Researchers at the University of New Mexico Comprehensive Cancer Center will use a two-year $453,000 grant to develop new treatments for slowly-progressing but very serious blood cancers in which the bone marrow makes too many red blood cells, white blood cells or platelets.
In many people, these disorders – Myeloproliferative neoplasms – can be traced to a mutation in a gene called JAK2, and they respond well to certain drugs. But other people have mutations in other genes and they don’t respond well to existing drugs.
“This is a problem where cell biology will really influence how we think about the disease,” says Bridget Wilson, PhD, one of the principal investigators of the grant from the U.S. Department of Defense.
Wilson and co-principal investigator Cédric Cleyrat, PhD, lead a team at the UNM Comprehensive Cancer Center that uses new advanced methods to see the proteins inside a cell. They will learn how the proteins work together — or don’t.
The proteins they will study play an important role in cellular protein quality control. Each cell uses a chaperone process which guides newly-formed proteins to their final destination, either in the cell or on its surface. But if this chaperone process becomes faulty, the cell doesn’t destroy malformed proteins as it should. Wilson and Cleyrat want to study this cellular process more deeply. Many patients with blood disorders who don’t have mutations in their JAK2 genes have mutations in genes that code for other proteins in this process.
Working with Cecilia Arana Yi, MD, Wilson and Cleyrat will examine blood and bone marrow samples from people with these blood cancers.
“Patients at UNM Cancer Center will be able to participate in these studies,” says Wilson, a professor of pathology in the UNM School of Medicine. “Our goal is to try to understand how these different proteins intersect with each other with the promise of new therapeutic concepts down the road.”