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New culprit discovered in T-cell acute lymphoblastic leukemia
Date:1/12/2012

potentially deadly disease," said lead author of the study Panagiotis Ntziachristos, PhD, of the Department of Pathology at NYU Langone. "The PRC2 genetic alteration amplifies the Notch oncogene's communication signals leading to T-ALL. Our study experiments uncover a specific epigenetic switch during the progression of the disease that can be further exploited for the development of targeted epigenetic therapies."

The study shows T-ALL as an epigenetic disease, regulated by a subtle equilibrium between oncogenes and tumor suppressors. Oncogenes like Notch can infiltrate the normal function of PRC2 in specific gene loci leading to cancerous cell transformation. Mutations in PRC2 assist oncogenes like Notch by altering their DNA gene expression.

"Our studies offer new therapy avenues for the treatment of T-ALL," said Dr. Aifantis. "The detection of new genetic alterations in T-ALL provides a new platform for selecting potential treatment strategies for the disease. Drugs that can target histone demethylases, enzymes that catalyze the H3K27me3 modification, could be used alone or in combination with Notch1 inhibitors for the treatment of the disease."


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Contact: Lauren Woods
lauren.woods@nyumc.org
212-404-3555
NYU Langone Medical Center / New York University School of Medicine
Source:Eurekalert

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