1. Additional file 1 of Mutations in ALK signaling pathways conferring resistance to ALK inhibitor treatment lead to collateral vulnerabilities in neuroblastoma cells
- Author
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Berlak, Mareike, Tucker, Elizabeth, Dorel, Mathurin, Winkler, Annika, McGearey, Aleixandria, Rodriguez-Fos, Elias, da Costa, Barbara Martins, Barker, Karen, Fyle, Elicia, Calton, Elizabeth, Eising, Selma, Ober, Kim, Hughes, Deborah, Koutroumanidou, Eleni, Carter, Paul, Stankunaite, Reda, Proszek, Paula, Jain, Neha, Rosswog, Carolina, Dorado-Garcia, Heathcliff, Molenaar, Jan Jasper, Hubank, Mike, Barone, Giuseppe, Anderson, John, Lang, Peter, Deubzer, Hedwig Elisabeth, Künkele, Annette, Fischer, Matthias, Eggert, Angelika, Kloft, Charlotte, Henssen, Anton George, Boettcher, Michael, Hertwig, Falk, Blüthgen, Nils, Chesler, Louis, and Schulte, Johannes Hubertus
- Abstract
Additional file 1: Figure S1: ALK inhibitor treatment of ALK-mutated neuroblastoma cell lines for optimized screeningconditions (related to Figure 1). Figure S2: Quality control of CRISPR/Cas9 knockout screen (related to Figure 1). Figure S3: Lorlatinib- and Ceritinib- resistant NBLW-R neuroblastoma cells grow as aggressive tumors in the kidney capsule of nude mice (related to Figure 3). Figure S4: Tetracycline induced NRASQ61K expression (related to Figure 4). Figure S5: Computational modeling of ALK downstream signaling using STASNet (related to Figure 6). Figure S6: MEK inhibitor treatment of ectopic NRASQ61K expression models (related to Figure 7). Figure S7: High-throughput drug screening of LAN-5 and LAN-5 NF1 KO#2 clone (related to Figure 7). Table S1. Full clinical data on neuroblastoma patients.
- Published
- 2022
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