 19% (P<.001), driven by GI events and decreased lymphocyte count; grade 3 nonhematologic 22% v 11% (P=.004).

ESPAC-1 reported adjuvant CXRT as detrimental, but accrued 1994-2000 with split-course lower-dose 2D planning, no postoperative imaging to exclude incomplete resection or early metastases, and no QA. RTOG 9704's post hoc analysis linked RT protocol deviations to worse survival, the specific failure mode 0848 designed its real-time review to prevent.

resected pancreatic head adenocarcinoma, progression-free after five cycles of gemcitabine-based adjuvant chemotherapy
Does not represent body/tail primaries, pts treated with FOLFIRINOX or neoadjuvant therapy, or margin-positive node-negative pts (10 total, five per arm).

Accrual took almost 9 years and the OS event rate ran below projection, so the trial read out on a follow-up trigger at 270 of 316 planned events (power 72% for the hypothesized HR 0.76). The node-negative arms hold 42 and 49 pts, and the subgroup rests on an interaction P=.022 across nine tested subgroups.

The negative primary settles that unselected adjuvant CXRT adds nothing after gemcitabine-based chemotherapy, while the safety profile removes the ESPAC-1-era objection that RT here is harmful. What stays open is whether the node-negative signal reflects a real locoregional benefit in pts with lower competing distant risk, and whether it survives a modern FOLFIRINOX backbone.

EndpointChemo (n=42)Chemo+CXRT (n=49)
5yr OS (95% CI)28.6 (14.9-42.2)48.1 (33.3-62.9)
Median OS, yr (95% CI)3.0 (2.2-4.0)3.9 (2.5-NR)
Median DFS, yr (95% CI)1.5 (0.8-2.7)2.3 (1.4-NR)
CONSORT flow
Randomized 354
Chemo
allocated 174
analyzed 174
5yr OS 23.1%
Chemo+CXRT
allocated 180
analyzed 180
5yr OS 27.9%

Prespecified stratified phase III, primary OS endpoint negative overall. Node-negative benefit rests on a subgroup interaction (P=.022) in 91 pts, hypothesis-generating not definitive.

📚 Sources · 📄 1 paper
📄 PAPER Ross A Abrams; Kathryn A Winter; Karyn A Goodman et al. · Journal of Clinical Oncology (2026-06)
Adjuvant Chemotherapy +/- Chemoradiotherapy for Adenocarcinoma of The Pancreatic Head: Results of The Radiotherapy Randomization of NRG Oncology/RTOG 0848

2026-05-31

Practice-changing

RASolute 302

ForPreviously treated metastatic pancreatic cancer, RAS G12-mutant

TL;DRMedian OS 13.2 vs 6.6 mo, HR 0.40 (95% CI 0.30-0.54), P<0.001, daraxonrasib over chemo in previously treated RAS G12 metastatic pancreatic cancer.

Monday clinic

In previously treated metastatic pancreatic cancer with a RAS G12 mutation, this supports daraxonrasib over investigator's choice chemotherapy on OS; it does not extend to treatment-naive or non-metastatic disease.

RASolute 302
PopulationArmNEvents, n (%)mOS, mo (95% CI)HR for death (95% CI)
RAS G12Daraxonrasib22872 (32)13.2 (10.0-NR)0.40 (0.30-0.54), P<0.001
RAS G12Chemotherapy231127 (55)6.6 (5.4-8.2)ref
OverallDaraxonrasib24879 (32)13.2 (10.0-NR)0.40 (0.30-0.53), P<0.001
OverallChemotherapy252141 (56)6.7 (5.8-8.0)ref
8 details 2 trials watching

Phase, randomization and primary endpoint not stated in source. HRs came from a stratified Cox model and P values from a stratified log-rank test. Presented at ASCO as abstract LBA5.

Previously treated metastatic pancreatic cancer. OS reported in a RAS G12 population (228 vs 231) and an overall population that also includes G13 or Q61 mutations or no RAS mutation identified (248 vs 252).

Daraxonrasib vs investigator's choice chemotherapy. Dose, schedule and the chemo options allowed are not stated in source.

OS favored daraxonrasib in both populations with HR 0.40, P<0.001; per-arm values are in the figure table.

Second-line metastatic pancreatic cancer has been a chemotherapy space, with NAPOLI-1 establishing a nal-IRI based option. An OS benefit for a RAS-directed agent over chemo is a different class of result; no cross-trial numbers are reported in source.

previously treated metastatic pancreatic cancer, principally RAS G12-mutant disease
Does not represent treatment-naive or non-metastatic disease, and gives no separate estimate for G13, Q61 or no-RAS-mutation tumors.

Safety and follow-up duration not reported in source; the daraxonrasib median OS upper CI is not reached. Composition of the investigator's-choice control is unknown, which bears on comparator strength.

The identical HR 0.40 in both populations reflects that the overall population is almost entirely RAS G12, not a demonstrated benefit beyond G12. Events of 32% vs 55% and 56% mean the daraxonrasib median of 13.2 mo rests on fewer events and may move with maturity.

OS HR 0.40 vs investigator's-choice chemo, P<0.001, consistent in RAS G12 and overall populations; source frames it as historic. Tweet omits phase and design.

📚 Sources · 🐦 1 tweet

2026-05-30 ASCO Annual Meeting 2026

Challenges SOC

Neo-CRAG

ForcT3N2-3M0 / cT4 gastric or Siewert II-III EGJ adenocarcinoma, D2-resectable

Disease-free survival surrogate

HR 0.750

95% CI 0.607-0.928, P=0.008; 3yr DFS 55.6% vs 42.4%

TL;DRAdding preop 45Gy/25fx to periop XELOX raised 3yr DFS 55.6% vs 42.4%, HR 0.750; mOS 67.5 vs 37.6mo.

Why it mattersRadiation oncology

The RT case here rests on locoregional control: LRR after R0 fell to 9.4% from 18.3%, tracking the ypN0 (56.1% vs 36.4%) and pCR gains, which is the mechanistic chain CRITICS and TOPGEAR never produced. Dose was conventional 45Gy/25fx preoperatively, and G3+ postop complications stayed flat (9.0% vs 7.6%), so the deliverability objection to preop RT before D2 loses force.

Monday clinic

In node-heavy cT3N2+ or cT4 gastric/Siewert II-III disease heading to D2 resection, this supports revisiting preoperative chemoRT rather than chemo alone; it does not speak to cT2N0-N1 disease or to pts already committed to a FLOT backbone.

The longer read
Neo-CRAG
EndpointCRTCTEffect size
3yr DFS55.6% (50.1-61.1)42.4% (36.9-47.9)HR 0.750 (0.607-0.928), P=0.008
Median DFS52.7 mo24.4 mon/a
5yr OS50.1%44.2%HR 0.781 (0.628-0.970), P=0.025
Median OS67.5 mo37.6 mon/a
9 details

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

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

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

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

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

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

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

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

high-risk cT3N2-3 / cT4 gastric and Siewert II-III EGJ adenocarcinoma treated with D2 gastrectomy and a doublet backbone
Does not represent cT2 or node-negative disease, Siewert I tumours, or pts planned for perioperative FLOT.

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

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

CONSORT flow
Randomized 620
CRT (chemoRT + XELOX)
allocated 310
3yr DFS 55.6%
CT (XELOX alone)
allocated 310
3yr DFS 42.4%

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

  • Does preoperative chemoRT still add benefit on a FLOT backbone?
  • Generalizability outside high-volume D2 centers
  • Optimal target volume and elective nodal coverage not reported in source
📚 Sources · 🐦 1 tweet