An existing cancer drug may be effective against a specific type of nerve tumour because of its ability to block a particular metabolic pathway.
Wade Clapp at the Indiana University School of Medicine in Indianapolis, Luis Parada at the University of Texas Southwestern Medical Center in Dallas and their colleagues studied mice with tumours that derived their cancerous nature from a mutation in a gene called Nf1. For the tumours to grow, a biochemical pathway, c-kit, must be activated in bone-marrow cells with only one healthy copy of the gene, and immune cells called 'mast' cells from the bone marrow must have migrated close to the tumour cells.
The authors suppressed the tumours' growth with the c-kit-inhibiting drug imatinib mesylate (Gleevec). Imatinib was then given to a child with a life-threatening NF1-dependent tumour, which subsequently shrank by about 70%.