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Activated ALK collaborates with MYCN in neuroblastoma pathogenesis.

Cancer cell | 2012

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.

Pubmed ID: 22439933 RIS Download

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Associated grants

  • Agency: NCI NIH HHS, United States
    Id: R01 CA104605-04
  • Agency: NCI NIH HHS, United States
    Id: K99 CA134743
  • Agency: NCI NIH HHS, United States
    Id: CA104605
  • Agency: NINDS NIH HHS, United States
    Id: R00 NS058608
  • Agency: NCI NIH HHS, United States
    Id: R01 CA104605
  • Agency: NCI NIH HHS, United States
    Id: K99CA134743
  • Agency: NCI NIH HHS, United States
    Id: R01 CA148688
  • Agency: NCI NIH HHS, United States
    Id: R00 CA134743

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