Dr. Tyler Jacks of MIT and the Howard Hughes Medical Institute, Karen Cichowski of Brigham and Women’s Hospital and Harvard Medical School, and their colleagues have discovered how neurofibromin, a key regulator of the ras oncogene, is, itself, regulated. This discovery has promising therapeutic implications for the treatment of neurofibromatosis type I (NF1), a common hereditary disease that results from mutations in the neurofibromin gene, as well as the ~30% of human tumors that have altered Ras activity.
The report is published in the February 15th issue of Genes & Development.
Neurofibromin is a tumor suppressor protein encoded by the Nf1 gene on human chromosome 17. Neurofibromin helps protect cells against cancer by suppressing Ras, a potent activator of cell growth and proliferation. People with mutations in the Nf1 gene develop neurofibromatosis type I (NF1), a neurological disorder that affects 1 in 3,500 people world-wide. NF1 patients develop benign tumors along their peripheral and optic nerves, as well as café-au-lait skin spots. NF1 is also associated with an increased risk of malignant neurological tumor development and childhood learning disabilities.
Michele McDonough | EurekAlert!
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