Platelet extravasation is arrested in the OvCa-Chip treated with atorvastatin. Confocal micrographs showing platelet (red) adhering to the vascular endothelium (Endo, green, VE-cadherin) (A), and corresponding extravasation of platelets into the cancer cells (cancer cells, blue, nuclei) (B) crossing the dysfunctional vascular barrier at increasing time points within OvCa-Chip (top) or OvCa-Chip treated with atorvastatin (Drug-OvCa-Chip; bottom). Bars represents 50 µm. Graph showing the quantitation of platelet adherence to the endothelium (C), and extravasated platelet concentration observed within the tumor chamber (D) (▪, OvCa-Chip; ▲, Drug-OvCa-Chip; and ●, Control-Chip). The shaded areas represent the 48-hour period before the introduction of platelets within OvCa-Chip when tumor-vessel coculture was established. P-values calculated vs Control-Chip; n = 3 individual experiments. (E) A representative immunohistochemical analysis of tumor tissue specimens obtained from healthy women and women with ovarian cancer showing platelets extravasated (CD42b⁺, brown, denoted by arrows) into the tumor stroma, in patients without statin drug treatment vs those with atorvastatin treatment. The bar represents 50 µm. Insets: original magnification ×40, of select regions. (F) Quantification of platelets observed with histology. Error bars are means ± SEM; n = 5 individual patient samples per group. One-way ANOVA, followed by Dunnett’s multiple-comparisons test. *P < .05; **P < .01.