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. Author manuscript; available in PMC: 2014 Sep 1.
Published in final edited form as: Cancer Discov. 2013 Sep;3(9):10.1158/2159-8290.CD-13-0358. doi: 10.1158/2159-8290.CD-13-0358

Figure 1.

Figure 1

A depiction of the model Clozel et al. proposed for the mechanism-based epigenetic chemosensitization of diffuse large B cell lymphoma upon low dose 5-aza-2-deoxycytidine, decitibine (DAC) treatment (1). Acquired resistance to anthracyclines may occur through DNMT1 methylation of CpG islands located in the promoter of genes such as SMAD1. Hypomethylation and reactivation of genes occurs after inhibition of DNMT1 by DAC. This hypomethylation, which is augmented in rapidly dividing cells, results in the reactivation of genes (e.g. SMAD1). SMAD1 confers chemosensitization upon its phosphorylation, trimerization, translocation into the nucleus and transcription of target genes including CDKN1A.