Mass General Brigham Cancer Institute Researchers Present Key Findings at AACR

Researchers from Mass General Brigham Cancer Institute will present research discoveries and outcomes from clinical trials in cancer at the 2026 American Association for Cancer Research (AACR) Annual Meeting, held April 17-22 in San Diego.

AACR brings together leading experts in cancer research to share the latest breakthroughs in cancer science and medicine. Presentations from Mass General Brigham Cancer Institute investigators will cover a wide range of topics, including clinical studies, cancer biology, screening, early detection, treatment and more.

Below are a few highlights from this year’s presentations. All times are local or Pacific time.

From persistence to relapse: Evolution of drug resistance in lung cancer
When: Saturday, April 18, 4:20-4:47 p.m.
Who: Aaron Hata, MD, PhD, physician investigator, Krantz Family Center for Cancer Research at Mass General Brigham Cancer Institute
What: In this Discovery Science Plenary, Dr. Hata will discuss his work addressing the emergence of drug resistance in lung cancer. He will highlight key features of cancer cells that persist in residual tumors after incomplete response to therapy. These persister cells can remain dormant for years but ultimately evolve into mechanisms of drug resistance that lead to disease relapse. Recent work in Dr. Hata’s laboratory using patient-derived models of EGFR and ALK-driven lung cancer has revealed that this evolutionary process is accelerated by increased expression of genes that induce mutations and promote lineage plasticity. The long term goal of this work is to better understand how cancer cells evade treatment to establish a foundation for adaptive therapies that can prevent or delay drug resistance.

Early-onset colorectal cancer: Advancing correlation to causation to prevention
When: Tuesday, April 21, 8:33-9:01 a.m.
Who: Andrew T. Chan, MD, MPH, Director of Cancer Epidemiology at Mass General Brigham Cancer Institute
What: In this plenary session on the rising incidence of early-onset cancers, Dr. Chan will discuss early-onset colorectal cancer, now the leading cause of cancer death in adults younger than age 50 in the U.S. He will review established and emerging risk factors for early-onset colorectal cancer as well as strategies to move from epidemiologic correlation toward causal understanding and prevention.

Age-stratified therapeutic strategies targeting tumor cell subclones that drive chemoresistance and immunosuppression in triple-negative breast cancer
When: Tuesday, April 21, 3:50-4:05 p.m.
Who: Milos Spasic, PhD, Investigator at Brigham and Women’s Hospital
What: Age is the biggest risk factor for developing most forms of cancer, including breast cancer. While over 50% of cancer cases occur in patients over 65, fewer than 25% of patients enrolled in clinical trials are in this age group. In a new study of triple negative breast cancer—an especially aggressive and treatment resistant form of the disease—scientists show that age dramatically alters how tumors respond to therapy. Using young and aged mouse models, the team found that standard chemotherapy and immunotherapy combinations were far less effective in older animals, in part because aging weakens immune responses and allows chemotherapy resistant cancer cell subtypes to expand. By tracking individual tumor cell lineages, the researchers identified a rare but dangerous subpopulation of cancer cells that thrive with age and resist chemotherapy. Importantly, this resistant group was vulnerable to a different class of drugs known as histone deacetylase inhibitors, which, when paired with immunotherapy, significantly reduced tumor growth and extended survival in older mice—without the need for chemotherapy. The findings suggest that tailoring cancer treatment to a patient’s age, rather than relying on one size fits all regimens, could lead to safer and more effective therapies for older adults.

Targeted therapy-induced chromosomal instability dictates mitotic dependency on Aurora kinase A
When: Tuesday, April 21, 4:05-4:20 p.m.
Who: Chendi Li, PhD, research fellow at Mass General Brigham Cancer Institute and Aaron Hata, MD, PhD (full title noted above)
What: Targeted cancer drugs are designed to shut down specific genetic drivers of tumor growth. However, researchers are recognizing that these treatments can also place hidden stresses on cancer cells, particularly in tumors that do not fully respond to therapy. In a new study of KRAS-mutant lung cancer, investigators found that, while effective at blocking cancer-driving signals, drugs targeting the KRAS G12C mutation can also induce DNA damage and chromosomal instability in some tumors, even at doses that do not kill the cells outright. By analyzing 15 lung cancer cell lines with diverse genetic backgrounds, the team observed that this treatment-induced chromosomal instability varied widely. In some cases, it created an unexpected vulnerability in cancer cells that were otherwise resistant to KRAS G12C inhibitors. Tumors with high levels of chromosomal disruption became particularly sensitive to drugs that interfere with cell division, especially inhibitors of Aurora kinase A. When combined, these therapies prevented cancer cells from completing cell division, ultimately leading to catastrophic cell death in both cell-based and mouse tumor models. These findings suggest that treatment-induced chromosomal instability could serve as a biomarker to identify patients most likely to benefit from combined KRAS and Aurora kinase A inhibition, offering a potential strategy to improve the effectiveness of KRAS-targeted therapies through a more precise, biomarker-driven approach.