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Title 

Activated ALK collaborates with MYCN in neuroblastoma pathogenesis

Authors 

S ZhuJeong Soo LeeF GuoJ ShinA R Perez-AtaydeJ L KutokS J RodigD S NeubergD HelmanH FengR A StewartW WangR E GeorgeJ P KankiA T Look

Publisher 

Elsevier (Cell Press)

Issue Date 

2012

Citation 

Cancer Cell, vol. 21, no. 3, pp. 362-373

Abstract 

Amplification of the MYCN oncogene in childhood neuroblastoma is often accompanied by mutational activation of ALK (anaplastic lymphoma kinase), suggesting their pathogenic cooperation. We generated a transgenic zebrafish model of neuroblastoma in which MYCN-induced tumors arise from a subpopulation of neuroblasts that migrate into the adrenal medulla analog following organogenesis. Coexpression of activated ALK with MYCN in this model triples the disease penetrance and markedly accelerates tumor onset. MYCN overexpression induces adrenal sympathetic neuroblast hyperplasia, blocks chromaffin cell differentiation, and ultimately triggers a developmentally-timed apoptotic response in the hyperplastic sympathoadrenal cells. Coexpression of activated ALK with MYCN provides prosurvival signals that block this apoptotic response and allow continued expansion and oncogenic transformation of hyperplastic neuroblasts, thus promoting progression to neuroblastoma.

ISSN 

1535-6108

Link 

http://dx.doi.org/10.1016/j.ccr.2012.02.010

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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