Overexpression of GATA2 predicts an adverse prognosis for patients with acute myeloid leukemia and it is associated with distinct molecular abnormalities

Acute myeloid leukemia (AML) represents a heterogeneous group of hematological neoplasms associated with the accumulation of acquired genetic and epigenetic aberrations in hematopoietic progenitor cells. Myeloid leukemogenesis is directly linked to the disruption of expression of transcription factors that regulate the proliferation, survival and differentiation of myeloid progenitors. Moreover, overexpression of particular genes has been associated with prognosis in AML, enabling patients with different survival rates to be identified within cytogenetic risk groups. The GATA2 gene encodes a transcription factor that mediates essential functions in hematopoietic stem cell and progenitor cell (HSC/HPC) compartments. The essential role of GATA2 in hematopoiesis is evident in mice lacking GATA2, which are anemic, have fewer HSC/HPC cells and that die by day 10–11 of gestation.