Assessment of Chemotherapy-Induced DNA Damage in Peripheral Blood Leukocytes of Cancer Patients Using the Alkaline Comet Assay (CROSBI ID 117131)
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Kopjar, Nevenka ; Garaj-Vrhovac, Vera ; Milas, Ivan
engleski
Assessment of Chemotherapy-Induced DNA Damage in Peripheral Blood Leukocytes of Cancer Patients Using the Alkaline Comet Assay
The alkaline comet assay was employed to assess the pre-and post-treatment levels of in in vivo DNA damage in peripheral blood leukocytes of cancer patients.During the study all patients were given antineoplastic drugs, mainly as polychemotherapy. To quantify the DNA damage, two different comet parameters were eveluated:the tail lenght and tail moment. Our results indicate marked interindividual variations between baseline DNA damage in peripheral blood leukocytes recorded among cancer patients prior to the chemotherapy. After intravenous administration of various antineoplastic drugs, a significantly increaesed level of dNA damage in all cancer patients compared to their pre-tretment values was recorded. The highest level of DNA damage was seen following administration of 5-fluorouracil, adriamycin, and cisplatin (FAP protocol). The results indicate that administration of antineoplastic drugs in standard protocol is accompanied by significant DNA damage in peripheral blood leukocytes. In order to diminish the potential risks of developing secong neoplasms, a continious biomonitoring of cancer patients after the ending of chemotherapy becomes important.Despite their limitations, present results confirm the usefulness of the alkaline comet asay as a sensitive biomarker of exposure that enables rapid and simple detection of primary DNA damage in peripheral blood leukocytes of cancer patienets. Together with standard cytogenetic endpoints, the comet assay provides a powerfull technique for the routine detection of critical DNA lesions produced after administration of antineoplastic drugs in the clinical seetings.
antineoplastic drugs; microgel electrophoresis; biomarker of exposure; cancer chemotherapy protocols; DNA lesions; second cancer risks; interindividual differences in response
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