leukemia and is proposed to play a role in the transformation of the chronic and/or accelerated phases of this disease to its blast crisis phase. Repression of GATA2 The repression of GATA2 expression due to methylation of promoter sites in the GATA2 gene rather than a mutation in this gene has been suggested to be an alternate cause for the GATA2 deficiency syndrome. This epigenetic gene silencing also occurs in certain types of non-small-cell lung carcinoma and is suggested to have a protective effect on progression of the disease. Overexpression of GATA2 Elevated levels of GATA2 transcription factor due to overexpression of its gene GATA2 is a common finding in AML. It is associated with a poor prognosis, appears to promote progression of the disease, and therefore proposed to be a target for therapeutic intervention. This overexpression is not due to mutation but rather caused at least in part by the overexpression of EVI1, a transcription factor that stimulates GATA2 expression. GATA2 overexpression also occurs in prostate cancer where it appears to increase metastasis in the early stages of androgen-dependent disease and to stimulate prostate cancer cell survival and proliferation through activating by an unknown mechanism the androgen pathway in androgen-independent (i.e. castration-resistant) disease). See also GATA transcription factor GATA2 deficiency MonoMAC Emberger syndrome References Further reading External links Transcription factors