Researchers identify mechanism, possible drug treatment for tumors in neurofi...(nvestigators discovered that neurofibrom...),Health
nvestigators discovered that neurofibromatosis type 1 is caused by loss-of-function mutations in a tumor suppressor gene, now known as NF1. People with the disease have the genetic makeup NF1+/-, meaning they have one functional copy of the gene and one non-functional or mutant copy.
Still, for many years the trigger for neurofibroma growth has been a mystery. Schwann cells, which form a protective sheath around nerve fibers, were a prime suspect. However, neurofibromas also contain nerve fibers themselves, connective tissue and mast cells, the latter of which circulate in the blood and contribute to inflammation.
Combined with previous findings, the new study suggests that the formation of plexiform neurofibromas requires two steps: complete loss of NF1 in Schwann cells (rendering them NF1-/-) and an interaction between NF1-/- Schwann cells and NF1+/- mast cells. While Schwann cells appear to be the primary tumor causing cell, mast cells appear to stimulate tumor growth by recruiting other cell types and blood vessels to the tumor.
"The mast cell inflammatory response appears to be co-opted by the tumor to enhance tumor growth," says Dr. Parada.
The researchers uncovered the role of mast cells in tumor growth through a series of technically challenging experiments. Previously, Dr. Parada had shown that mice with a targeted deletion of the NF1 gene in their Schwann cells and an NF1+/- genetic background develop plexiform neurofibromas, while mice with the same targeted deletion and an NF1+/+ genetic makeup do not develop the tumors. Drs. Parada and Clapp now show that in these non-tumorigenic mice, it is possible to induce plexiform neurofibromas by transplantation of NF1+/- bone marrow (which contains mast cells and other blood cells).
The researchers also examined the role of c-kit, a molecule that is expressed by mast cells and other cell types, and is known to become overactive in some kinds of cancer. When c-
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| Contact: Daniel Stimson stimsond@ninds.nih.gov 301-496-5751 NIH/National Institute of Neurological Disorders and Stroke Source:Eurekalert |
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