Immuno therapy with autologous DCs and CIK cells was found to be a promising candidate for treatment of AML in elderly patients.

It is believed that there are key differences in the genomic profile between adult and childhood acute myeloid leukemia (AML). Relapse is the significant contributor of mortality in patients with AML and remains as the leading cause of cancer death among children, posing great challenges in the treatment of AML. The knowledge about the genomic lesions in childhood AML is still premature as most genomic events defined in children were derived from adult cohorts. However, the emerging technologies of next generation sequencing have narrowed the gap of knowledge in the biology of AML by the detection of gene mutations for each sub-type which have led to the improvement in terms of prognostication as well as the use of targeted therapies. In this review, we describe the recent understanding of the genomic landscape including the prevalence of mutation, prognostic impact, and targeted therapies that will provide an insight into the pathogenesis of AML relapse in both adult and childhood cases.

B-cell precursor acute lymphoblastic leukemia (B-ALL) is the commonest cancer in children, comprising over 80% of the entire childhood leukemia. However, the etiology of childhood B-ALL remains poorly understood and genetic susceptibility is a major risk factor for this disease. ARID5B appeared as one of the most promising genetic markers with nearly a 3-fold increased risk of disease. Method: In this meta-analysis, a total of six candidate ARID5B polymorphisms (i.e. rs10821936, rs10994982, rs7089424, rs10821938, rs10740055, and rs7073837) which have been analyzed in at least 2 studies were included for analysis of the risk association between ARID5B polymorphisms and childhood B-ALL. Results: Pooled analysis revealed that the dominant model of these six ARID5B polymorphisms was associated with an increased risk of childhood B-ALL. However, subgroup analysis based on ethnicity suggested that only four polymorphisms (i.e. rs10821936, rs10994982, rs7089424 and rs10821938) consistently conferred increased risk to childhood B-ALL across different populations, whereas the other 2 polymorphisms (rs10740055, rs7073837) were causative to Caucasians (OR=2.01, 95% CI=1.66-2.44; OR= 1.98, 95% CI=1.69-2.31) but maybe protective for Asian (OR=0.49, 95% CI=0.22-1.09; OR=0.95, 95% CI=0.43-2.09) respectively. Conclusion: Our meta-analysis demonstrated could serve as promising markers for assessing the susceptibility risk to childhood B-ALL in both the Asian and Caucasian populations. Further development of a multigene panel inclusive of ARID5B is desirable for screening children with a higher risk of developing B-ALL and to improve clinical management of the disease.