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Ectopic expression of LMO2 occurs in approximately 45% of T-lineage acute lymphoblastic leukemias (T-ALL), sometimes in association with chromosomal translocations. Recently, a lymphoproliferative disorder developed in two participants in a gene therapy trial due to LMO2 activation via integration of the retroviral vector. To investigate these regulatory disruptions, we analyzed the promoter region and identified a tissue-specific repressor. The fragment containing this element could also produce tissue-specific suppression of transcription from the SV40 promoter. This suppression involves histone acetylation which can be relieved with Trichostatin A (TSA). The negative element is in a region consistently removed from LMO2 in the known chromosomal translocations.

Original publication

DOI

10.1016/j.leukres.2004.05.013

Type

Journal article

Journal

Leuk Res

Publication Date

01/2005

Volume

29

Pages

89 - 97

Keywords

Adaptor Proteins, Signal Transducing, Base Sequence, Consensus Sequence, DNA-Binding Proteins, Histone Deacetylases, Humans, Hydroxamic Acids, Jurkat Cells, K562 Cells, LIM Domain Proteins, Leukemia, Metalloproteins, Molecular Sequence Data, Organ Specificity, Proto-Oncogene Proteins, Proto-Oncogenes, Regulatory Sequences, Nucleic Acid, Transcription, Genetic, Transfection