Acute B lymphoblastic leukemia (B-ALL) is a clonal heterogeneous disease caused by mutations in genes associated with the development and proliferation of B lymphocytes, which obstructs the normal differentiation and maturation of B lymphocyte progenitor cells. Although the complete remission rate for adult ALL patients can exceed 80% after induction remission therapy, most patients eventually relapse, resulting in a low long-term survival rate. Recently, many new gene mutation types have been detected in relapsed B-ALL patients using technologies such as gene chips and second-generation sequencing. However, the exact pathogenesis of these gene mutations and their co-synergistic fusion genes in B-ALL remains unclear. At the recently concluded 28th European Hematology Association (EHA) annual meeting, a study (Abstract No: P346) by the team of Liu Hongxing and Wang Tong from Beijing Lu Daopei Hematology Institute was selected for this year's EHA. The research aims to decode the structural changes of PAX5 and analyze other pathological fusion genes and gene mutations in B-ALL, while following up on the treatment and outcome of patients.
