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Significance Our findings identify a type of oncogene addiction process driven by a lipid that controls prosurvival effector protein secretion. The crosstalk between functionally redundant phosphatidylinositol (PI) 4-kinases maintains addiction and can be targeted with small molecule kinase inhibitors that might be applicable to a genetically defined subset of cancers for which there are no effective targeted therapies.

Addiction to Golgi-resident PI4P synthesis in chromosome 1q21.3–amplified lung adenocarcinoma cells