Researchers at the McMaster University have found that promoting the growth of adipocytes, also called fat cells, can help kill cancer cells found in leukemia patients.
Members of the research team were surprised to find that fat cells in the bone marrow had the ability to suppress cancer cells and cause the regeneration of healthy blood cells.
In a study published on October 16 in the journal Nature Cell Biology, the team explained that analysis from Acute myeloid leukemia (AML) patients showed that leukemic cells suppressed adipocytes in the bone marrow (BM). This led to imbalanced regulation of endogenous hematopoietic stem and progenitor cells which caused impaired myelo-erythroid maturation.
“In vivo administration of PPARγ agonists induced BM adipogenesis, which rescued healthy hematopoietic maturation while repressing leukemic growth,” according to the study. “Our study identifies a previously unappreciated axis between BM adipogenesis and normal myelo-erythroid maturation that is therapeutically accessible to improve symptoms of BM failure in AML via non-cell autonomous targeting of the niche.”
The study was conducted over a period of three and half years. Bone marrow samples were collected to patients at The Ottawa Hospital, as well as those from Western University and Hamilton Health Sciences.
The approach taken by the team represents a “different way of looking at leukemia and considers the entire bone marrow as an ecosystem,” rather than trying to destroy the diseased cells themselves, Allison Boyd, a postdoctoral fellow with McMaster and first author of the study, said in in an interview with DailyNewsMcMaster.ca.
To induce fat cell production, the team used a drug that is commonly used to moderate diabetes. They found the drug helped boost red blood cell production and suppress leukemic disease.
While traditional methods such as chemotherapy and other existing standards-of-care focus on killing cancer cells, the team took an approach that “changes the environment the cancer cells live in,” according to Mick Bhatia, director and senior scientist with the McMaster Stem Cell and Cancer Research Institute.
“This not only suppressed the ‘bad’ cancer cells but also bolstered the ‘good’ healthy cells allowing them to regenerate in the new drug-induced environment,” he said. “The fact that we can target one cell type in one tissue using an existing drug makes us excited about the possibilities of testing this in patients.”
The team foresees their approach being added to existing treatments or even replacing some of them in the future.