Abstract: Studies on Comparative Genomic Hybridization between Multiple Types of Paclitaxel-resistantNasopharyngeal Carcinoma Cells and the Parent Cell LinesWei LI, Yanhong MA, Yunpeng DONG, Xinli ZHANG, Guolin TANCorrespondence to: Guolin TAN, E-mail: guolintan@xysm.netDepartment of Otolaryngology Head and Neck Surgery, The Third Xiangya Hospital of Central South University, Changsha 410013, ChinaThis work was supported by National Natural Science Foundation of China (No. 30772403； 30471874)Abstract Objective: Comparative genomic hybridization ( CGH ) is a new molecular and cellular technology developed fromfluorescence in situ hybridization ( FISH ). It is a molecular cytogenetics method used to examine genomic imbalances, especially thedeletion and amplification of chromosomes, and to locate these alterations in certain chromosome regions. To completely understandthe possible differences in genomic DNA between three paclitaxel-resistant nasopharyngeal carcinoma cell lines ( CNE1/Taxol, HNE2/Taxol, 5-8F/Taxol ) and corresponding parent cells ( CNE1, HNE2, 5-8F ) which were sensitive to paclitaxel medication, and the signifi-cance of the differences in nasopharyngeal carcinoma acquired drug-resistance, the genomic DNA of three paclitaxel-resistant nasopha-ryngeal carcinoma cell lines and their parent cell lines were detected and analyzed using comparative genomic hybridization ( CGH ).Methods: The three paclitaxel-resistant nasopharyngeal carcinoma cell lines ( CNE1/Taxol, HNE2/Taxol, 5-8F/Taxol ) were created bycombining high-dose pulse therapy in the parent cells with stepwise dose increments of paclitaxel. The resistance index was determinedby colony formation. Cell CGH was performed on paclitaxel-resistant nasopharyngeal carcinoma cell lines and the parent cell lines toexplore the changes in chromosomal DNA regions. Results: The resistance indices of the three paclitaxel-resistant nasopharyngeal car-cinoma cell lines ( CNE1/Taxol, HNE2/Taxol, 5-8F/Taxol ) were 8.43, 8.27 and 5.26, respectively. There were extensive chromosomalchanges in the three parent cell lines when compared to normal genomic DNA, mainly seen in the co-amplification of 3q21-qter,5p13-pter, 12 and 20qll-qter, and the common deletion of 10q11-qter, 18 and X in all three parent cell lines. However, the three paclitax-el-resistant cell lines showed a relatively normal karyotype with changes mainly in the co-amplification of 3q21-qter, 5p13-pter, 12,20qll-qter and 8q21-qter. Compared with the common amplifications in parent cell lines, a new co-amplification of 8q21-qter was de-tected in the three paclitaxel-resistant nasopharyngeal carcinoma cell lines. Conclusion: Co-amplification of 3q21-qter, 5p13-pter, 12and 20 qll-qter, and deletion of 10q11-qter, 18, and X may be associated with nasopharyngeal carcinoma. Chromosomal amplificationof 8q21-qter may be related to paclitaxel-resistance in nasopharyngeal carcinoma cell lines. Further studies on these chromosome re-gions may supply new clues on the occurrence of nasopharyngeal carcinoma and the mechanism of acquired resistance of nasopharyn-geal carcinoma to paclitaxel.Keywords Nasopharyngeal carcinoma; Paclitaxel-resistant nasopharyngeal carcinoma cell lines; CGH