t(10;11)-acute leukemias with MLL-AF10 and MLL-AB11 chimeric transcripts: Specific expression patterns of AB11 gene in leukemia and solid tumor cell lines

The recurrent translocation t(10;11) is associated with acute myeloid leuke mia (AML). The AF10 gene on chromosome 10 at band p12 and MLL at 11q23 fuse in the t(10;11)(p12;q23). Recently, we have identified ABII as a new partn er gene for MLL in an AML patient with a t(10;11)(p11.2;q23). The ABII is a human homologue of the mouse Abi-interactor I (Abil), encoding an Abl-bind ing protein. The ABI I protein exhibits sequence similarity to homeotic gen es, and contains several polyproline stretches and a src homology 3 (SH3) d omain. To clarify the clinical features of t(10;11)-leukemias, we investiga ted 6 samples from acute leukemia patients with t(10;11) and MLL rearrangem ent and detected MLL-AF10 chimeric transcripts in 5 samples and MLL-ABII in one. The patient with MLL-ABII chimeric transcript is the second case desc ribed, thus confirming that the fusion of the MLL and ABII genes is a recur ring abnormality. Both of the patients with MLL-ABII chimeric transcript ar e surviving, suggesting that these patients have a better prognosis than th e patients with MLL-AF10. To investigate the roles of AF10 and ABII further , we examined the expression of these genes in various cell lines and fresh tumor samples using the reverse transcriptase-polymerase chain reaction me thod. Although AF10 was expressed in almost all cell lines similarly, the e xpression patterns of ABI I were different between leukemia and solid tumor cell lines, suggesting the distinctive role of each isoform of ABI I in th ese cell lines. We also determined the complete mouse Abi I sequence and fo und that the sequence matched with human ABII better than the originally re ported Abil sequence. Further functional analysis of the MLL-AF10 and MLL-A BII fusion proteins will provide new insights into the leukemogenesis of t( 10; I I)-AML. (C) 2001 Wiley-Liss, Inc.