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Sperm DNA Damage in Cancer Patients

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Genetic Damage in Human Spermatozoa

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 1166))

Abstract

Fertility is a growing healthcare issue for a rising number of cancer survivors. In men, cancer itself and its treatment can negatively affect spermatogenesis by targeting the dividing spermatogonia and their cellular environment, ultimately leading to a reduction of testicular germ cells and sperm count. Experimental data and prospective longitudinal studies have shown that sperm production can recover after cancer treatment. But despite this, yet unpredictable, recovery in sperm production, cancer survivors are more at risk to produce sperm with aneuploidy, DNA damage, abnormal chromatin structure, and epigenetic defects even 2 years post-treatment. Sperm DNA alteration is of clinical concern, as these patients may father children or seek assisted reproduction technologies (ART) using gametes with damaged genome that could result in adverse progeny outcomes. Interestingly, large cohort studies revealed lower birth rate but no significant impact on the health of the children born from male cancer survivors (naturally or using ART). Nevertheless, a better understanding of how cocktail of chemotherapy and new anticancer agents affect spermatogenesis and sperm quality is needed to reduce side effects. Moreover, developing new fertility preservation strategies is essential as sperm cryopreservation before treatment is currently the only option but does not apply for prepubertal/young postpubertal patients.

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Abbreviations

ART:

Assisted reproductive technologies

CED:

Cyclophosphamide equivalent dose

DFI:

DNA fragmentation index

HDS:

High DNA stainability

SCSA:

Sperm chromatin structure assay

SSCs:

Spermatogonial stem cells

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Correspondence to Geraldine Delbes .

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Beaud, H., Tremblay, A.R., Chan, P.T.K., Delbes, G. (2019). Sperm DNA Damage in Cancer Patients. In: Baldi, E., Muratori, M. (eds) Genetic Damage in Human Spermatozoa. Advances in Experimental Medicine and Biology, vol 1166. Springer, Cham. https://doi.org/10.1007/978-3-030-21664-1_11

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