ALK pERKs up MYCN in neuroblastoma

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Item Type:	Article
Title:	ALK pERKs up MYCN in neuroblastoma
Creators Name:	Lindner, S., Henssen, A., Astrahantseff, K. and Schulte, J.H.
Abstract:	The gene expressing the receptor tyrosine kinase anaplastic lymphoma kinase (ALK) is mutated and aberrantly expressed in several cancers. The clinical efficacy of the ALK inhibitor, crizotinib, lags behind expectations for treating MYCN-amplified, ALK-mutant neuroblastoma, a deadly childhood cancer. In this issue of Science Signaling, Umapathy et al. identify the kinase extracellular signal-regulated kinase 5 (ERK5) as a central mediator that enables ALK to boost MYCN expression, and they show that inhibiting ERK5 in concert with ALK reduced neuroblastoma cell viability in vitro and in xenograft tumor models. This report has important clinical implications for the treatment of patients with neuroblastoma or other tumors that overexpress MYC(N) and harbor ALK mutations, such as non-small-cell lung cancer.
Keywords:	Anaplastic Lymphoma Kinase, Mitogen-Activated Protein Kinase 7, Mutation, N-Myc Proto-Oncogene Protein, Neoplastic Gene Expression Regulation, Neuroblastoma, Nuclear Proteins, Oncogene Proteins, Receptor Protein-Tyrosine Kinases, Signal Transduction
Source:	Science Signaling
ISSN:	1945-0877
Publisher:	American Association for the Advancement of Science
Volume:	7
Number:	349
Page Range:	pe27
Date:	28 October 2014
Official Publication:	https://doi.org/10.1126/scisignal.2005940
PubMed:	View item in PubMed

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