Targeting and blocking the activity of a newly discovered signaling pathway known as cyclin dependent kinase 1 (CDK1) may improve the treatment of people living with a particular type of AML.
"If you feel really tired over a period of time, see your doctor."
Physician scientists at Harvard University, led by Daniel Tenen, MD, director of the Blood Program of the Harvard Stem Cell Institute, made the discovery.
Scientists know that the so-called FLT3 receptor is a common mutation in AML, occurring in 20-30 percent of patients. Its presence complicates the outlook.
These mutations are believed to switch on several signaling pathways that are involved in cancer development.
In a recent study, the researchers found that CDK1 is active in leukemias with the FLT3 mutation. Blocking its activity helps to treat AML.
Based on this study data, researchers suggest that drug therapies targeting the CDK1 pathway could be effective in treating AML with FLT3 mutations.
The researchers further conclude that this approach may be especially helpful for patients who are resistant to drugs that block FLT3.
An article on this research was published July 16 in The Journal of Clinical Investigation.
This research was supported by the National Institutes of Health.
The authors have declared that no conflict of interest exists.