Epigenetics in pediatric acute lymphoblastic leukemia
Recent technical advances and decreasing costs of methods for high-throughput DNA sequencing and SNP genotyping have stimulated systematic studies of the epigenetic changes in leukemic cells from pediatric ALL patients. The results emerging from these studies are increasing our understanding of the epigenetic component of leukemogenesis and have demonstrated the potential of DNA methylation as a biomarker for lineage and subtype classification, prognostication, and disease progression in ALL. In
Although the survival rate for patients with pediatric ALL treated on
modern protocols is high (> 90%), the outcome of ALL patients that relapse is poor [1]. Thus it would be highly beneficial if new biomarkers that predict relapse of ALL at diagnosis could be identified. As DNA methylation marks cellular states and is reversible, DNA methylation has good potential both as biomarker and as a potential treatment target.
6.1. 
In combination with recent re- ductions in DNA sequencing costs, single-cell sequencing offers a breakthrough for future analysis of DNA methylation in single cells from heterogeneous tumor populations [26,27,28].
https://www.cancer.org/cancer/cancer-in-children/differences-adults-children.html
With some exceptions, childhood cancers tend to respond better to certain treatments.. Children might seem to do better with cancer treatments than adults because they usually do not have other health problems that can get worse with cancer treatment. On the other hand, children (especially very young children) are more likely to be affected by radiation therapy if it is needed as part of treatment. Both chemo, radiation therapy, and other cancer treatments also can cause long-term side effects, so children who have had cancer will need careful follow-up for the rest of their lives.
Researchers are now studying the causes, diagnosis, and treatment of leukemia at many medical centers, university hospitals, and other institutions.
https://www.cancer.org/cancer/cancer-in-children/key-statistics.html#written_by
Because of major treatment advances in recent decades, more than 80% of children with cancer now survive 5 years or more. Overall, this is a huge increase since the mid-1970s, when the 5-year survival rate was about 58%. Still, survival rates vary depending on the type of cancer and other factors. The survival rates for a specific type of childhood cancer can be found in our information for that cancer type. 
After accidents, cancer is the second leading cause of death in children ages 1 to 14 . About 1,180 children younger than 15 years old are expected to die from cancer in 2018.
The levels of 5hmC in cancer are strongly reduced relative to the corresponding normal tissue surrounding the tumor [47]. Using liquid chromatography-mass spectrometry, anti-5hmC antibody-based immuno-dot blots, and immunohistochemistry, we demonstrated tumor-associated loss of 5hmC for cancers of the lung, brain, breast, liver, kidney, prostate, intestine, uterus and melanoma [47]. Other investigators confirmed this observation by showing loss of 5hmC in different types of solid tumors [57-60]
https://www.ncbi.nlm.nih.gov/pubmed/22052461
The data, therefore, suggest that 5hmdC is strongly depleted in human malignant tumors, a finding that adds another layer of complexity to the aberrant epigenome found in cancer tissue. In addition, a lack of 5hmC may become a useful biomarker for cancer diagnosis.
https://www.ncbi.nlm.nih.gov/pubmed/22980977
Here, we report that "loss of 5-hmC" is an epigenetic hallmark of melanoma, with diagnostic and prognostic implications. Genome-wide mapping of 5-hmC reveals loss of the 5-hmC landscape in the melanoma epigenome. We show that downregulation of isocitrate dehydrogenase 2 (IDH2) and TET family enzymes are likely one of the mechanisms underlying 5-hmC loss in melanoma. Rebuilding the 5-hmC landscape in melanoma cells by reintroducing active TET2 or IDH2 suppresses melanoma growth and increases tumor-free survival in animal models. Thus, our study reveals a critical function of 5-hmC in melanoma development and directly links the IDH and TET activity-dependent epigenetic pathway to 5-hmC-mediated suppression of melanoma progression, suggesting a new strategy for epigenetic cancer therapy.
https://www.urmc.rochester.edu/pediatrics/steiner-lab/current-research-projects/tet2-5-hmc-hematopoiesis-leukemogenesis.aspx
Epigenetic modifications are covalent modifications to DNA, or DNA binding proteins (histones), which are maintained throughout multiple cell divisions and are important for the regulation of DNA expression. Epigenetic modifications are a critical mechanism of gene regulation during hematopoiesis, and disruptions of these regulatory mechanisms have been associated with malignant transformation.