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Chromosomal Rearrangements Leading to MLL Gene Fusions: Clinical and Biological Aspects

¹ Genetics Branch, Center for Cancer Research, National Cancer Institute, NIH and ² Department of Pediatrics, Uniformed Services University of the Health Sciences, Bethesda, Maryland

Requests for reprints: Peter D. Aplan, Genetics Branch, National Cancer Institute, NIH, National Naval Medical Center, Building 8 Room 5101, 8901 Rockville Pike, Bethesda, MD 20889. Phone: 301-496-0901; Fax: 301-496-0047; E-mail: aplanp{at}mail.nih.gov.

Key Words: MLL • chromosomal translocation • infant leukemia • DNA topoisomerase II • nonhomologous end-joining • homeobox

Rearrangements of the MLL gene located at 11q23 are common chromosomal abnormalities associated with acute leukemia, especially infant and therapy-related leukemias. A variety of chimeric oncoproteins resulting from these rearrangements has been described; all of these include the NH₂-terminal region of MLL implicated in protein-protein interactions and transcriptional repression. Although the molecular basis for the oncogenic activity of MLL chimeric proteins is incompletely understood, it seems to be derived, at least in part, through activation of clustered homeobox (HOX) genes. Here, we survey MLL gene rearrangements that are associated with acute leukemia and discuss molecular pathways leading to these rearrangements. [Cancer Res 2008;68(24):10024–7]

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