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. 2018 Nov 6;293(52):20123–20136. doi: 10.1074/jbc.RA118.005395

Figure 2.

Figure 2.

Conditional expression of the mouse Met transgene and homozygous Pten deletion in mouse prostate leads to development of HGPIN and prostatic adenocarcinomas. A and B, histology of 3-month-old PtenL/L:PB-Cre4 (A) and H11Met/+/PtenL/L:PB-Cre4 (B) mouse prostates. ×200 magnification images of mPIN lesions in AP/DLP/VP are shown in A1–A3 and B1–B3. Boxes, ×400 magnification images (A1′–A3′ and B1′–B3′). C and D, immunohistochemical analysis of 4-month-old PtenL/L:PB-Cre4 (C1–C9) and H11Met/+/PtenL/L:PB-Cre4 (D1–D9) mouse prostates with different antibodies as labeled. E and F, histology of 12-month-old PtenL/L:PB-Cre4 (E) and H11Met/+/PtenL/L:PB-Cre4 (F) mouse prostates. ×200 magnification images of prostatic adenocarcinomas are shown in E1–E3 and F1–F3. Boxes, ×400 magnification images of invasive adenocarcinoma (E1′–E3′ and F1′–F3′), as well as an expansion of EMT pattern with nuclear atypia, polygonal cell pattern, and pleomorphism (F3′) in H11Met/+/PtenL/L:PB-Cre4 tumor. G and H, immunohistochemical analysis of PtenL/L:PB-Cre4 (G1–G6) and H11Met/+/PtenL/L:PB-Cre4 (H1–H6) adenocarcinoma with different antibodies as labeled.