Obesity can act as fuel for leukemia, according to a study led by Indiana University School of Medicine scientists, published on Jul. 14. The research team identified a potential new treatment strategy that combines popular weight-loss medications with anti-inflammatory drugs for patients facing aggressive blood cancers.
The researchers analyzed electronic health record data from more than 440,000 people in the UK Biobank and conducted experiments in mouse models. They found that obesity creates chronic inflammation, accelerating the growth of mutated, leukemia-causing blood stem cells. This environment is characterized by high levels of an inflammatory molecule called IL-17A and decreased GLP-1 metabolic signaling.
Both pathways can be targeted with existing medications. The study tested a dual-therapy approach using anti–IL-17A antibodies—currently used to treat autoimmune diseases—and drugs that boost GLP-1 signaling, which are found in several diabetes and weight-loss medicines. The combination successfully lowered leukemia levels and improved immune function in obese mice.
"Because these therapies are already available and have established safety profiles, our results raise the possibility of repurposing them either alone or in combination to improve outcomes for patients with high-risk myeloid leukemias," said Santhosh K. Pasupuleti, PhD, assistant research professor of pediatrics at the IU School of Medicine and co-senior author of the study. "This strategy could help reduce leukemia progression while simultaneously improving metabolic health and restoring anti-tumor immunity."
The team plans to evaluate this therapeutic approach further through clinical studies to determine whether combining IL-17A inhibitors with GLP-1 drugs can safely benefit patients with obesity-associated leukemia. Future research will also identify which patients may benefit most from this treatment and assess its application to other cancer types.
"The broader significance of this work extends beyond leukemia," Kapur said. "The demonstration that metabolic dysfunction can reprogram immune responses to promote cancer progression has implications for multiple malignancies and suggests that metabolic interventions could become a foundational component of cancer prevention and therapy."
