correlating factor for poor AML prognosis. The oncogene has been found to increase proliferative rates of HSCs whilst impairing their differentiation. The HOXA9 fusion oncogene causes an 8 times greater proliferation rate of HSCs after 5 weeks of cell culture when compared to control cells, and doubles the period of time over which HSCs can self-renew to an average of 54.3 days, compared to control human HSCs which stopped proliferating after 27.3 days. There are conflicting results regarding the effect of the oncogene on the differentiation of HSCs into the erythroid lineage. One study observed that the oncogene had a detrimental effect on the differentiation of HSCs, especially in the erythroid lineage, as proerythroblast colonies derived in vitro from mutated HSCs were fewer in number when compared to those derived from control HSCs, regardless of growth factors such as erythropoietin and interleukins which were introduced into the cultures. However, another study noted that the erythroid colonies were twice as populated in cultures of oncogene HSCs when compared to control HSCs. It is possible that these differing observations are due to a delayed differentiation of HSCs affected by the oncogene. The study which observed an increase in erythroid cell number noted that this proliferative effect could only be observed after around 3 weeks, and before this, cell numbers were comparable if not lower for the oncogene culture. The study observing a decreased number of cells did not quote the time of measurement, so if it was within three weeks of the culture, the reduced number may be attributed to this delay. Morphology alteration Proerythroblasts formed in the densely populated colonies of oncogene HSC cultures are strikingly different from those formed in the control colonies. By staining the colonies with giemsa, the oncogene-derived cells were shown to be non-hemoglobinized, larger, much less uniform in shape and had a distinctly large nucleus. These are some of the key morphological differences between primitive erythrocytes and adult erythrocytes. Thus, the NUP98-HOXA9 fusion may give rise to a new population of primitive erythrocytes in cases of AML, and by investigating the various proteins coded by this oncogene, it may be possible to not only establish some molecular causes of AML, but also identify some crucial proteins involved in early erythropoiesis which are absent during adult erythropoiesis. Pure erythroid leukemia There exists a rare form of AML, pure erythroid leukemia, where only the erythroid precursors of myeloid