Effect of ALK kinase inhibitor, ceritinib, on the gene expression profile of SUDHL-1 cell line

Tyrosine kinase receptor anaplastic lymphoma kinase (ALK) is physiologically expressed during embryogenesis. However, chromosomal rearrangements, especially translocations, cause expression of pathogenic ALK fusion proteins that drive tumor formation and maintenance. For instance, the translocation between chromosomes 2 and 5 (t(2;5)) fuses the nucleophosmin 1 (NPM1) gene with ALK, leading to anaplastic large cell lymphoma (ALCL). The constitutive active NPM1::ALK tyrosine kinase drives tumor transformation and tumor cells inevitably depend on ALK kinase activity for survival. For this reason, ALK kinase inhibitors showed great success in treating ALK-positive ALCL. Here, we explored gene expression changes induced by ceritinib, second generation ALK inhibitor, on a representative cell line, SUDHL-1.