Journal
SEMINARS IN CANCER BIOLOGY
Volume 15, Issue 3, Pages 175-188Publisher
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.semcancer.2005.01.007
Keywords
leukaemia; chromosomal translocations; oncogenes; fusion genes; therapy
Categories
Ask authors/readers for more resources
The marked association of abnormalities of chromosome I I long arm, band q23, with human leukaemia led to the identification of the 11 q23 gene called MLL (or HTRX, HRX, TRX1, ALL-1). MLL can become fused with one of a remarkable panoply of genes from other chromosome locations in individual leukaemias, leading to either acute myeloid or lymphoid tumours (hence the name MLL for mixed lineage leukaemia). The unusual finding that a single protein could be involved in both myeloid and lymphoid malignancies and that the truncated protein could do so as a fusion with very disparate partners has prompted studies to define the molecular role of MLL-fusions in leukaemogenesis and to the development of MLL-controlled mouse models of leukaemogenesis. These studies have defined MLL-fusion proteins as regulators of gene expression, controlling such elements as HOX genes, and have indicated a variety of mechanisms by which MLL-fusion proteins contribute to leukaemogenesis. (c) 2005 Elsevier Ltd. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available