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Background   SET-NUP214  fusion resulting from a recurrent cryptic deletion, del(9)(q34.11q34.13) has recently been described in T-cell acute lymphoblastic leukemia (T-ALL) and in one case of acute myeloid leukemia (AML). The fusion protein appears to promote elevated expression of  HOXA  cluster genes in T-ALL and may contribute to the pathogenesis of the disease. We screened a panel of ALL and AML cell lines for  SET-NUP214  expression to find model systems that might help to elucidate the cellular function of this fusion gene.    Results  Of 141 human leukemia/lymphoma cell lines tested, only the T-ALL cell line LOUCY and the AML cell line MEGAL expressed the  SET(TAF- Iβ)- NUP214  fusion gene transcript. RT-PCR analysis specifically recognizing the alternative first exons of the two  TAF- I isoforms revealed that the cell lines also expressed  TAF- Iα- NUP214  mRNA. Results of fluorescence in situ hybridization (FISH) and array-based copy number analysis were both consistent with del(9)(q34.11q34.13) as described. Quantitative genomic PCR also confirmed loss of genomic material between  SET  and  NUP214  in both cell lines. Genomic sequencing localized the breakpoints of the  SET  gene to regions downstream of the stop codon and to  NUP214  intron 17/18 in both LOUCY and MEGAL cells. Both cell lines expressed the 140 kDa SET-NUP214 fusion protein.    Conclusion  Cell lines LOUCY and MEGAL express the recently described  SET-NUP214  fusion gene. Of special note is that the formation of the  SET  exon 7/ NUP214  exon 18 gene transcript requires alternative splicing as the  SET  breakpoint is located downstream of the stop codon in exon 8. The cell lines are promising model systems for  SET-NUP214  studies and should facilitate investigating cellular functions of the the SET-NUP214 protein.

SET-NUP214 fusion in acute myeloid leukemia- and T-cell acute lymphoblastic leukemia-derived cell lines