Description
We found that mice deficient in both IRF-4 and IRF-8 develop from a very early age a more aggressive CML-like disease than mice deficient in IRF-8 alone. IRF-4 deficiency dramatically enhanced the effect of IRF-8 deficiency on expansion of granulocyte-monocyte progenitors (GMPs). All mice deficient in both IRF-4 and IRF-8 eventually develop and succumb to a B-lymphoblastic leukemia/lymphoma at approximately 25 weeks of age. The results demonstrate that IRF-4 and IRF-8 deficiencies can cooperate in the development of both myeloid and lymphoid tumors.