Researchers have found that a particularly aggressive type of blood cancer called mixed lineage leukemia (MLL) requires the normal version of a translocated gene (the MLL gene) to survive. The findings were featured as the cover article in the February 17, 2010 issue of Cancer Cell. MLL develops when a piece of chromosome 11 breaks at the normal MLL gene. The chromosome piece attaches to another broken chromosome, resulting in the joining of the MLL gene to a now-neighboring gene on the other chromosome. The joined genes code for a new “fusion protein” that eventually causes uncontrolled growth of blood cells. The researchers found that the runaway growth triggered by the fusion protein is blocked when the gene for the normal MLL protein is deleted from leukemia cells. The results showed that the normal protein is required for fusion-protein generation of the leukemia and for the maintenance of transformed cells. This suggested that the normal protein cooperates with the fusion protein in the generation of the leukemia. "This research not only uncovers the crucial role of a normal protein key to the development of MLL, but also how the cancer cells stay alive in the first place," said Dr. Xianxin Hua, from the University of Pennsylvania, senior author of the article. The results point to the normal MLL gene as a potential target for new therapies, possibly through repression of the gene in leukemia stem cells. [Press release] [Cancer Cell abstract]
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