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Fig. 3 | Molecular Cancer

Fig. 3

From: Mutations in ALK signaling pathways conferring resistance to ALK inhibitor treatment lead to collateral vulnerabilities in neuroblastoma cells

Fig. 3

Continuous treatment with ALKis leads to de novo NRAS mutations and ALKi resistance in NBLW-R a Schematic to illustrate the induction of resistance to either lorlatinib or ceritinib in NBLW-R within 3 months. b and c 10-day GI50 of lorlatinib (0.073 μM) and ceritinib (0.109 μM) in NBLW-R parental line and 5-day GI50 of lorlatinib and ceritinib in lorlatinib-resistant NBLW-R (NBLW-R.LR (mean of L1, 2 and 3)) and ceritinib-resistant NBLW-R (NBLW-R.CR (mean of C1, 2 and 3)). NBLW-R.LR lorlatinib > 20 μM; NBLW-R.LR ceritinib > 900 nM; NBLW-R.CR lorlatinib 14 μM; NBLW-R.CR ceritinib > 1 μM. d and e Immunoblots and ALK immunoassay of cell lysates from NBLW-R versus NBLW-R.L2, and NBLW-R versus NBLW-R.C1 following treatment of cells with indicated ALKi for 1 hour, values represent mean ± SD, n = 3

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Molecular Cancer

ISSN: 1476-4598