Scientists at the University of Texas Health Science Center at San Antonio have identified the FOXM1 protein as a key factor enabling certain cancers to evade the body’s immune response, potentially opening latest avenues for immunotherapy development. The research, published in Nature Communications in April 2025, details how FOXM1 initiates a cascade of events that allows cancer cells to avoid detection by the immune system.
For years, researchers have observed elevated levels of FOXM1 in a variety of cancers, including ovarian, breast, and pediatric malignancies. The UT Health San Antonio study is the first to define the specific mechanisms by which this protein facilitates immune evasion. Manjeet Rao, PhD, professor in the Department of Cell Systems and Anatomy and deputy director of the Greehey Children’s Cancer Research Institute, explained that FOXM1 supports cancer cell survival and progression by suppressing the anti-tumor immune response.
Cancer cells, as they multiply and mutate, actively manipulate their surrounding environment to shield themselves from immune attack. Typically, T-cells identify and destroy abnormal cells. However, tumors release chemical signals that can exhaust immune cells or create conditions that prevent them from functioning effectively. A critical tactic involves suppressing cell-surface proteins called stress ligands, which normally alert the immune system to the presence of cancer cells.
The discovery builds on a broader understanding of the cancer-immunity cycle, which outlines the steps involved in generating an anti-cancer immune response. Research into this cycle has been ongoing for the past decade, with scientists working to identify challenges and opportunities for improving immunotherapy, according to a recent review published in Immunity.
Further research indicates that metabolic changes within cancer cells also play a role in suppressing immune responses. A review published in Nature in January 2024 details how alterations in glucose, lactate, fatty acid, and nucleotide metabolism can interfere with both innate and adaptive immune functions, promoting tumor progression. The study suggests that targeting these metabolic alterations could enhance the effectiveness of anti-cancer immunotherapies.
Scientists at UT Southwestern Medical Center have also identified a hormone-receptor interaction that weakens immunity, allowing cancer cells to evade the body’s defenses. This research, published in Nature Immunology, points to potential therapeutic targets for bolstering the immune response against cancer.
