Abstract
Since the initial discovery of the NPM-ALK fusion gene in patients suffering from anaplastic large cell lymphoma, ALK rearrangements have been described in a variety of other tumor entities origination from various cell types. Non-small cell lung cancer, inflammatory myofibroblastic tumors, squamous cell carcinoma and – as most recently discovered – neuroblastoma are associated with gain-of-function mutations of the receptor tyrosine kinase ALK. Besides reviewing the pathobiology of aberrant ALK signalling, I will demonstrate that ALK is activated in a rare myeloproliferative disorder in children.
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