Oncogenic mutations of ALK kinase in neuroblastoma

By Yuyan Chen, J. Takita, Y. L. Choi, Motohiro Kato, M. Ohira, M. Sanada, Lili Wang, M. Soda, A. Kikuchi, T. Igarashi and 4 more. Nature, 2008

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Drug Resistance in Cancer: An Overview (2014, background): “Other genetic alterations such as chromosomal rearrangements and mutations in anaplastic lymphoma kinase are seen in anaplastic large-cell lymphoma [14,23].”
PI3K/AKT/mTOR signaling transduction pathway and targeted therapies in cancer (2023, background): “Alterations in epidermal growth factor receptor (EGFR) [36, 37], fibroblast growth factor receptor (FGFR) [38, 39], platelet-derived growth factor receptor (PDGFR) [40, 41], vascular endothelial growth factor receptor (VEGFR) [42, 43], hepatocyte growth factor (HGF) [44, 45], leukocyte receptor tyro”
Unique Clinicopathologic Features Characterize ALK-rearranged Lung Adenocarcinoma in the Western Population (2009, background): “Since their discovery in ALCL, ALK rearrangements or mutations have been identified in inflammatory myofibroblastic tumors, a subset of diffuse large B-cell lymphomas (42–45), and a subset of neuroblastomas (46, 47).”
Neuroblastoma and MYCN (2013, background): “Gain of function mutations in the receptor tyrosine kinase ALK (chromosome 2p23) occur in 50% of familial neuroblastoma cases, and 7% of sporadic neuroblastoma cases (Chen et al. 2008; George et al. 2008; Janoueix-Lerosey et al. 2008; Mossé et al. 2008; Molenaaret al. 2012b).”