Unknown,Transcriptomics,Genomics,Proteomics

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Characterization of t(15;21) translocations in myeloid disorders


ABSTRACT: We report on two novel t(15;21) alterations [t(15;21)(q24;q22) and t(15;21)(q21;q22)], which led to concurrent disruption of RUNX1 and two translocation partner genes encoding for transcription factors (SIN3A, TCF12) Examination of four different patients with myeloid disorders. 2 out of 4 have been analyzed by means RNAseq

ORGANISM(S): Homo sapiens

SUBMITTER: Alberto L'Abbate 

PROVIDER: E-GEOD-71551 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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

L'Abbate Alberto A   Tolomeo Doron D   De Astis Francesca F   Lonoce Angelo A   Lo Cunsolo Crocifissa C   Mühlematter Dominique D   Schoumans Jacqueline J   Vandenberghe Peter P   Van Hoof Achilles A   Palumbo Orazio O   Carella Massimo M   Mazza Tommaso T   Storlazzi Clelia Tiziana CT  

Molecular cancer 20151216


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  ...[more]

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