Abstract
Neuroblastoma (NBL) is one of the most common solid tumors and around 15% of cancer mortality in children. Amplification of the N-Myc proto-oncogene is strongly correlated with advanced disease and poor clinical outcome in NBL. Recent studies described that ubiquitin-specific protease 7 (USP7; also known as HAUSP) interacts with N-Myc, induces deubiquitination and subsequent stabilization of N-Myc that in-turn potentiates N-Myc function, and treatment with the HAUSP inhibitor (P22077) blocked such effects.
Highlights
Neuroblastoma (NBL), the most common solid tumor of childhood, is originated from the neural crest cells of the developing sympathetic nervous system [1]
Like C-Myc, N-Myc is stabilized by activation of phosphatidylinositol 3-kinase (PI3K) [24], and inhibition of PI3K and mTOR leading to reduced secretion of VEGF and decreased levels of N-Myc protein [25] [26] [27]
Chanthery Y.H. et al demonstrated that a clinical PI3K/mTOR inhibitor, NVP-BEZ235, decreased angiogenesis and improved survival on N-Myc dependent mechanism in both primary human and transgenic mouse models for N-Myc-driven neuroblastoma, suggesting that NVP-BEZ235 should be tested in children with high-risk, N-Myc-amplified neuroblastoma [28]
Summary
Neuroblastoma (NBL), the most common solid tumor of childhood, is originated from the neural crest cells of the developing sympathetic nervous system [1]. Neuroblastoma (NBL) is one of the most common solid tumors and around 15% of cancer mortality in children. Amplification of the N-Myc proto-oncogene is strongly correlated with advanced disease and poor clinical outcome in NBL.
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