Human C-reactive protein does not bind to fcγRIIa on phagocyti cells

Sullivan et al. reply — Our paper (1) demonstrated that the expression of MRP1 at the level of transcription, translation, and function was repressed by wild-type p53 in human prostate cancer, human melanoma, and human colon carcinoma cell lines. In these cell lines, we used either transfection of a human p53 temperature-sensitive mutant, or isogenic cell lines in which p53 was inactivated by either the E6 protein of human papilloma virus 16, or a dominant-negative p53 mutant. We demonstrated that shifting the control cells from 38°C to 32°C had no effect on MRP expression or function (Figures 5, 6, and 8). Previously, Wang and Beck reported the ability of wild-type p53 to repress MRP1 promoter activity (2). We did not investigate the expression of MDR1, since we had previously shown that P-glycoprotein was not expressed in over 90 human prostate cancer specimens obtained at the time of surgery (3).

The strength of our observations rests on the fact that a human in vitro model was constructed based on the study of human in vivo gene expression and it yielded similar alterations upon p53 mutation. In contrast, Bahr et al. transfected a murine gene into human cells. Whether murine genes have the same transcriptional effects on the human genome as human genes would require further elucidation. This may, in part, account for why the findings in the letter of Bahr and colleagues differ from those in our paper and from those reported in the literature. Additionally, it may be as the authors suggest that different genetic alterations exist in individual glioma cell lines; these too would require further elucidation.