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lüll Oncogenic NOTCH1 control of MYC and PI3K: challenges and opportunities for anti-NOTCH1 therapy in T-cell acute lymphoblastic leukemias and lymphomas Palomero T; Ferrando AClin Cancer Res 2008[Sep]; 14 (17): 5314-7The 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.|Drug Delivery Systems[MESH]|Gene Expression Regulation, Neoplastic[MESH]|Humans[MESH]|Leukemia-Lymphoma, Adult T-Cell/*genetics[MESH]|Lymphoma/*genetics[MESH]|Models, Biological[MESH]|Mutation[MESH]|Phosphatidylinositol 3-Kinases/*metabolism[MESH]|Proto-Oncogene Proteins c-myc/*metabolism[MESH]|Receptor, Notch1/antagonists & inhibitors/*genetics[MESH]|Signal Transduction/genetics[MESH] |