The implementation of cancer chemotherapy has resulted in the development of an area of concern recognized as chemoresistance.  Platinum compounds such as cisplatin are being used as anticancer drugs, but the success factor is not always actualized. This is because some forms of cancer like ovarian cancer have become resistant to the cisplatin chemotherapy. As a result, the effectiveness of these drugs has diminished leading to increased mortality. The aspect calls for the need of investing in research and development to help identify other treatments that will be able to resensitize chemoresistant tumors. The objective of the study is to help gain a comprehension of how these ovarian cells manage to become resistant to cisplatin. This will be important to help analyze the factors that bring about the resistance. The study has measured interstrand cross-link (ICL) formation and repair coupled with base excision repair (BER) in chemosensitive (OCI-P5x and A2780) and chemoresistant (SKOV-3) ovarian cancer cell lines using modified comet assays. The method was preferred due to its ability of analyzing DNA damage formation and repair at the single cell level. There was the presence of significant differences among the ovarian cancer cell lines with regards to cisplatin treatment, according to the available data. Compared to the chemosensitive lines, a significant DNA crosslink formation attenuation was noted in the chemoresistant cell line SKOV-3 as a result of increased nucleotide excision repair over the first 12h. This is despite making an observation that the peak of crosslink formation for the three cell lines was at 12h. However, between the cell lines there were no differences in BER. There was also a study of the function of nuclear organization on DNA damage formation using ICL comet assay by comparing response in intact cells and nucleoid bodies. Based on the results, intact cells and nucleoid bodies demonstrated similar rank order of dose-response, but at all doses cisplatin, chemoresistant cells showed to be more resistant to damage formation. Fascinating insights have been provided by these data regarding the differences in the DNA damage response between chemosensitive and chemoresistant cells. Molecular basis of these differences will be explored in future experiments.

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