Mutated NPM1 in combination with overexpression of Meis1 or Hoxa9 is not sufficient to induce acute myeloid leukemia

Background Acute myeloid leukemia (AML) carrying nucleophosmin 1 (NPM1) mutations (NPMc+) is regarded as a separate entity of myeloid neoplasms due to its distinct biological and clinical features. However, NPMc+ alone displays low leukemogenic activity and cooperating events appear crucial for AML to develop. Dysregulation of homeobox genes, such as HOXA9 and MEIS1, is a common transcriptional signature of NPMc+ AML. Furthermore, the pathogenic role for NPMc+ in AML remains incompletely understood.