very imp:
https://www.gavinpublishers.com/articles/Review-Article/Infectious-Diseases-Diagnosis-Treatment-ISSN-2577-1515/Genomic-Epigenomic-Abnormality-in-Pediatric-Cancer
https://genomemedicine.biomedcentral.com/articles/10.1186/s13073-015-0134-6
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.
Conclusion and future direction:
DNA methylation patterns are markedly abnormal in malignant cells in comparison with normal tissues. Abnormal methylation has been postulated to inactivate tumor suppressor genes through cytosine methylation and to activate oncogenes through cytosine hydroxymethylation and demethylation (Figure 3). An unexpected number of oxidized cytosine forms have been uncovered, whose specific functions need to be investigated. Specific techniques allowing their thorough investigation at the nucleotide level are under development and will enable us to investigate the specific functions of these cytosines in normal cells. This is a requirement for understanding their roles in cellular transformation, because mutations detected in cancer can inactivate or impair DNA methylation (for example, DNMT3A mutations) or DNA demethylation (for example, TET2 or IDH mutations).