Title : Evaluation of noncytotoxic DNMT1-depleting therapy in patients with myelodysplastic syndromes.

Pub. Date : 2015 Mar 2

PMID : 25621498






1 Functional Relationships(s)
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1 Preclinical studies suggest that noncytotoxic concentrations of the DNA methyltransferase 1 (DNMT1) inhibitor decitabine produce p53-independent cell-cycle exits by reversing aberrant epigenetic repression of proliferation-terminating (MYC-antagonizing) differentiation genes in cancer cells. Decitabine tumor protein p53 Homo sapiens