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BookmarkScienceDaily (Aug. 26, 2008) — Some cases of a form of leukemia known as pre–B cell acute lymphoblastic leukemia (pre–B-ALL) are caused by a genetic event that leads to the generation of a rogue chromosome known as the Philadelphia (Ph) chomosome, and individuals with Ph+ pre–B-ALL tend to have a poor outlook. As current treatments for Ph+ pre–B-ALL are not very effective, researchers are looking for new drugs to combat this disease.
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And now, David Fruman and colleagues, at the University of California, at Irvine, have generated data in mice and human cells that might provide insight into a new molecule to target in this clinical setting.
In the study, deletion of two genes responsible for generating a molecule known as PI3K prevented the development of disease in a mouse model of Ph+ pre–B-ALL. Consistent with an important role for PI3K in the development of Ph+ pre–B-ALL, a drug that inhibits PI3K as well as another signaling molecule known as mTOR suppressed the growth of mouse B-ALL and human Ph+ ALL leukemia cells in vitro.
The authors therefore suggest that targeting PI3K, either alone or together with mTOR, might prove beneficial to individuals with of Ph+ pre–B-ALL.
Journal reference:
- Kharas et al. Ablation of PI3K blocks BCR-ABL leukemogenesis in mice, and a dual PI3K/mTOR inhibitor prevents expansion of human BCR-ABL leukemia cells
. Journal of Clinical Investigation, 2008; DOI: 10.1172/JCI33337
