Growth Response of Neurofibroma Explants to FGF-Basic Human Single–Plex Beads In -Vitro Cell-Culture Analysis

Neurofibromatosis type 1 (NF-1), also known as von Recklinghausen disease is caused by disorder of a single gene on chromosome 17 that usually restrains cell division. The NF1 gene is mapped to chromosome 17(17p21). Its protein product neurofibromin, negatively regulate oncogenic Ras, and thus regulate cell proliferation. Neurofibromas are heterogeneous and complex benign tumours, consisting of Schwann cells (NF-/-) and fibroblasts (NF1+/+, NF+/-) and other cell types including perineurial cells, mast cells, pericytes and endothelial cells. Human basic fibroblasts growth factor (b-FGF) is expressed by Schwann cells, macrophages and fibroblasts at the distal nerve stump, thereby preparing the local environment for axonal regeneration. Thus, b-FGF is apparently imperative in Schwann cell proliferation. This study was undertaken in order to elucidate any growth advantage conferred on benign neurofibroma explants following the introduction of b-FGF. Neurofibroma specimens from 22 patients were processed in accordance to the standard operating procedure of primary cell culture laboratory. Cell culture analysis suggests an increased in cell proliferation as positive response to b-FGF in cell phenotypes with NF1-/+. Conversely, cell phenotypes with NF1+/+ did not respond to the addition of (b-FGF) in terms of cell proliferation. Indeed, the cells with NF1+/+ phenotypes exhibited the features reminiscence of cell arrest and / senescence. It is hypothesize herein, that cells with haploinsufficient NF1 gene (NF1+/-) and those with null genotypes (NF1-/-) may be responsible for the proliferation of the neurofibroma in vivo and thus can be utilize as critical targets for therapeutic management of neurofibromatosis type-1.