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Inhibition of ALK signaling for cancer therapy Mosse YP; Wood A; Maris JMClin Cancer Res 2009[Sep]; 15 (18): 5609-14Paradigm shifting advances in cancer can occur after discovering the key oncogenic drivers of the malignant process, understanding their detailed molecular mechanisms, and exploiting this transdisciplinary knowledge therapeutically. A variety of human malignancies have anaplastic lymphoma kinase (ALK) translocations, amplifications, or oncogenic mutations, including anaplastic large cell lymphoma, inflammatory myofibroblastic tumors, non-small cell lung cancer, and neuroblastoma. This finding has focused intense interest in inhibiting ALK signaling as an effective molecular therapy against diseases with ALK-driven pathways. Recent progress in the elucidation of the major canonical signaling pathways postulated to be activated by NPM-ALK signaling has provided insight into which pathways may present a rational therapeutic approach. The identification of the downstream effector pathways controlled by ALK should pave the way for the rational design of ALK-inhibition therapies for the treatment of a subset of human cancers that harbor ALK aberrations.|*Signal Transduction[MESH]|Anaplastic Lymphoma Kinase[MESH]|Humans[MESH]|Neoplasms/*enzymology/metabolism/*therapy[MESH]|Protein-Tyrosine Kinases/*antagonists & inhibitors/genetics/*metabolism[MESH]|Receptor Protein-Tyrosine Kinases[MESH] |
