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Testicular cancer and sperm DNA damage: Short- and long-term effects of antineoplastic treatment

TitleTesticular cancer and sperm DNA damage: Short- and long-term effects of antineoplastic treatment
Publication TypeArticolo su Rivista peer-reviewed
Year of Publication2015
AuthorsPaoli, D., Gallo M., Rizzo F., Spanò M., Leter Giorgio, Lombardo F., Lenzi A., and Gandini L.
Keywordsadolescent, adult, adverse effects, antineoplastic agent, Antineoplastic Agents, article, Bleomycin, cancer radiotherapy, cancer staging, carboplatin, chromatin assembly and disassembly, chromatin condensation, cisplatin, combination chemotherapy, controlled study, cryptorchism, DNA damage, DNA denaturation, DNA fragmentation, drug effect, drug effects, etoposide, Fertility, genetics, human, Humans, Longitudinal Studies, longitudinal study, major clinical study, male, multimodality cancer therapy, multiple cycle treatment, Neoplasm Staging, paraaortic lymph node, Pathology, priority journal, radiation response, radiotherapy, scrotum, semen analysis, seminoma, sperm, Sperm Count, Sperm Motility, sperm quality, Spermatozoa, spermatozoon, spermatozoon count, spermatozoon motility, Testicular Neoplasms, testis cancer, testis descent, Time, Time Factors, treatment outcome

The aim of this study was to investigate sperm DNA damage induced by chemo- and radiotherapy in patients with testicular cancer to provide data on the extent and persistence of nuclear damage that might affect individual reproductive potential. We evaluated pre- and post-antineoplastic treatment sperm DNA integrity, expressed as DNA Fragmentation Index (DFI), in a large caseload of testicular cancer patients by sperm chromatin structure assay. The mean total DFI for all patients at T0 was 18.0 ± 12.5%. Sperm chromatin profile was markedly impaired at T3 (27.7 ± 17.4%) and T6 (23.2 ± 15.3%), improving considerably at T12 and T24 (14.0 ± 8.9% and 14.4 ± 10.3%). After chemotherapy, we found a marked increase in DFI at T3 and T6 and a significant reduction at T12 and T24 in comparison with the baseline. In contrast, DFI increased at T3 and T6 after radiotherapy but the subsequent reduction was far less marked, reaching baseline values at T12 and T24. Finally, post-treatment DNA damage was not age or histotype dependent, but was more marked in the advanced stage of cancer. In this study, we showed that the chromatin profile may be affected in the months immediately following the end of the treatment, improving after 12-24 months. Our results thus indicate that post-treatment DNA damage is influenced both by the type and intensity of the therapy and by the pathological and clinical stage of the disease. © 2014 American Society of Andrology and European Academy of Andrology.


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Citation KeyPaoli2015122