Mll rearrangements emerge during spontaneous apoptosis of clinical blood samples

Access through your institution Buy or subscribe The _MLL_ gene (11q23) is frequently involved in genetic aberrations in _de novo_ and therapy-related acute myeloid leukemia (t-AML). In

t-AML, _MLL_ translocations are detectable in up to 10% of all cases.1 Typically, these t-AML are characterized by a short latency period of up to 2 years and are associated with previous

topoisomerase inhibitor treatment.2 The initiating event is thought to be a breakage at the topoisomerase binding site within the breakpoint cluster region (bcr; exons 5–11) of the _MLL_

gene. In more than 70% of _MLL_-positive t-AML, the _MLL_ breakpoint is localized in the telomeric region of the bcr, whereas in _de novo_ AML, it is in the centromeric region.3 MLL

aberrations (deletions, insertions, translocations) can be induced in normal hematopoietic progenitors _in vitro_ by exposure to topoisomerase II inhibitors,4 and by retrospective analysis,

t-AML-associated _MLL_ aberrations have been backtracked up to a few months after topoisomerase II inhibitor therapy in clinical samples.5 As the incidence of t-AML may be up to 10% in

high-dose, myeloablative treatment schedules, it is of certain interest to identify patients who are at an increased risk to attract this complication. Recently, Ng _et al._6 investigated

clinical samples of children who were treated with topoisomerase inhibitors/anthracyclines by Southern blot and panhandle PCR and observed _MLL_ aberrations (_MLL_ breakage and illegitimate

recombination) in 7% (5/71) of the patients. This is a preview of subscription content, access via your institution ACCESS OPTIONS Access through your institution Subscribe to this journal

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REFERENCES * Schoch C, Schnittger S, Klaus M, Kern W, Hiddemann W, Haferlach T . AML with 11q23/MLL abnormalities as defined by the WHO classification: incidence, partner chromosomes, FAB

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Scholar  * Betti CJ, Villalobos MJ, Jiang Q, Cline E, Diaz MO, Loredo G _et al_. Cleavage of the MLL gene by activators of apoptosis is independent of topoisomerase II activity. _Leukemia_

2005; 19: 2289–2295. Article  CAS  Google Scholar  Download references AUTHOR INFORMATION Author notes * J Basecke and F Griesinger: This work was supported by the German Hector-Stiftung

(grant M18). AUTHORS AND AFFILIATIONS * Department of Hematology and Oncology, University of Goettingen, Goettingen, Germany J Basecke, K Karim, M Podleschny, A Becker, B Glass, L Trumper 

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this author inPubMed Google Scholar * B Glass View author publications You can also search for this author inPubMed Google Scholar * L Trumper View author publications You can also search

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ABOUT THIS ARTICLE CITE THIS ARTICLE Basecke, J., Karim, K., Podleschny, M. _et al._ MLL rearrangements emerge during spontaneous apoptosis of clinical blood samples. _Leukemia_ 20,

1193–1194 (2006). https://doi.org/10.1038/sj.leu.2404211 Download citation * Published: 06 April 2006 * Issue Date: 01 June 2006 * DOI: https://doi.org/10.1038/sj.leu.2404211 SHARE THIS

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