The mechanism of B cell acute lymphoblastic leukemia development

Abstract

B cell acute lymphoblastic leukemia (B-ALL) is a common malignant disease in children. Gene mutations in transcriptional factors and signal transduction molecules result in differentiation block and abnormal proliferation of B lymphoid progenitor cells. Children with B-ALL generally have a good prognosis, but about 20% of the pediatric patients and 60% adult patients still suffer from the high risk of relapse. Better understanding of the mechanism of leukemogenesis leads to significant improvement in treatment of ALL patients. Gene expression analysis and whole genome sequencing technologies have identified a number of novel gene mutations, but the roles of those mutations in leukemogenesisis remain unclear. This review mainly summarizes the so far identified cooperating gene mutations related to cell development and differentiation, epigenetic regulation, cell cycle and apoptosis, signal pathway, non-coding RNA, and leukemia clone evolution, some of which may be tightly associated with the relapse of B-ALL. In addition, we also review mouse models of B-ALL which may be useful for study of pathogenesis, risk classification, and design of future therapy.