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Neurofibromatosis type 1 (NF1) is a common inherited cancer predisposition syndrome. The  NF1  gene product, neurofibromin, is hypothesized to function as a tumor suppressor and nearly all NF1 patients develop benign peripheral nerve tumors. These neurofibromas presumably arise from  NF1  inactivation in S100 +  Schwann cells, but there is no formal proof for this mechanism. We demonstrate that fibroblasts isolated from neurofibromas carried at least one normal  NF1  allele and expressed both  NF1  mRNA and protein, whereas   the S100 +  cells typically lacked the  NF1  transcript. Our findings further indicate that additional molecular events aside from  NF1  inactivation in Schwann cells and/or other neural crest derivatives contribute to neurofibroma formation.

Genetic and cellular defects contributing to benign tumor formation in neurofibromatosis type 1