The results were shared today during the Plenary Session at the American Society of Clinical Oncology Annual Meeting by Dr. Jonathan Goldman, Health Sciences Clinical Professor in the Department of Medicine at the David Geffen School of Medicine at UCLA, and published in the New England Journal of Medicine. 

 

CHICAGO, MAY 31, 2026 ― Updated results from the Phase 3 BREAKWATER trial, led by researchers at The University of Texas MD Anderson Cancer Center, demonstrated a 56% reduction in the risk of disease progression or death for patients with BRAF V600E mutant metastatic colorectal cancer treated with a targeted therapy combination. 

High-risk localized and locally advanced prostate cancer patients treated with apalutamide — a next generation neoadjuvant androgen-receptor pathway inhibitor (ARPI) — plus hormone therapy before and after prostate cancer surgery resulted in more major pathologic responses and reduced the risk of metastasis or death, meeting both primary endpoints, in an international phase 3 clinical trial led by principal investigator Mary-Ellen Taplin, MD, medical oncologist at Dana-Farber Cancer Institute, and Adam Kibel, MD, chair of the Department of Urology at Mass General Brigham.  

About The Study: Regional participation in a population-based multicancer early detection (MCED) screening trial was associated with a modest increase in diagnostic delay rates for patients referred for suspected head and neck, lung, and upper gastrointestinal cancers. This increase is unlikely to have materially affected interpretation of the MCED screening trial primary findings. Future trials of population-based screening interventions likely to affect demand for limited health care resources should consider monitoring for system-level spillover effects. 

Adeno‑associated virus (AAV) vectors offer safety and durable expression but lack tumor specificity. This hypothesis proposes an NSCLC‑directed, hypoxia‑responsive AAV platform that integrates MGS4 peptide‑guided capsid targeting with dual hypoxia‑responsive element (HRE)‑gated promoters driving Q‑CXCL9‑Fc (chemokine) and miR‑30‑based shRNA against mesothelin (MSLN). The design aims to restrict entry to NSCLC lesions, confine transgene expression to hypoxic, BIRC5‑active tumor regions, and synergistically enhance antitumor immunity while suppressing invasion. This multimodal, hypoxia‑responsive AAV represents a precision oncology strategy that combines environmental sensing, tumor‑specific transcription, and peptide‑defined tropism within a single vector.