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Phosphoproteome and gene expression profiling of ALK inhibition in neuroblastoma cell lines reveals conserved oncogenic pathways.

Journal article
Authors Jimmy Van den Eynden
Ganesh Umapathy
Arghavan Ashouri
Diana Lizeth Cervantes-Madrid
Joanna Szydzik
Kristina Ruuth
Jan Koster
Erik Larsson
Jikui Guan
Ruth H. Palmer
Bengt Hallberg
Published in Science signaling
Volume 11
Issue 557
ISSN 1937-9145
Publication year 2018
Published at Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology
Language en
Links dx.doi.org/10.1126/scisignal.aar568...
www.ncbi.nlm.nih.gov/entrez/query.f...
Subject categories Biochemistry and Molecular Biology, Cell and Molecular Biology

Abstract

Anaplastic lymphoma kinase (ALK) is a tyrosine kinase receptor that is a clinical target of major interest in cancer. Mutations and rearrangements in ALK trigger the activation of the encoded receptor and its downstream signaling pathways. ALK mutations have been identified in both familial and sporadic neuroblastoma cases as well as in 30 to 40% of relapses, which makes ALK a bona fide target in neuroblastoma therapy. Tyrosine kinase inhibitors (TKIs) that target ALK are currently in clinical use for the treatment of patients with ALK-positive non-small cell lung cancer. However, monotherapy with the ALK inhibitor crizotinib has been less encouraging in neuroblastoma patients with ALK alterations, raising the question of whether combinatorial therapy would be more effective. In this study, we established both phosphoproteomic and gene expression profiles of ALK activity in neuroblastoma cells exposed to first- and third-generation ALK TKIs, to identify the underlying molecular mechanisms and identify relevant biomarkers, signaling networks, and new therapeutic targets. This analysis has unveiled various important leads for novel combinatorial treatment strategies for patients with neuroblastoma and an increased understanding of ALK signaling involved in this disease.

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