Abstract Title:

Camptothecin acts synergistically with imatinib and overcomes imatinib resistance through Bcr-Abl independence in human K562 cells.

Abstract Source:

Cancer Lett. 2007 Jul 8;252(1):75-85. Epub 2007 Jan 16. PMID: 17223257

Abstract Author(s):

Dong-Sik Ju, Mi-Ju Kim, Jae-Ho Bae, Hye-Soon Song, Byung-Seon Chung, Min-Ki Lee, Chi-Dug Kang, Hyun-Sun Lee, Dong-Wan Kim, Sun-Hee Kim

Abstract:

In this study, we have tried to find new targets and effective drugs for imatinib-resistant chronic myelogenous leukemia (CML) cells displaying loss of Bcr-Abl kinase target dependence. The imatinib-resistant K562/R1, -R2 and -R3 cells showed profound declines of Bcr-Abl level and concurrently exhibited up-regulation of Bcl-2 and Ku70/80, and down-regulation of Bax, DNA-PKcs and BRCA1, suggesting that loss of Bcr-Abl after exposure to imatinib might be accompanied by other cell survival mechanism. K562/R3 cells were more sensitive to camptothecin (CPT)- and radiation-induced apoptosis than K562 cells, indicating hypersensitivity of imatinib-resistant cells to DNA damaging agents. Moreover, when K562 cells were treated with the combination of imatinib with CPT, the level of Bax and the cleavage of PARP-1 and DNA-PK were significantly increased in comparison with the effects of each drug. Therefore, our study suggests that CPT can be used to treat CML with loss of Bcr-Abl expression.

Study Type : In Vitro Study

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