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Through a combined approach integrating RNA-Seq, SNP-array, FISH and PCR techniques, we identified two novel t(15;21) translocations leading to the inactivation of  RUNX1  and its partners  SIN3A  and  TCF12 . One is a complex t(15;21)(q24;q22), with both breakpoints mapped at the nucleotide level, joining  RUNX1  to  SIN3A  and  UBL7-AS1  in a patient with myelodysplasia. The other is a recurrent t(15;21)(q21;q22), juxtaposing  RUNX1  and  TCF12,  with an opposite transcriptional orientation, in three myeloid leukemia cases. Since our transcriptome analysis indicated a significant number of differentially expressed genes associated with both translocations, we speculate an important pathogenetic role for these alterations involving  RUNX1 .   Electronic supplementary material  The online version of this article (doi:10.1186/s12943-015-0484-0) contains supplementary material, which is available to authorized users.

molecular cancer

t(15;21) translocations leading to the concurrent downregulation of RUNX1 and its transcription factor partner genes SIN3A and TCF12 in myeloid disorders