MYC deregulates TET1 and TET2 expression to control global DNA (hydroxy)methylation and gene expression to maintain a neoplastic phenotype in T-ALL.

The results indicate that upon ectopic TET2 expression, there is a decreasing trend for genes involved in cell cycle arrest ( n = 84), negative regulation of extrinsic apoptotic signaling ( n = 66), positive regulation of endothelial cell proliferation ( n = 77), and regulation of transcription from RNA Pol II promoter in response to stress ( n = 58) (Fig. 7 f).

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