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Clinical Cancer Research 14, 5314-5317, September 1, 2008. doi: 10.1158/1078-0432.CCR-07-4864
© 2008 American Association for Cancer Research

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Molecular Pathways

Oncogenic NOTCH1 Control of MYC and PI3K: Challenges and Opportunities for Anti-NOTCH1 Therapy in T-Cell Acute Lymphoblastic Leukemias and Lymphomas

Teresa Palomero1,2 and Adolfo Ferrando1,2,3

Authors' Affiliations: 1 Institute for Cancer Genetics-Columbia University, Departments of 2 Pathology, and 3 Pediatrics, Columbia University Medical Center, New York, New York

Requests for reprints: Adolfo Ferrando, Columbia University Medical Center, Pathology and Pediatrics, 1130 St. Nicholas Avenue, ICRC 505A, New York, NY 10032. Phone: 212-851-4611; Fax: 212-851-5256; E-mail: af2196{at}columbia.edu.

Abstract

The identification of activating mutations in NOTCH1 in the majority of T-cell acute lymphoblastic leukemias and lymphomas (T-ALL) has brought much interest in inhibiting NOTCH1 signaling as therapeutic target in this disease. Small-molecule inhibitors of the {gamma}-secretase complex, which mediates a critical proteolytic cleavage required for NOTCH1 activation, hold the promise of becoming an effective molecular therapy against relapsed and refractory T-ALL. Recent progress in the elucidation of the transcriptional regulatory networks downstream of oncogenic NOTCH1 has uncovered a central role of NOTCH1 signaling in promoting leukemic cell growth and revealed an intricate circuitry that connects NOTCH1 signaling with MYC and the PI3K-AKT signaling pathway. The identification of the downstream effector pathways controlled by NOTCH1 should pave the way for the rational design of anti-NOTCH1 therapies for the treatment of T-ALL.







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Copyright © 2008 by the American Association for Cancer Research.