Multiple myeloma is an invariably fatal B-cell malignancy that accounts for about 10% of hematopoietic cancers. Mutations in a receptor protein, Fibroblast Growth Factor Receptor 3
(FGFR3), are responsible for the common form of human skeletal dwarfism and also the lethal neonatal syndrome, Thanatophoric Dysplasia. Several of these same FGFR3 mutations have also been found to occur in about 25% of human multiple myeloma patients. We have recently demonstrated an interaction between FGFR3 and another important regulatory protein, Pyk2, which has been shown by others to regulate scheduled cell death of multiple myeloma cells. We wish to further explore the molecular mechanism whereby FGFR3 contributes to the cancerous properties of multiple myeloma cells, possibly by acting through the regulatory protein Pyk2.