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. 2008 Nov 25;105(49):19444–19449. doi: 10.1073/pnas.0807691105

Fig. 2.

Fig. 2.

Prostate specific homozygous deletion of Grp78 blocks prostate tumorigenesis resulting from PTEN inactivation. (A) The cPtenf/fGrp78f/+, cPtenf/fGrp78f/f, and cPtenf/fGrp78f/− male mice were genotyped by PCR analysis. (B) The gross anatomy of the prostate of the mice with the indicated genotypes at 20 wk. All lobes of cPtenf/fGrp78+/+ mice formed solid tumor mass. In cPtenf/fGrp78f/+ mice, only AP developed solid tumor mass. The cPtenf/fGrp78f/f and cPtenf/fGrp78f/− mice are normal and cancer free. AP, anterior prostate; DLP, dorsolateral prostate; VP, ventral prostate; B, bladder; SV, seminal vesicle. (C) Histological comparison of H&E staining prostate sections of the mice in B. The cPtenf/fGrp78+/+ mice developed invasive adenocarcinoma in all prostate lobes. In cPtenf/fGrp78f/+ mice, AP had extensive invasive adenocarcinoma, whereas DLP and VP only developed diffusive prostate intraepithelial neoplasia (PIN). All lobes of the cPtenf/fGrp78f/f, and cPtenf/fGrp78f/− mouse prostates were normal. (D) The distribution of prostate lobes in 3 histological states, normal, PIN, and adenocarcinoma, for each genotype: Ptenf/fGrp78f/f (I), cPtenf/fGrp78+/+ (II), cPtenf/fGrp78f/+ (III), cPtenf/fGrp78f/f (IV), and cPtenf/fGrp78f/− (V).