Intratumoral administration of DMXAA resulted in tumor regression and complete rejection in mouse xenografts. Tumor regression induced by DMXAA results from a cascade of cellular events which include disruption of tumor vasculature followed by the release of chemokines which trigger the recruitment of immune cells. DMXAA induced expression of IFN-β resulting in a striking expansion of leukemia-specific T cells extending survival in two acute myeloid leukemia models.