Our preliminary investigations demonstrate no significant compromising affects on the cell's structure at a cytogenetic or physiological level, post-treatment. Thus, further establishing these protocols as unique direct cell-engineering approaches with a host of biological and medical applications, from the development of tissues to perhaps even organs in the future.

SummaryHere, we report a high incidence of PAX5 abnormalities observed in 32/68 (47%) of patients with genetically unclassified childhood precursor B-cell acute lymphoblastic leukaemia (pre-B ALL). Various deletions, gains, mutations and rearrangements of PAX5 comprised 45%, 12%, 29% and 14%, respectively, of the abnormalities found. 28% of patients showed more than one abnormality of the gene, implying bi-allelic impairment of PAX5. Novel PAX5-RHOXF2, PAX5-ELK3 and PAX5-CBFA2T2 rearrangements, which lead to aberrant expression of PAX5, were also identified. PAX5 rearrangements demonstrated a complex mechanism of formation including concurrent duplications/deletions of PAX5 and its partner genes. Finally, the splice variant c.1013-2A>G, seen in two patients with loss of one PAX5 allele, was confirmed to be germ-line in one patient and somatic in the other. PAX5 alterations were also found to be clinically associated with a higher white blood cell count (P = 0Á015). These findings contribute to the knowledge of PAX5 alterations and their role in the pathogenesis of pre-B ALL.

No abstract

834 Scientific correspondence NAN 2015; 41: 832-836