The 'promiscuous' E2A gene, at 19p13.3, is fused with two different molecul
ar partners, PBX1 and HLF, following two chromosome translocations recurren
t in childhood pre-B ALL. We have identified a novel gene, FB1, by Virtue o
f its fusion with E2A and by a combination of molecular techniques. FB1 was
localized on 19q13.4, suggesting that the novel chimera originated by a cr
yptic rearrangement of chromosome 19. Two FB1 transcripts, of 1.2 kb and 1.
1 kb, are differentially expressed at low level in a variety of human tissu
es, including hemopoietic cell lines from different lineages. Accordingly,
FB1 cDNA displays high homology with a number of cDNA clones from different
human tissues. High homology was found also with cDNA clones from mouse an
d rat, suggesting that the sequence might be conserved at least among mamma
ls. The function of the putative FB1 protein, however, is currently unknown
as database sequence comparisons have failed to reveal strong homology wit
h known proteins. The E2A/FB1 fusion appears to be a recurrent feature of p
re-B ALLs, suggesting that it might have a role in the development and/or p
rogression of leukemogenesis.