Moreover, the binding of the E2A-PBX1 chimeric protein to the <i>BAFFR</i> promoter suggests that the transcriptional activator promotes the increase in <i>BAFFR</i> expression observed in about 50% of pre-B-ALL patients carrying the <i>t</i><sub>(1, 19)</sub> translocation.
In this study, we describe remodeling of signaling networks by E2A-PBX1 in pre-B-ALL, which results in hyperactivation of the key oncogenic effector enzyme PLCγ2.
Translocation t(1;19)(q23;p13) plays a crucial role in the pathogenesis of childhood pre-B cell leukemia and results in the formation of a fusion gene E2A-PBX1 that encodes a hybrid transcription factor with oncogenic potential.
Here we described a new fusion site of the E2A and PBX1 genes, which was detected in the leukemic blasts of a child with t(1;19) pre-B ALL using the reverse transcriptase polymerase chain reaction and direct sequencing.
A new E2A-PBX-1 fusion transcript positive t(1;19) pre-B ALL cell line (designated LC1;19) with the composite immunophenotype CD7-CD10+CD19+CD45-HLA-DR+C mu+ was established by expanding BM blasts from a SCID mouse, which died of human t(1;19) ALL at 7 weeks after inoculation of primary leukemic blasts from a t(1;19) ALL patient.