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A BACH2-BCL2L1 fusion gene resulting from a t(6;20)(q15;q11.2) chromosomal translocation in the lymphoma cell line BLUE-1

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http://pubman.mpdl.mpg.de/cone/persons/resource/persons50605

Turkmen,  S.
Dept. of Human Molecular Genetics (Head: Hans-Hilger Ropers), Max Planck Institute for Molecular Genetics, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons50386

Klopocki,  E.
Research Group Development & Disease (Head: Stefan Mundlos), Max Planck Institute for Molecular Genetics, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons50488

Reinhardt,  R.
High Throughput Technologies, Max Planck Institute for Molecular Genetics, Max Planck Society;

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Citation

Turkmen, S., Riehn, M., Klopocki, E., Molkentin, M., Reinhardt, R., & Burmeister, T. (2011). A BACH2-BCL2L1 fusion gene resulting from a t(6;20)(q15;q11.2) chromosomal translocation in the lymphoma cell line BLUE-1. Genes Chromosomes Cancer, 50(6), 389-96. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/21412927 http://onlinelibrary.wiley.com/store/10.1002/gcc.20863/asset/20863_ftp.pdf?v=1&t=gyzw8vx9&s=d7a278cbc50ee7f48bdf3f0dd1c5fcba6b1e3e4e.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0010-77FA-6
Abstract
Abnormalities of the long arm of chromosome 6 are a common feature in various B-cell malignancies. In most cases, the genes involved have not yet been clearly identified. We have molecularly characterized the recently established Burkitt lymphoma cell line BLUE-1 that carries a t(6;20)(q15;q11.2) rearrangement in addition to the typical t(8;14) with MYC-IGH fusion. To identify the gene loci involved on both chromosomes we applied a sequential BAC clone mapping strategy. By using RT-PCR we were finally able to detect a chimeric mRNA transcript showing a fusion of the first (non-coding) exon of BACH2 (BTB and CNC homology 1, basic leucine zipper transcription factor 2) on 6q15 to the second exon of BCL2L1 (BCL-X) on 20q11. Various fusion transcripts were detected for different BCL2L1 (BCL-XL) isoforms. The fusion ultimately results in strong expression of the BCL2L1 (BCL-XL) anti-apoptosis protein, as demonstrated by immunoblotting. This is the first report that shows the involvement of both BCL2L1 and the transcription factor BACH2 in a chromosomal rearrangement. It points to BACH2 as a possibly important target in lymphomas with 6q aberrations, although other genes on 6q are probably also involved in these cases. Moreover, it suggests that members of the BCL2 anti-apoptosis gene family other than BCL2 itself might also be involved in lymphoma.