Prothrombotic effects of TCs. (A) Jimt1, A2058, and H1 TCs (10 000 cells per 100 µL) were added to isolated platelets, and platelet aggregation was monitored using LTA. Thrombin was used as positive control (4 to 6 replicates in 2 independent experiments). Thrombin vs TCs: Jimt1, P < .0001; A2058, P < .0001; H1, P = .003. Error bars: 95% CI. (B) FACS analysis of the TC surface molecule TF. The procoagulatory TF molecule was upregulated in Jimt1 breast cancer cells in vitro. (C) Plasma coagulation time depends on different TC lines: Jimt1 breast cancer shows the biggest decrease in plasma coagulation time. Jimt1 vs A2058, P = .001; Jimt1 vs H1, P = .003; A2058 vs H1, P = .038. Error bars: ±1 SD. (D) Jimt1, A2058, and H1 TCs (10 000 cells per 100 µL) were supplemented with human plasma, and thrombin generation was quantified. Human plasma was used as control (100%, horizontal dotted line) (n = 3 replicates of different cell passages). Jimt1 vs A2058, P = .299; Jimt1 vs H1, P = .002; A2058 vs H1, P = .017. Error bars: 95% CI. (E) After Jimt1, A2058, and H1 TCs (10 000 cells per 100 µL) were incubated with human plasma with or without tinzaparin (100 IU/mL), the supernatant was added to isolated platelets, and platelet aggregation was monitored using LTA. Thrombin was used as a positive control (n = 5 to 6 replicates in 2 independent experiments). Thrombin vs TCs: Jimt1, P < .0001; A2058, P < .0001; H1, P = .003. TCs vs tinzaparin: Jimt1, P < .0001; A2058, P < .0001; H1, P < .0001. Error bars: 95% CI. P values from Student t test. *P < .05. iso-ctr, isotype control; PE, phycoerythrin.