by Researchers at The University of Texas at Austin have made a groundbreaking discovery in the fight against acute myeloid leukemia (AML), an aggressive and deadly form of blood cancer. In an experimental study, scientists were able to inhibit the growth of the cancer without harming healthy cells. This finding could provide valuable insights for future drug development and increase the effectiveness of a certain type of chemotherapy. The study, led by Xiaolu Cambronne from the Department of Molecular Biosciences, in collaboration with researchers at Dell Medical School and the Department of Nutritional Sciences, was published in the journal Cell Metabolism.
AML is known for its rapid expansion and claims the lives of approximately 11,000 Americans each year. The majority of AML cases occur in adults over the age of 65, a demographic that often responds poorly to aggressive treatments like bone marrow transplants, leaving them with limited options.
The researchers made a significant discovery when they found that AML patients with poorer outcomes had elevated levels of a cellular transporter known as SLC25A51. In healthy cells, this transporter moves cellular fuel into the mitochondria, providing energy for the cell’s processes. However, in AML cells, the increased levels of the transporter essentially result in a “bigger fuel line,” causing the rapid replication of cancer cells.
By lowering the levels of the transporter, researchers effectively slowed down the progression of the disease and lengthened survival rates in animal models. Importantly, this approach did not harm normal bone marrow cells, only the cancerous ones.
Xiaolu Cambronne described this discovery as a new potential therapeutic target for a hard-to-treat disease. Lowering SLC25A51 levels appears to be a more targeted therapy for AML, as it does not negatively impact healthy cells.
Furthermore, when the lowered transporter levels were combined with 5-azacytidine, a type of chemotherapy used in AML patients, the survivability rate increased, and tumors shrank. The lower transporter levels made the cancer cells more vulnerable to the chemotherapy drug.
Currently, there are no drugs available that can lower SLC25A51 levels. The next step for researchers is to develop a compound that can safely accomplish this in the human body. In the animal study, researchers used gene editing to create sensitivity to a common antibiotic, which allowed them to control transporter levels.
This breakthrough offers hope for the development of more effective treatments for AML, particularly for individuals who do not respond well to current therapies. By targeting the cancer’s fuel supply, researchers have discovered a promising pathway to combat the aggressive growth of AML cells. However, further research and clinical trials are necessary to translate these findings into a viable treatment option for patients.
*Note:
1. Source: Coherent Market Insights, Public sources, Desk research
2. We have leveraged AI tools to mine information and compile it
