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. Author manuscript; available in PMC: 2011 Apr 25.
Published in final edited form as: Cancer Biol Ther. 2008 Apr 21;7(7):986–994. doi: 10.4161/cbt.7.7.6181

Figure 2.

Figure 2

The pharmacogenetic window of 5-FU compared to imatinib. (A) Preclinical foundation for imatinib, demonstrating promising pharmacogenetic window. In this in vitro model of CML, imatinib exposure inhibited cell growth selectively in leukemia cells expressing the bcr-abl protein. Adapted with permission from Druker et al.33 (B) Clinical results of imatinib (left) versus previous standard therapy (right) for newly diagnosed chronic-phased CML, as reported by O’Brien et al.34 Imatinib was developed for human trials based upon preclinical data (A) that demonstrated promising activity in cell lines expressing the bcr-abl protein. CCR = complete cytogenetic response. Other = less than complete cytogenetic response.