LOS ANGELES, April 16, 2026
City of Hope announced that its scientists will present groundbreaking research findings on cancer risk, immune resistance, and AI-driven discovery at the AACR Annual Meeting 2026, one of the world’s most influential oncology conferences. The presentations, spanning over 100 sessions, highlight innovative approaches to understanding early cancer development, overcoming treatment resistance, and leveraging artificial intelligence to accelerate precision oncology, reinforcing the institution’s leadership in translating advanced science into patient-focused solutions.
AI Unlocks New Insights into Early Cancer Risk
A major highlight of the research is the use of artificial intelligence to uncover microbiome patterns linked to early-onset colorectal cancer, a growing global concern. Researchers demonstrated that patients diagnosed at younger ages show distinct gut microbiome compositions and reduced microbial diversity, suggesting a potential biological basis for the rising incidence of colorectal cancer in younger populations. By integrating genomic, clinical, and social health data, the AI-driven analysis identified previously undetectable correlations between microbial profiles and disease characteristics.
These findings emphasize the importance of multi-dimensional data analysis in cancer research, offering new pathways for early detection, risk stratification, and personalized prevention strategies. The study underscores how AI can transform complex biomedical datasets into actionable insights, potentially reshaping screening and prevention frameworks.
New Mechanisms Identified in Tumor Immune Resistance
City of Hope scientists also revealed a novel molecular pathway responsible for immune evasion in colorectal cancer, addressing a major limitation in current immunotherapy treatments. The research identified the NAT10-MYC-autophagy axis as a key driver of resistance, particularly in microsatellite-stable tumors, which account for the majority of colorectal cancer cases. Elevated NAT10 activity was shown to reduce immune system recognition by degrading MHC class I molecules, creating so-called “immune-cold” tumor environments.
Importantly, preclinical models demonstrated that targeting this pathway restored immune signaling, increased immune cell infiltration, and significantly enhanced responses to immunotherapy, especially when combined with checkpoint inhibitors. These findings provide a promising new therapeutic target that could expand the benefits of immunotherapy to a broader patient population, addressing a critical unmet need in oncology..

