Systemic Chemotherapy Is Modulated by Platelet-Activating Factor-Receptor Agonists

Figure 1

Modulation of B16F10 tumor growth by systemic chemotherapy with etoposide (ETOP) and the effect of PAF-R agonist (CPAF). (a) Murine B16F10 melanoma tumor cells (0.5 × 10⁶) were implanted into the shaved dorsal hind flanks of syngeneic C57BL/6-WT mice (5–7 mice/group) subcutaneously (day 0). Mice were treated with or without ETOP (36 mg/kg) intraperitoneally either at day 0, day 3, or day 6 repeated at every 3 days until the end of the experiment. Control mice received the vehicle (0.5% DMSO in 100 μL PBS) by the same route. Tumor growth was monitored and measured with digital caliper and tumor volume (major circumference × minor circumference²/2) was expressed as mean ± SEM per group. Statistical differences () were noted between vehicle and ETOP treatment (day 0) at day 15. (b) Following subcutaneous B16F10 tumor cell implantation, C57BL/6-WT mice were treated with or without ETOP (36 mg/kg) intraperitoneally at day 0 repeated every 3 days until the end of the experiment. CPAF treatment (250 ng/mouse) was given intraperitoneally at days 0, 6, and 12. Control mice received the vehicle (0.5% DMSO in 100 μL PBS) by the same route. Tumor growth was measured and tumor volume (major circumference × minor circumference²/2) was expressed as mean ± SEM per group and compared between the groups. Statistical differences were noted between (1) , vehicle and ETOP groups; (2) , vehicle and CPAF groups; and (3) , ETOP and CPAF and ETOP and ETOP + CPAF groups at day 15.

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