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Although NF1 gene inactivation and loss of neurofibromin expression characterize the majority of MPNST cases [12], biallelic NF1 loss is insufficient for malignant transformation, and mutations in TP53, CDKN2A, EGFR, and SUZ12 have all been reported as secondary cooperating mutations facilitating malignant progression [13,14,15,16,17]

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