Fig. 1: CRISPR screens identify genes involved in resistance to AKT and PI3Kβ inhibitors in PTEN-deficient breast cancer cell lines. | Oncogene

Fig. 1: CRISPR screens identify genes involved in resistance to AKT and PI3Kβ inhibitors in PTEN-deficient breast cancer cell lines.

From: AKT-mTORC1 reactivation is the dominant resistance driver for PI3Kβ/AKT inhibitors in PTEN-null breast cancer and can be overcome by combining with Mcl-1 inhibitors

Fig. 1

A Outline of CRISPR screening approach used to identify gene knockouts that increase or decrease sensitivity to capivasertib and AZD8186. B Venn diagram showing overlap in AZD8186 and capivasertib resistance genes identified across the lines. C STRING network analysis of AZD8186 (left) and capivasertib (right) resistance genes identified in at least two cell lines (n = 9 for AZD8186 and n = 19 for capivasertib). Node size represents resistance effect caused by gene KO (mean gRNA FC for each gene in drug treated relative to DMSO control across three cell lines). Smallest and largest node represent mean gRNA FC of 1.5 and 15, respectively. Node colour represents pathway or associated gene function. Colour and size of node on STRING network were modified manually.

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