The focus of my laboratory is the development of cancer therapies that target pathways responsible for cancer initiation and progression. I am particularly interested in the study of cancers dependent upon alterations in tyrosine kinase and steroid receptor signaling. In pursuit of this goal, we have established relevant model systems in which changes in a drugs proposed molecular target can be correlated with drug dose, serum level, and anticancer activity. Our hypothesis is that the consequences of pathway inhibition will vary as a function of cell lineage and the complement of mutations within a tumor cells. Therefore, in order to improve the treat of cancer patients, one must understand not only which genetic changes are commonly found within particular tumor types but the mechanisms whereby these genetic alterations support tumor growth, survival, metastasis or other hallmarks of the cancer phenotype.