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Expression of ‘drugable’ tyrosine kinase receptors in malignant peripheral nerve sheath tumour: potential molecular therapeutic targets for a chemoresistant cancer

Malignant peripheral nerve sheath tumors (MPNSTs) are aggressive malignancies developing sporadically (~50%) or in neurofibromatosis type-1 contexts (NF1; ~50%).1. Surgical resection is the only curative intervention for these highly chemoresistant tumors 1. Unfortunately many MPNSTs progress during treatment; inoperable disease is generally lethal, 2, 3 mandating improved molecular-targeted MPNST therapeutic strategies. 
 
While Nf1 protein loss with enhanced RAS pathway signaling activation may contribute to initial transformation, 1,2 additional genetic/epigenetic molecular aberrations are required for tumorigenesis and MPNST progression.6 Tyrosine kinase receptor (TKR) over-expression and deregulated signaling occur in many malignancies, inducing activation of signaling pathways mediating tumor progression.3 Several of these receptors (e.g. EGFR, HER2, KIT) have been successfully utilized as anti-cancer therapeutic targets, providing strong rationales for blocking cancer-type specific deregulated TKRs. Several TKRs may be over-expressed in MPNST.4 However, due to tumor rarity, such insights are generally made using small MPNST sample cohorts. With an overarching goal of developing MPNST clinical trials using molecularly-targeted therapies, we evaluated protein expression levels of multiple TKRs in a large MPNST cohort assembled on a previously described tissue microarray (TMA).2