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NYU Langone scientists find key pathway implicated in progression of childhood cancer
Date:9/13/2010

lf of T-ALL patients and current estimates suggest that the gene's regulatory influence might be implicated in nearly 90 percent of cases.

In the new study, the researchers found that Notch targeted a protein called NF-kB (short for nuclear factor kB), an important transcription factor that regulates genes involved in cell division and the immune response. Transcription factors bind to the DNA of genes, thereby activating them. Previous studies had suggested that cross talk between Notch and NF-kB occurred, but the new study reveals the molecular characters involved in the cross talk, and shows that blocking NF-kB eliminated leukemic cells carrying activating Notch mutations.

The researchers then found that the way that Notch1 can induce NF-kB signaling is by suppressing the expression of an enzyme called CYLD, a negative regulator of the NF-kB pathway. In other words, the enzyme normally shuts down the pathway of genes regulated by NF-kB.

"Presently, drugs that inhibit NF-kB are already in development and some of them are being tested in humans for inflammatory diseases," said Dr. Aifantis, "If used for patients with T-ALL leukemia, such drugs could be used alone or in combination with more established protocols like chemotherapy and radiation."


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Contact: Dorie Klissas
Dorie.Klissas@nyumc.org
212-404-3525
NYU Langone Medical Center / New York University School of Medicine
Source:Eurekalert

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