Non-Hodgkin's lymphoma is diagnosed in nearly 70,000 Americans per year. Treatment with targeted therapies, including the Bruton's tyrosine kinase inhibitor ibrutinib, has been extremely successful at promoting patient responses (>90% in some subtypes). However, in many cases, ibrutinib eventually fails due to acquired drug resistance. The James lab uses quantitative proteomics and small molecule screening to identify signals that are required for the survival of drug-resistant lymphoma cell populations and to find phosphorylation events regulated by BTK (1). Ultimately, our goal is to use "signaling signatures" to determine, for a given patient, which additional therapies are likely to be successful when given in combination or sequence with targeted therapies like ibrutinib.
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