Chronic myelogenous leukemia is a clonal myeloproliferative disorder resulting from the neoplastic transformation of-a hematopoietic stem cell. While indicating extraordinary clinical exercise against chronic phase CML, in the accelerated and blastic phases of CML the results after imatinib therapy is unacceptably poor. Resistance to TK inhibitors was initially identified in patients with high level CML who’d a while receiving imatinib. This resistance was associated with point mutations that rendered ABL kinase resistant ubiquitin-conjugating towards the drug or-less commonly associated with BCR/ABL gene amplification. Furthermore, various other as yet not known mechanisms might be in charge of the develop-ment of resistance against imatinib. These studies highlight the requirement to identify novel anti BCR/ABL therapies to overcome the imatinib resistance. Cyclooxygenases will be the key enzymes that catalyze the conversion of arachidonic acid to prostaglandins and other eicosanoids. In many tissues, COX 1 is expressed constitutively, although COX 2 is induced by growth factors, cytokines, and carcinogens. Epidemiologic and experimental studies show that COX 2 inhibitors are Endosymbiotic theory effective chemopreventive brokers, reducing the risks of numerous kinds of tumors, including prostate, lung, colon, and gastric cancers. Recently, COX 2 inhibitors have also gained interest, either alone or in combination with other chemotherapeutic agents and/or radiation therapy, in the treatment of cancer. For example, celecoxib, a COX 2 selective inhibitor, applied antitumor effects in a large number of cancers. It also showed synergistic antitumor effects when mixed with gemcitaine or 5 fluorouracil in patients with higher level pancreatic cancer, and it enhanced the reaction to paclitaxel and carboplatin in early-stage non small cell lung cancer. Subhashini et al. showed that celecoxib exerts antileukemic results in K562 cells by cell cycle arrest, caspase 3 activation and down regulation of COX 2 term. These effects of celecoxib were shown to be complete with hydroxyurea or imatinib. The mechanism underlying the anti-tumor activity of COX 2 inhibitors is considered to involve inhibition of COX 2 enzyme activity, but it PF299804 ic50 is unclear whether COX 2 inhibition must induce apoptosis. In today’s study, imatinib resistant K562 cells were developed by continuous exposure of cells to imatinib. In a attempt to elucidate the possible mechanism of resistance, we analyzed the expression of MDR 1 and COX 2 and the results confirmed that MDR 1 and COX 2 are around expressed in IR K562 cells compared to K562 cells. We examined the result of celecoxib o-n cells and elucidated the possible participation ofCOX 2 in the development of resistance to imatinib.