-5mC and 5hmC defects in hematopoiesis malignancy
My writing:
Hematopoiesis is a developmental process that is characterized by a dynamic equilibrium between self-renewal and a well-regulated differentiation of hematopoietic stem cells (HSCs).  Both extrinsic and intrinsic factors such as signal transduction pathways, transcription factors, and chromatin modifiers regulate these processes. Due to either dysfunctioning or misregulation of any extrinsic or intrinsic factors, normal hematopoiesis may go awry to further drive severe hematological malignancies including three main forms of blood cancer i.e. leukemia, lymphoma, and myeloma. 
General stats of Leukemia:
https://www.nature.com/articles/s41568-018-0015-6

A causal mechanism for childhood acute lymphoblastic leukaemia

In this Review, I present evidence supporting a multifactorial causation of childhood acute lymphoblastic leukaemia (ALL), a major subtype of paediatric cancer. ALL evolves in two discrete steps. First, in utero initiation by fusion gene formation or hyperdiploidy generates a covert, pre-leukaemic clone. Second, in a small fraction of these cases, the postnatal acquisition of secondary genetic changes (primarily V(D)J recombination-activating protein (RAG) and activation-induced cytidine deaminase (AID)-driven copy number alterations in the case of ETS translocation variant 6 (ETV6)–runt-related transcription factor 1 (RUNX1)+ ALL) drives conversion to overt leukaemia. Epidemiological and modelling studies endorse a dual role for common infections. Microbial exposures earlier in life are protective but, in their absence, later infections trigger the critical secondary mutations. Risk is further modified by inherited genetics, chance and, probably, diet. Childhood ALL can be viewed as a paradoxical consequence of progress in modern societies, where behavioral changes have restrained early microbial exposure. This engenders an evolutionary mismatch between historical adaptations of the immune system and contemporary lifestyles. Childhood ALL may be preventable cancer.
Epigenetic modifiers have emerged recently as potential drivers of hematological malignancies through the sequencing of blood cancer. However, the molecular basis for hematopoietic transformation by many of these chromatin modifiers is still largely unclear.

Epigenetics in pediatric acute lymphoblastic leukemia