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Abstract
Abstract Paclitaxel (P) and carboplatin (C) chemotherapy is reported to be a platelet-sparing drug combination. We investigated possible mechanisms for this by studying P & C's effects on: 1] normal human, and P- and C- treated patient-derived erythroid (BFU-E), myeloid (CFU-GM), and megakaryocyte (CFU-Meg) progenitor cell growth; 2] P-glycoprotein (P-gp) protein and glutathione S-transferase (GST) mRNA expression; 3] P & C patient serum levels of TPO, SCF, IL-6, IL-11, IL-1b, IL-8 and TNFa; and 4] marrow stromal cell production of TPO and SCF after P & C exposure. We found that CFU-Meg were more resistant to P alone, or in combination with C, than CFU-GM and BFU-E. We also found that CFU-Meg express P-gp protein and GST mRNA. That the former might play a role in drug resistance is suggested by the finding that verapamil treatment significantly increased P & C's toxicity to CFU-Meg (colony formation decreased ∼70%, p
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