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. Author manuscript; available in PMC: 2009 Oct 19.
Published in final edited form as: J Cell Biochem. 2008 Jul 1;104(4):1311–1323. doi: 10.1002/jcb.21709

Fig. 1.

Fig. 1

Aspirin and apyrase decreased tumor cell-induced platelet aggregation and increased bleeding times but did not affect local tumor growth. A: Platelets were pre-incubated with ASA (10 mM), potato apyrase (5 U), the combination or nothing for 3-min priorto addition of B16-FL cells. All four aggregometry tracings of treated platelets were flat prior to tumor cell addition. B16-FL cells were added to the platelets at time 0 min and aggregation was measured for 6 min. ASA, apyrase, and ASA + apyrase treatment decreased B16-FL tumor cell-induced platelet aggregation. B: B16-FL adhesion to a lawn of wild type and β3−/− platelets or BSA (B16-FL alone) was measured by Cyquant Elisa Kit. B16-FL cells adhered to both wildtype and β3−/− platelets in vitro. C: Bleeding times (s = seconds) were measured in C57BL/6 mice treated 30 min prior with vehicle (n = 5), APT102 (n = 5), ASA (n = 5), or ASA + APT102 (n = 5). The treatment groups are denoted on the bottom of the graph. ASA and ASA + APT102 pretreatment elevated bleeding times compared to vehicle (*P = 0.0061, **P = 0.0002, ***P = 0.0001, ****P< 0.0001). D: 4T1-GFP-FL s.c. tumors were established in Balb/c mice for 7 days. ASA +APT102 (n = 5) or vehicle (n = 5) was then administered and BLI was performed at days 7 (pretreatment) and 14. No significant differences in s.c. tumor burden were observed between vehicle and ASA +APT102 (P = 0.23).