Fig. 3: AR mutations accelerate hepatocarcinogenesis in vivo. | Communications Biology

Fig. 3: AR mutations accelerate hepatocarcinogenesis in vivo.

From: Two somatic mutations in the androgen receptor N-terminal domain are oncogenic drivers in hepatocellular carcinoma

Fig. 3

a The experimental design of NRAS/AR-mutation-driven liver tumorigenesis model in male mice. b Kaplan-Meier analysis and log rank test of the survival rates of the mice after HDT injection of NRAS/pT3-Vector (n = 5), NRAS/AR-WT (n = 8), NRAS/AR-Q62L (n = 8) and NRAS/AR-E81Q (n = 8). No mortality was observed with the NRAS group during the course of the study. The mean survival of NRAS/AR-WT group was 28 W post HDT, and with AR-Q62L and AR-E81Q, the mean survival of mice was reduced to 15 and 22 W respectively. ***p < 0.001. c AR mutations accelerate hepatocarcinogenesis of NRAS-driven mice compared with WT. The morphological pictures of a representative liver of NRAS/pT3-Vector, NRAS/AR-WT, NRAS/AR-Q62L and NRAS/AR-E81Q HDT mice of different time were shown. d The liver weight of different HDT mice at 10 W and 18 W was testes. All error bars represent Standard Deviation. e The HE stain of a representative liver of NRAS/pT3-Vector, NRAS/AR-WT, NRAS/AR-Q62L and NRAS/AR-E81Q HDT mice of different time were shown N: normal liver, T: tumor liver (Scale bar = 50 μm). f AR mutations have stronger malignancy than WT. The IHC stain of different groups liver cancer at tumor formation time were shown. NRAS/AR-Q62L liver cancer at 10 W post HDT and NRAS/AR-E81Q liver cancer at 18 W post HDT showed higher KI67 stain with 23 W AR-WT mouse. N: normal liver, T: tumor liver (Scale bar = 50 μm).

Back to article page