Abstract

Comment on: Lubanska D and Porter LA. The atypical cell cycle regulator Spy1 suppresses differentiation of the neuroblastoma stem cell population. Oncoscience. 2014; 1: 336-348.

Highlights

  • Neuroblastoma (NB) is a highly malignant pediatric tumor derived from primordial neural crest cells that give rise to sympathetic neural ganglia and adrenal medulla

  • Spy1 has been shown to be upregulated in a number of human cancers including gliomas, where expression levels are increased in higher grade tumors, and amplification of the Spy1 encoding SPDYA gene and overexpression of the Spy1 effector CDK2 correlate with poor survival [3]

  • Spy1 overexpression in CD133- NB cells resulted in increased neurosphere formation and levels of CD133, c-MYC and Ki67, while Spy1 knockdown in CD133+ NB cells resulted in significant decline in the number of spheres formed and decreased levels of Ki67 and c-MYC

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Summary

Introduction

Neuroblastoma (NB) is a highly malignant pediatric tumor derived from primordial neural crest cells that give rise to sympathetic neural ganglia and adrenal medulla. Spy1 has been shown to be upregulated in a number of human cancers including gliomas, where expression levels are increased in higher grade tumors, and amplification of the Spy1 encoding SPDYA gene and overexpression of the Spy1 effector CDK2 correlate with poor survival [3]. In May issue of Oncoscience, Porter and colleagues characterize the roles of Spy1 in proliferation, differentiation and self-renewal of the peripheral nervous system tumor NB [4].

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