Researchers uncover gene related to acute leukemia

The product of the new gene created by inv(16) alters the activity of a protein called AML-1. AML-1 is a transcription factor--a protein that turns other genes on and off. It is what Hiebert calls a "master regulator" because it controls major cellular pathways that participate in the proliferation, survival, and differentiation of blood cells.

The importance of AML-1 is underscored by the fact that its gene is one of the most commonly mutated in human leukemia. Translocations disrupting the AML-1 gene are associated with both acute myeloid and acute lymphocytic leukemias. Whereas previous models held that inv(16) simply kept AML-1 from doing its job of turning genes on and off, Hiebert and colleagues now demonstrate that inv(16) joins with AML-1 to actively turn genes off, even those that AML-1 usually turns on.

It is likely that inv(16) recruits other proteins to help it force AML-1 to always turn genes off, Hiebert said, and possible treatments may hinge on the proteins that join it.

Based on other studies, one of these proteins might be an enzyme called histone deacetylase (HDAC). Hiebert and colleagues will now determine whether HDAC is part of the group working with inv(16).

"If HDAC is involved, then drugs that block its activity--HDAC inhibitors--might have an impact," Hiebert said. "We have these HDAC inhibitors, and they're being tried for other diseases. Our data suggest that they might provide effective treatment for AML."

In addition to determining what other proteins associate with inv(16), Hiebert is interested in defining the genes that are being turned off by the group. His preliminary data suggest that the complex is turning off tumor suppressor genes.

Tumor suppressors protect against malignancy by sending threatening cells down a suicide pathway.

"The model for how translocations cause leukemia is then rather simple: translocation products turn off multiple tumor suppressors, and from there it only takes one or two mo

Contact: Cynthia Manley/Matt Scanlan
Vanderbilt University Medical Center

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