Total RNA was isolated from IR K562 cells treated with imatinib celecoxib and in mix of imatinib and celecoxib using TRIzol reagent. Reverse transcription of 1 g Docetaxel Taxotere of total RNA isolated was attained by combining the RNA with 10 l of 2 PCR master mix, 1 l of deoxynucleotides, 1 l of oligo dT, 0. 2-5 r RNAase inhibitor, and 0. 5 l of Reverse Transcriptase in a-20 l volume. This is followed by incubation of the mixture at 4-2 C for 60 min, and then for 5 min at 95 C. Four microliters of the merchandise in the RT response was used for PCR. The PCR conditions and the primer sequences are given in the Table 1. The PCR products were visualized on 1% agarose ties in under UV light. The GAPDH primers served as control. Total RNA was isolated from K562 and IR K562 cells using TRIzol reagent. Reverse transcription of 1 g of total RNA isolated was attained by combining the RNA with 10 l of 2 PCR grasp blend, 1 l of deoxynucleotides, 1 l of oligo dT, 0. 2-5 d RNAase inhibitor, and 0. 5 l of Reverse Transcriptase in a-20 l volume. Thiswas followed closely by incubation of the mixture at 4-2 C for 60 min, and then for 5 min at 9-5 C. An extended PCR technique was used to improve the ABL kinase domain of the BCR/ABL allele with forward primer BCRF and reverse primer ABLkinaseR. An additional period PCR used forward Gene expression primer ABLkinaseF and reverse primer ABLkinaseR used within the first step. The entire kinase domain was sequenced in-the forward and reverse directions; this region included 863 angles. The launch from IR K562 cells treated with celecoxib, imatinib and imatinib and celecoxib was estimated depending on manufacturers instructions. Data were reported as the mean S. E. Of-three in-dependent studies. Statistical analysis of differences was completed by one-way analysis of variance. A value of less than 0. 0-5 was considered supplier Gemcitabine as important. In order to define IR K562 cells for the mechanism of resistance devel-opment, series analysis of the Abl kinase domain was performed for existence of any point mutations. The expression of MDR 1 and COX 2 was examined, to learn the choice mechanisms. Imatinib resistant K562 cells showed over expression of both COX 2 and MDR 1, indicating a possible function for COX 2 and MDR 1 in-the devel-opment of resistance in K562 cells against imatinib. So that you can test this IRK562 and K562 cells were confronted with celecoxib, a COX 2 selective inhibitor. To understand the role of COX 2-in the improvement of resistance, IR K562 cells were treated with different levels of celecoxib alone or in mixture with imatinib and the cell growth was checked by MTT assay. As shown in Fig. 2a and b, a dose dependent reduction in the growth of cells was observed with increasing levels of imatinib and celecoxib.