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. Author manuscript; available in PMC: 2022 Oct 1.
Published in final edited form as: J Hepatol. 2021 May 28;75(4):888–899. doi: 10.1016/j.jhep.2021.05.018

Figure 1. FAK is activated in human iCCA patients and Akt/YAP-induced iCCA mouse lesions.

Figure 1.

(A) PTK2 mRNA levels in human intrahepatic cholangiocarcinoma (iCCA) from The Cancer Genome Atlas (TCGA) and National Cancer Institute (NCI) datasets. (B) Quantitative real-time RT-PCR analysis of PTK2 expression in iCCA (n = 50) and corresponding non-tumorous surrounding liver tissues (ST; n = 50) from our cohort. (C) Kaplan–Meier survival curves of human iCCA specimens from our cohort with high and low PTK2 mRNA levels, showing the unfavorable outcome of patients with elevated expression of this gene. (D) GSEA analysis of FAK pathway-related proteins in iCCA from TCGA. (E-F) FAK activation in the Akt/YAP-induced iCCA mouse model.