Figure 3.

Histological characteristics of endometrial tumors formed in the Pten^−/−Kras^G12D MECPK model. A) i) Low magnification (4X) (left) showing tumor interface with normal tissue and high magnification (20X) of ii) normal (center) and iii) cancer tissues (right) with H&E. H&E of tumors from Pten^−/−Kras^G12D MECPK mice are endometrioid, lack glandular formation, and have minimal stroma. Ki67 confirmed these lesions were highly proliferative. iv-vi). As expected, PTEN was not detected in the cancer cells of the tumor tissue (vii-ix). Tumors expressed pAKT (x-xii), AKT (xiii-xv), pERK1/2 (xvi-xviii) and ERK1/2 (xix-xxi) important markers of PI3K and MAPK activation. Primary tumors were Vimentin positive in stroma and largely negative in epithelium and cancer cells (xxii-xxiv) and were negative for CDH1 in the stroma and positive in normal epithelium and in cancer cells (xxv-xxvii). n = 3 independent tissue samples. B) Comparison of MECPK tumor histology to human endometrial cancer samples. i) Representative H&E of a MECPK tumor at 1 month post-injection. In vivo tumor formation displays histological characteristics similar to that of grade 3 endometrioid endometrial cancers (ii-iii). Notably, cells are tightly compacted with visible mitotic events and near complete loss of stroma. Scale bar: 50 μm.