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DNA Damage Can Stall the Cell Cycle02:36

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In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
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In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
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The journey of sperm from its origin to the point of ejaculation begins within the seminiferous tubules of the testis. Here, Sertoli cells produce fluid that propels non-motile sperm through a series of conduits, starting with the straight tubules leading to the rete testis. This interconnected network of tubules acts as the initial pathway for sperm, guiding them into the efferent ductules and then into the epididymis for maturation.
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Overview of DNA Repair02:25

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In order to be passed through generations, genomic DNA must be undamaged and error-free. However, every day, DNA in a cell undergoes several thousand to a million damaging events by natural causes and external factors. Ionizing radiation such as UV rays, free radicals produced during cellular respiration, and hydrolytic damage from metabolic reactions can alter the structure of DNA. Damages caused include single-base alteration, base dimerization, chain breaks, and cross-linkage.
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Translesion DNA Polymerases02:10

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Translesion (TLS) polymerases rescue stalled DNA polymerases at sites of damaged bases by replacing the replicative polymerase and installing a nucleotide across the damaged site. Doing so, TLS allows additional time for the cell to repair the damage before resuming regular DNA replication.
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During ejaculation, males release around 2-5 milliliters of semen, which is a complex mixture of mature sperm and various fluids produced by accessory glands. The mature sperm cells measure approximately 60 micrometers in length and consist of a head, neck, midpiece, and tail. The head is flattened and tapered, measuring about 4 to 5 micrometers in length. It contains a nucleus with condensed chromosomes and an acrosome, a cap-like structure filled with enzymes essential for penetrating the...
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Visualizing DNA Damage Repair Proteins in Patient-Derived Ovarian Cancer Organoids via Immunofluorescence Assays
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Sperm DNA Damage in Cancer Patients.

Hermance Beaud1, Amelie R Tremblay1, Peter T K Chan2

  • 1Institut national de la recherche scientifique, Centre INRS - Institut Armand-Frappier, QC, Canada.

Advances in Experimental Medicine and Biology
|July 14, 2019
PubMed
Summary
This summary is machine-generated.

Cancer treatments can harm male fertility, affecting sperm quality long-term. While sperm production may recover, DNA damage persists, posing risks for fathering children, necessitating improved fertility preservation methods.

Keywords:
CancerChemotherapyFertilityProgenyRadiotherapySperm DNASperm chromatinSperm epigenome

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Area of Science:

  • Reproductive Medicine
  • Oncology
  • Genetics

Background:

  • Male fertility is a significant concern for cancer survivors.
  • Cancer and its treatments can impair spermatogenesis, reducing sperm count and quality.
  • Sperm DNA damage, including aneuploidy and epigenetic defects, can persist post-treatment.

Purpose of the Study:

  • To review the impact of cancer and treatments on male fertility and sperm quality.
  • To discuss the implications of sperm DNA alterations for reproductive outcomes.
  • To highlight the need for enhanced fertility preservation strategies for cancer patients.

Main Methods:

  • Review of experimental data and longitudinal studies on male cancer survivors.
  • Analysis of cohort studies examining birth rates and child health outcomes.
  • Assessment of the effects of chemotherapy and novel anticancer agents on spermatogenesis.

Main Results:

  • Sperm production can recover post-cancer treatment, but sperm DNA damage remains a concern.
  • Male cancer survivors have an increased risk of producing sperm with genetic and epigenetic abnormalities.
  • Large cohort studies show a lower birth rate but no significant adverse health effects in children born to male cancer survivors.

Conclusions:

  • Male cancer survivors face long-term risks of impaired sperm quality due to treatment-induced DNA damage.
  • Understanding the effects of various cancer therapies on sperm is crucial for mitigating side effects.
  • Current fertility preservation options, primarily sperm cryopreservation, are insufficient for prepubertal or young postpubertal patients, necessitating new strategies.