Researchers at MUSC Hollings Cancer Center have identified a signaling loop involved in the growth and persistence of leukemia cells – and developed a novel immunotherapy that can disrupt that loop to boost immune function and improve survival.
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Acute myeloid leukemia (AML) is one of the most aggressive blood cancers, with poor response to chemotherapy or CAR-T cell therapy. This is notably due to a self-sustaining signaling loop that allows leukemia stem cells to grow and evade treatment. A study published in Nature Communications has just outlined a groundbreaking bispecific antibody that disrupts this mechanism. The novel antibody tackles leukemia on two fronts : it blocks the IL-33/IL1RL1 protective feedback loop, while recruiting T-cells that target IL1RL1-expressing leukemia cells. In preclinical models, this dual-action strategy eradicated the shielded cancer cells, enhanced immune response, reduced relapse, and improved survival, all without significant toxicity. While Phase I trials are to follow, this approach may be replicated for cancers where IL1RL1 is also expressed in the tumor microenvironement.