Very recent: \citep{Nordlund_2018}
Etiologies of pediatric cancers including childhood AML/ALL and brain tumors have been substantially explored. The findings have helped us illustrate a landscape of initiation and progression of tumor genesis, diagnosis/prognosis, and targeted treatments. Owing to the versatility of Next gen sequencing, an unprecedented amount of data in cancer patients have been generated in order to characterize the complexity of genetic regulatory mechanisms. Many investigators have started to address cancer-related questions using gene expression profiles, genetic variations, epigenetic profiles, and functional genetic regulatory elements at the chromatin level. In this article, we systematically review how various genomic elements, such as gene fusion, mRNA and long non-coding RNA, may contribute to the development of pediatric cancers.
From: Cooperating gene mutations in childhood acute myeloid leukemia with special reference on mutations of ASXL1, TET2, IDH1, IDH2, and DNMT3A:
TET proteins encode a-ketoglutarate-dependent oxygenases, which are involved in the conversion of 5-methylcytosine to 5-hydroxymethylcytosine. TET2 protein is important for normal myelopoiesis, and disruption of TET2 enzymatic activity results in altered DNA methylation and favors myeloid neoplasm transformation. There have been no published reports on TET2 mutations in pediatric AML except in abstract form.