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Wednesday, 12 December 2012

Researchers identify therapeutic targets in neurofibromatosis

In the latest issue of the Journal of Clinical Investigation, three independent groups of researchers report that MAPK hyperactivation is a critical mediator of disease pathogenesis in neurofibromatosis. Taken together, these studies demonstrate that hyperactivation of MEK and ERK underlies NF1-associated disorders and provide a rationale for testing MEK and ERK inhibitors in neurofibromatosis patients. Read more here.

Study mentioned: Staser K, et al. Normal hematopoiesis and neurofibromin-deficient myeloproliferative disease require Erk. J Clin Invest. 2012 Dec 10. [Epub ahead of print] PMID: 23221339

Study mentioned: Chang T, et al. Sustained MEK inhibition abrogates myeloproliferative disease in Nf1 mutant mice. J Clin Invest. 2012 Dec 10. [Epub ahead of print] PMID: 23221337

Study mentioned: Jessen WJ, et al. MEK inhibition exhibits efficacy in human and mouse neurofibromatosis tumors. J Clin Invest. 2012 Dec 10. [Epub ahead of print] PMID: 23221341

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