Multiple myeloma (MM) is an incurable malignancy of plasma cells marked by extreme genetic and phenotypic heterogeneity. Chromosomal hyperdiploidy or recurrent chromosomal translocations involving the immunoglobulin heavy chain locus primarily characterize this disease, with an abundance of mutations chiefly targeting the RAS and NF-kB pathways. While the genetics of MM have been well-annotated, much less is known about pathogenic signaling in MM and how common mutations contribute to oncogenic signaling. My research program utilizes cutting-edge proteogenomic techniques, high-resolution microscopy imaging and biochemical approaches to elucidate molecular mechanisms underlying oncogenic signaling in MM. The goal of my lab is to find new opportunities for the targeted treatment of MM by exploiting druggable pathways, even in tumors with undruggable driver oncogenes.

Current projects in the laboratory focus on: 1) discovering new modes of pathogenic signaling emanating from mutant KRAS and NRAS in MM;  2) characterizing the origins of NF-kB survival signaling that is prevalent in MM; and 3) identifying novel genes that control protein stability of commonly expressed oncogenes and tumor suppressors in lymphoid malignancies.