More active mitochondria may help chronic myeloid leukemia cells withstand treatment
Researchers in Adelaide and Singapore have uncovered new clues as to why some people with chronic myeloid leukemia (CML) respond better to treatment than others, finding that mitochondrial function in cancer cells could be targeted to improve responses.
Researchers in Adelaide and Singapore have discovered a potential link between mitochondrial function in chronic myeloid leukemia (CML) cells and treatment response. The study, published in HemaSphere, found that mitochondrial DNA mutations in patients with CML were associated with how well they responded to treatment with tyrosine kinase inhibitors (TKIs).
Patients with poorer responses had more active mitochondria, suggesting that these cells may rely more heavily on mitochondrial energy production. The team treated CML stem and progenitor cells with a mitochondrial inhibitor, which reduced the cells' ability to grow and survive. When combined with TKIs, the treatment showed even greater effectiveness.
While mitochondrial inhibitors are not currently used in CML treatment, this research provides a proof of concept that targeting mitochondrial energy production could improve treatment outcomes. Additionally, the study highlights the potential of using mitochondrial genetics to identify metabolic vulnerabilities in other cancers treated with targeted therapies, paving the way for more personalized treatment approaches.
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