Health UK (Commonwealth Union) – A drug in development, designed to combat metabolic disorders like type 2 diabetes and Alzheimer’s disease, could potentially provide a ray of hope for individuals battling chronic myeloid leukemia (CML), a type of blood cancer.
In a recent study conducted by the University of Glasgow and published in Nature Communications, researchers delved into the distinctive role of glucose in the behavior of treatment-resistant CML cancer cells. Encouragingly, their investigations revealed that employing an experimental diabetes medication to target CML cells hindered their glucose absorption, weakening them and potentially rendering them more susceptible to cancer therapies.
Prior research has already suggested that disrupting how cancer cells utilize essential nutrients like glucose for survival could unlock promising avenues for new treatments.
In this particular study, researchers uncovered that CML stem cells, which are pivotal in driving the disease, relied on glucose to energize their mitochondria, the cellular energy powerhouses. This glucose dependency also equipped these stem cells to elude current treatments.
To counteract this phenomenon, scientists effectively zeroed in on CML stem cells using a drug that obstructed glucose entry into their mitochondria. Remarkably, this very same drug had previously undergone clinical trials for the treatment of type 2 diabetes and Alzheimer’s disease. Now, the research team is exploring the potential of transitioning these findings into clinical trials to assess whether combining this drug with existing CML treatments could benefit patients.
Presently, individuals with CML receive tyrosine kinase inhibitors (TKIs), a treatment that has had its involvement in the clinical management of the disease. The researchers pointed out that while TKIs rarely offer a complete cure, they do effectively halt its progression. Consequently, most patients must remain on TKIs for life, facing associated side effects and the risk of developing drug resistance. The primary obstacle to finding a cure for CML lies in the fact that TKIs do not effectively target the crucial CML stem cells responsible for perpetuating the disease.
Professor Vignir Helgason, the lead author of the study at the University of Glasgow, indicated that the research has revealed that cancer cells often depend on increased uptake of specific nutrients—sugar, proteins, or fats—to survive. This suggests that if they can employ drugs to target that nutrient uptake, it may ultimately enhance cancer treatments.
“Our study investigated specific nutrient “addictions” in CML cancer cells. We were able to reveal that CML cancer cells use an increased amount of glucose to support their nutritional needs. Encouragingly, we were also able to show that the same cancer cells were sensitive to a newly developed anti-diabetic drug that prevents a normal breakdown of glucose, blocking the cells’ ability to absorb it.”
Dr Kevin Rattigan, co-author of the study, from the University of Glasgow’s School of Cancer Sciences, says “Our study has revealed that the addiction to glucose is an Achilles heel for the CML stem cells that are resistant to current therapies. We were also able to show that a newly developed drug can prevent CML stem cells using glucose for energy. This breakthrough may lead to improved therapy options and outcomes for patients.”
Jerry Colca, co-founder of Metabolic Solutions Development Company, the organization behind the development of the investigational drug MSDC-0160 scrutinized in this study, expressed enthusiasm about the potential of the drug’s mechanism of action, remarking, indicated that they are excited about the potential of the mechanism of action of new insulin sensitizers demonstrated in this study.
Researchers in recent years have often emphasized the role of the mitochondria and metabolism in cancer and other diseases. Professor Thomas Seyfried a leading cancer researcher from Boston College has often pointed the need to draw our attention to mitochondrial disruption in cancer treatment.
