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. 2016 Dec 12;213(13):2989–3005. doi: 10.1084/jem.20160817

Figure 3.

Figure 3.

Pten silencing drives increased vascularity in synovial sarcoma. (A) Plot of tumor mass at harvest against time elapsed after TATCre injection into mice bearing conditional SS18-SSX and either Ptenw/w (triangles) or Ptenfl/fl (circles). Filled shapes indicate tumors with associated histologically detected metastasis. (B) Pie chart demonstrating histological subtype fractions for metastatic tumors in hSS;Ptenfl/fl mice (n = 59). (C) Flow cytometry of a primary tumor and lung metastasis stained with E-cadherin and analyzed for intrinsic GFP expression. Tumor population (open arrow) and endothelial cells (filled arrow) both express higher levels of E-cadherin than the immune infiltrates (lower left). (D) Example photomicrographs of tumors with retained histological appearance between primary tumor and metastasis. (E) Example anti–Ki-67 immunohistochemistry photomicrographs and chart of proliferative indices for SS18-SSX-induced tumors in each Pten genotype (student’s t test). (F) Example H&E photomicrographs of necrosis (right side of each) identified in tumors and graph of the mean necrotic area per tumor cross section by histology (Student’s t test). (G) Example anti-CD31 immunohistochemistry photomicrographs demonstrating vascular density in hSS tumors arising with wild-type or silenced Pten. Graph presents mean vascular density in primary tumors of each genotype (Student’s t test). (H) Plot of vascular density indicated as vessel perimeter per cross-sectional area against cross-sectional area of each metastasis in hSS;Ptenfl/fl mice. Bars, 50 µm.