Studies to better understand the conditions that foster the initiation of leukemias and lymphomas are currently a major thrust of the lab. We have developed an evolutionary based model for cancer development, Adaptive Oncogenesis.  Using mouse models, we are currently exploring how reduced progenitor cellular fitness resulting from carcinogen exposure, irradiation, inadequate diet or aging can select for adaptive oncogenic events and thereby promote the expansion and fixation of oncogenically initiated cells. While current views of carcinogenesis focus on oncogenic mutations as the limiting step, our studies support a novel rationale for links between tumorigenesis and carcinogenic contexts: these contexts may promote the clonal expansion of cells bearing particular initiating events, in part by reducing progenitor pool fitness which selects for adaptive oncogenic mutations.