Leukemia is the most common childhood malignancy and cause of pediatric cancer death. Significant advances in the cure rates of B-cell acute lymphoblastic leukemia (B-ALL) and T-cell acute lymphoblastic leukemia (T-ALL) have been achieved; however, patients with refractory or relapsed B-ALL or T-ALL continue to have poor outcomes. Immunotherapy is a revolutionary treatment aimed to improve survival and reduce the toxicity of chemotherapy by harnessing the patient’s own immune system to target cancer cells.

Significant milestones and seminal discoveries during 1674-1966, by individuals who have made crucial contributions toward progress in the diagnosis of hematologic neoplasms as we understand today are depicted chronologically. It is notable that the path to progress in the understanding of disease and neoplasms initially took centuries for significant discoveries (17^th-18^th centuries), and subsequently, many decades (19^th-20^th centuries) for a breakthrough or a change from the prevailing norm. 

Chronic lymphoid leukemia (CLL) is a malignant hematological disease characterized by the accumulation of mature lymphocytes with a defect in the induction of apoptosis that massively accumulate in peripheral blood (PB), bone marrow (BM) and lymphoid tissues.

Acute myeloid leukemia (AML) is a type of hematological malignancies that originate from hematopoietic stem/ progenitor cells in myeloid lineage. The genetic heterogeneity of AML causes varied responses to the existing treatment options, as well as drug resistance and refractory/ recurrent, posing a challenge to personalized precision medicine. Therefore, it is urgent to identify novel molecular targets, discover patient specific and disease specific risk factors, and explore effective combinations of modalities and drugs in the foreseeable future.

IDH2 gene mutations, typically at residues R140 and R172, occur in 8–19% of patients with acute myeloid leukemia (AML). These mutations induce production of 2-hydroxyglutarate (2-HG), an oncometabolite that causes DNA and histone hypermethylation, and subsequent blockade of hematopoietic cell differentiation.