B cell acute lymphoblastic leukemia (ALL), caused by too many immature white blood cells in the blood and bone marrow, has become one of the most curable cancers in children—approximately 90 percent who get it will survive. In spite of this progress, the survival rate for adults is lower, while the toxicity of treatments can worsen outcomes for many.
Michael Farrar, part of the U’s laboratory medicine and pathology faculty, is eager to curb the negative effects of B cell ALL.
While past studies suggest that a protein called SOS1 may be connected to B cell ALL, researchers do not know how the protein advances the disease or the mutations that cause it to unravel. However, Farrar recently found a mutation in mice that appears to alter SOS1 and correlate with overall survival. “The more truncated SOS1 we observed in their leukemia cells, the faster the mice died,” he says.
Farrar’s team is now working to identify similar SOS1-altering mutations in people and to determine how the protein gets rearranged to speed the progression of B cell ALL. Their ultimate goal is to launch clinical trials that would test the impact of different SOS1-targeting drugs against leukemia.
“What I like best about my work at the U is that every day there is the possibility that we may discover something new about how cancer develops and how we might develop new strategies to combat it. Support from Minnesota Masonic Charities is critical to moving these studies forward.”