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Practice-changing

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Practice-changing

STAMPEDE (abiraterone ± enzalutamide, high-risk non-metastatic) NCT00268476

ForHigh-risk M0 prostate: node+ or ≥2 of T3-4/Gleason 8-10/PSA≥40

TL;DRMFS HR 0.53 (6yr 82% vs 69%) and OS HR 0.60 adding 2yr abiraterone to ADT in high-risk M0 prostate (85% also had RT).

Why it mattersRadiation oncology

The RT read: abiraterone sits on top of definitive ADT+RT (74Gy/37fx to prostate+SV in the 85% who got RT), not RT vs no-RT. It moves systemic intensification for the high-risk M0 pt you're already irradiating; enzalutamide adds nothing over abiraterone (interaction HR 1.02, p=0.91).

8 details 2 trials watching

Pooled meta-analysis of two open-label phase 3 RCTs within the STAMPEDE platform, 113 UK/Swiss sites, N=1974, randomized 1:1. Median follow-up 72 mo (60-84).

High-risk non-metastatic disease: node-positive, or if node-negative ≥2 of T3/T4, Gleason 8-10, PSA ≥40; or high-risk relapse. Median age 68, median PSA 34; 39% node-positive.

Abiraterone 1000mg + prednisolone 5mg daily for 2yr added to 3yr ADT; the second trial's combination arm also received enzalutamide 160mg. Control = ADT alone.

RT planned in 85% (1684/1974): 74Gy/37fx to prostate + seminal vesicles or hypofractionated equivalent. Mandated if node-negative, encouraged if node-positive.

Primary: metastasis-free survival. Secondary: OS, prostate cancer-specific survival, biochemical failure-free survival, PFS, and toxicity.

Adding enzalutamide to abiraterone gave no extra MFS benefit (interaction HR 1.02, p=0.91), with no between-trial heterogeneity.

high-risk non-metastatic prostate cancer treated with definitive ADT plus radiotherapy
Does not represent metastatic disease, lower-risk localized disease, or patients managed without radiotherapy.

Open-label design, though MFS/OS are hard endpoints less prone to ascertainment bias. Pooled across two platform trials; no radiotherapy-treated subgroup HR reported in the source excerpt.

Two randomised phase 3 trials pooled; MFS primary hit (HR 0.53) with concordant OS benefit at 72mo, applicable high-risk M0 population. Adding enzalutamide gave no extra benefit.

In high-risk M0 prostate (node+, or ≥2 of T3-4/Gleason 8-10/PSA≥40) going to definitive ADT+RT, this supports adding 2yr abiraterone; it does not extend to lower-risk localized disease, and adding enzalutamide buys nothing.

📚 Sources · 📄 1 paper
📄 PAPER Attard, Gerhardt; Murphy, Laura; Clarke, Noel W et al. · The Lancet (2022-01)
Abiraterone acetate and prednisolone with or without enzalutamide for high-risk non-metastatic prostate cancer: a meta-analysis of primary results from two randomised controlled phase 3 trials of the STAMPEDE platform protocol
Practice-changing

RASolute 302

ForPreviously treated metastatic pancreatic cancer (RAS-mut or WT)

Overall survival

HR 0.40

95% CI 0.30-0.53, P<0.001; mOS 13.2 vs 6.7 mo (overall pop)

TL;DRmOS 13.2 vs 6.7mo, HR 0.40 (0.30-0.53), P<0.001 for daraxonrasib vs investigator's-choice chemo in previously treated metastatic pancreatic cancer.

Monday clinic

In previously treated metastatic pancreatic cancer with a RAS mutation, daraxonrasib's OS benefit supports it as a systemic option over chemotherapy; the signal does not extend to treatment-naive or localized disease.

RASolute 302
Population · ArmMedian OSHR (death)12-mo OS
G12 · Daraxonrasib13.2 mo (10.0-NR)0.40 (0.30-0.54)53.3%
G12 · Chemo6.6 mo (5.4-8.2)8.7%
Overall · Daraxonrasib13.2 mo (10.0-NR)0.40 (0.30-0.53)53.2%
Overall · Chemo6.7 mo (5.8-8.0)17.3%
7 details 1 trial watching

Phase 3 RCT, daraxonrasib vs investigator's-choice chemotherapy in previously treated metastatic pancreatic cancer. Two prespecified populations: RAS G12-mutant and overall (G12/G13/Q61 or no RAS mutation identified).

Previously treated metastatic pancreatic cancer. RAS G12 arm n=228 vs 231; overall n=248 vs 252. Overall population also includes tumors with no identified RAS mutation.

Daraxonrasib, an oral RAS(ON) multi-selective inhibitor targeting active GTP-bound RAS, vs investigator's choice cytotoxic chemotherapy.

Primary OS met: median 13.2 vs 6.7 mo, HR 0.40 (0.30-0.53), P<0.001 (overall); HR 0.40 (0.30-0.54) in RAS G12. 12-mo OS 53% vs 17% (overall). Deaths 32% vs 55-56%.

previously treated metastatic pancreatic cancer with RAS mutations (G12/G13/Q61) or no identified RAS mutation
Does not represent treatment-naive or localized/resectable pancreatic cancer.

Chemo control (6.6-6.7 mo) matches the historic 2L metastatic PDAC benchmark; no prior targeted agent has shown an OS signal of this magnitude in this setting.

Data limited to a single ASCO LBA OS figure; full safety and PFS not yet reported. Open-label; daraxonrasib median OS upper CI not reached (10.0-NR), so tail durability is immature.

Randomized phase 3, OS primary hit HR 0.40 in 2L metastatic PDAC where no targeted SOC exists; hard endpoint, unprecedented magnitude. Full LBA data pending.

📚 Sources · 🐦 1 tweet