Dear Cash Kumar,

The following review article depicts some of TET inhibitors such as 2HG, FH and SDH inhibitors, Dnmt3a Inhibitors; IDH 1 & IDH 2:

TET proteins and the control of cytosine demethylation in cancer

Laurianne Scourzic, Enguerran Mouly and Olivier A BernardEmail author

Genome Medicine20157:9

DOI: 10.1186/s13073-015-0134-6

©  Scourzic et al.; licensee BioMed Central. 2015

Published: 29 January 2015

Abstract

The discovery that ten-eleven translocation (TET) proteins are α-ketoglutarate-dependent dioxygenases involved in the conversion of 5-methylcytosines (5-mC) to 5-hydroxymethylcytosine (5-hmC), 5-formylcytosine and 5-carboxycytosine has revealed new pathways in the cytosine methylation and demethylation process. The description of inactivating mutations in TET2 suggests that cellular transformation is in part caused by the deregulation of this 5-mC conversion. The direct and indirect deregulation of methylation control through mutations in DNA methyltransferase and isocitrate dehydrogenase (IDH) genes, respectively, along with the importance of cytosine methylation in the control of normal and malignant cellular differentiation have provided a conceptual framework for understanding the early steps in cancer development. Here, we review recent advances in our understanding of the cytosine methylation cycle and its implication in cellular transformation, with an emphasis on TET enzymes and 5-hmC. Ongoing clinical trials targeting the activity of mutated IDH enzymes provide a proof of principle that DNA methylation is targetable, and will trigger further therapeutic applications aimed at controlling both early and late stages of cancer development.

https://genomemedicine.biomedcentral.com/articles/10.1186/s13073-015-0134-6

Hoping this will be helpful,

Rafik