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The genetic mechanisms involved in the transformation from a benign neurofibroma to a malignant sarcoma in patients with neurofibromatosis-type-1- (NF1-)associated or sporadic malignant peripheral nerve sheath tumors (MPNSTs) remain unclear. It is hypothesized that many genetic changes are involved in transformation. Recently, it has been shown that both  phosphatase and tensin homolog  ( PTEN ) and  epidermal growth factor receptor  ( EGFR ) play important roles in the initiation of peripheral nerve sheath tumors (PNSTs). In human MPNSTs,  PTEN  expression is often reduced, while  EGFR  expression is often induced. We tested if these two genes cooperate in the evolution of PNSTs. Transgenic mice were generated carrying conditional floxed alleles of  Pten , and  EGFR  was expressed under the control of the 2′,3′- cyclic nucleotide  3′ phosphodiesterase  ( Cnp ) promoter and a  desert hedgehog  ( Dhh ) regulatory element driving Cre recombinase transgenic mice ( Dhh -Cre). Complete loss of  Pten  and  EGFR  overexpression in Schwann cells led to the development of high-grade PNSTs.  In vitro  experiments using immortalized human Schwann cells demonstrated that loss of  PTEN  and overexpression of  EGFR  cooperate to increase cellular proliferation and anchorage-independent colony formation. This mouse model can rapidly recapitulate PNST onset and progression to high-grade PNSTs, as seen in sporadic MPNST patients.

Conditional Inactivation ofPtenwithEGFROverexpression in Schwann Cells Models Sporadic MPNST