Ruth Palmer Lab
Ruth Palmer Lab
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Jikui Guan
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Novel activating SNRNP70-ALK fusion in congenital infant-type hemispheric glioma displays clinical response to lorlatinib: a case-report
Alk(Tango) reveals a role for Jeb/Alk signaling in the Drosophila heart
ALK F1174S mutation impairs ALK kinase activity in EML4-ALK variant 1 and sensitizes EML4-ALK variant 3 to crizotinib
ALK signaling primes the DNA damage response sensitizing ALK-driven neuroblastoma to therapeutic ATR inhibition
IGF1R Contributes to Cell Proliferation in ALK-Mutated Neuroblastoma with Preference for Activating the PI3K-AKT Signaling Pathway
Sustained Response to Entrectinib in an Infant With a Germline ALKAL2 Variant and Refractory Metastatic Neuroblastoma
Chromosome Imbalances in Neuroblastoma—Recent Molecular Insight into Chromosome 1p-deletion, 2p-gain, and 11q-deletion Identifies New Friends and Foes for the Future
Mapping the Phospho-dependent ALK Interactome to Identify Novel Components in ALK Signaling
BioID-Screening Identifies PEAK1 and SHP2 as Components of the ALK Proximitome in Neuroblastoma Cells
Extracellular domain shedding of the ALK receptor mediates neuroblastoma cell migration
Loss of RET Promotes Mesenchymal Identity in Neuroblastoma Cells
ALK ligand ALKAL2 potentiates MYCN-driven neuroblastoma in the absence of ALK mutation
Phosphoproteome and gene expression profiling of ALK inhibition in neuroblastoma cell lines reveals conserved oncogenic pathways
Clinical response of the novel activating ALK-I1171T mutation in neuroblastoma to the ALK inhibitor ceritinib
ALKALs are in vivo ligands for ALK family receptor tyrosine kinases in the neural crest and derived cells
MEK inhibitor trametinib does not prevent the growth of anaplastic lymphoma kinase (ALK)-addicted neuroblastomas
Novel Mechanisms of ALK Activation Revealed by Analysis of the Y1278S Neuroblastoma Mutation
The ALK inhibitor PF-06463922 is effective as a single agent in neuroblastoma driven by expression of ALK and MYCN
Brigatinib, an anaplastic lymphoma kinase inhibitor, abrogates activity and growth in ALK-positive neuroblastoma cells, Drosophila and mice
FAM150A and FAM150B are activating ligands for anaplastic lymphoma kinase
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