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Penn study on silencing of tumor suppressor gene suggests new target for lymphoma
Date:8/9/2011

The silencing affects gene promoter regions within DNA, in two ways: methylation of the DNA and modification of histones and other proteins. The methylation is mediated by enzymes called DNA methyltransferases (DNMTs). Histones are modified by histone deacetylases.

Silencing of the IL-2Rγ promoter via methylation is induced in malignant T cells by NPM-ALK by activating another protein called STAT3. STAT3 increases expression of one of the DNMTs and facilitates attachment of this and other DNMTs to the IL-2Rγ gene promoter. Strikingly, when IL-2Rγ is expressed, NPM-ALK disappears from the cancerous T cells, and they eventually die. These results demonstrate that NPM-ALK induces epigenetic silencing of the IL-2Rγ gene and that IL-2Rγ acts as a tumor suppressor by reciprocally inhibiting expression of NPM-ALK.

"Epigenetic silencing is not an independent event, and genetics in the form of the aberrant fusion protein drives an epigenetic change," says Wasik. "Is this phenomenon generalizable? Can we overcome the tumor suppressor gene silencing using inhibitors of DNA methylation, which are already approved to treat some forms of blood cancer, to inhibit the expression of NPM-ALK and possibly other cancer-causing proteins in patients?"

This approach could potentially complement inhibition of fusion protein activity as is routinely done for BCR-ABL in chronic myelogeneous leukemia and experimentally for ALK in lung carcinoma, lymphoma and other malignancies expressing ALK.


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Contact: Karen Kreeger
karen.kreeger@uphs.upenn.edu
215-349-5658
University of Pennsylvania School of Medicine
Source:Eurekalert

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