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CSHL scientists reveal mechanism behind 'oncogene addiction' in acute leukemia
Date:7/31/2011

and were soon eliminated altogether from all affected organs. This result confirmed the cancer cells' addiction to MLL-AF9, and provided a unique system to reveal the underlying genetic networks.

To further explore components of these networks, the team used RNA interference, or RNAi, an experimental tool to suppress gene function, which in prior work they had adapted for use in animal models. These recent advances now provide a means to switch off virtually any gene in an established cancer, and thereby enable the identification and evaluation of new potential drug targets. While the current study focused on the dramatic effects of suppressing Myb in AML, the approach validates a general method for understanding oncogene addiction in vivo that can be applied in other cancer types.

The RNA interference technique used in the experiments to block Myb is not applicable in humans, for a variety of still-daunting technical reasons. The hope is to find a small molecule that specifically targets the Myb protein, which can be the basis for a human drug. None has yet been developed, although the search is on.

But, says Lowe, "our results show that suppressing a single mediator of aberrant self-renewal can re-establish pre-existing cell-fate programs and eliminate aggressive AML. This suggests that pre-existing cell-fate programs remain hard-wired even in cancer cells, and raises our hope that agents that inhibit these programs will be less prone to resistance mechanisms that prevent targeted therapies from producing a lasting effect in other cancers."


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Contact: Peter Tarr
tarr@cshl.edu
516-367-8455
Cold Spring Harbor Laboratory
Source:Eurekalert

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