ArticleProceedings of the National Academy of Sciences of the United States of America2001
Etoposide induces heritable chromosomal aberrations and aneuploidy during male meiosis in the mouse.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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26 citing papers in PubMed, 168 citations in OpenAlex.
- A simple method to efficiently generate structural variation in plants.PLoS genetics · 2025Article
- Non-alkylating agents-induced gonadotoxicity in pre-pubertal males: Insights on the clinical and pre-clinical front.Clinical and translational science · 2024Review
- Checkpoint Kinase 1 Is a Key Signal Transducer of DNA Damage in the Early Mammalian Cleavage Embryo.International journal of molecular sciences · 2023Review
- Cleavage of Early Mouse Embryo with Damaged DNA.International journal of molecular sciences · 2022Article
- Endogenous localization of TOP-2 inmicroPublication biology · 2021Article
- A Role forCells · 2020Article
- Exposure to Chemotherapy During Childhood or Adulthood and Consequences on Spermatogenesis and Male Fertility.International journal of molecular sciences · 2020Review
- GCNA Interacts with Spartan and Topoisomerase II to Regulate Genome Stability.Developmental cell · 2020Article
- Observational
- Article
- Etoposide damages female germ cells in the developing ovary.BMC cancer · 2016Article
- Maternal exposure to radiographic exams and major structural birth defects.Birth defects research. Part A, Clinical and molecular teratology · 2016Article
- Genetic Effect of Chemotherapy Exposure in Children of Testicular Cancer Survivors.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016Article
- Induction of centrosome amplification by formaldehyde, but not hydroquinone, in human lymphoblastoid TK6 cells.Environmental and molecular mutagenesis · 2015Article
- Maternal occupational exposure to ionizing radiation and major structural birth defects.Birth defects research. Part A, Clinical and molecular teratology · 2015Article
- Meiotic interstrand DNA damage escapes paternal repair and causes chromosomal aberrations in the zygote by maternal misrepair.Scientific reports · 2015Article
- The analysis of mutant alleles of different strength reveals multiple functions of topoisomerase 2 in regulation of Drosophila chromosome structure.PLoS genetics · 2014Article
- Cohesin removal precedes topoisomerase IIα-dependent decatenation at centromeres in male mammalian meiosis II.Chromosoma · 2014Article
- Article
- An extracellular S1-type nuclease of marine fungus Penicillium melinii.Marine biotechnology (New York, N.Y.) · 2012Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Etoposide, a topoisomerase II inhibitor widely used in cancer therapy, is suspected of inducing secondary tumors and affecting the genetic constitution of germ cells. A better understanding of the potential heritable risk of etoposide is needed to provide sound genetic counseling to cancer patients treated with this drug in their reproductive years. We used a mouse model to investigate the effects of clinical doses of etoposide on the induction of chromosomal abnormalities in spermatocytes and their transmission to zygotes by using a combination of chromosome painting and 4',6-diamidino-2-phenylindole staining. High frequencies of chromosomal aberrations were detected in spermatocytes within 64 h after treatment when over 30% of the metaphases analyzed had structural aberrations (P < 0.01). Significant increases in the percentages of zygotic metaphases with structural aberrations were found only for matings that sampled treated pachytene (28-fold, P < 0.0001) and preleptotene spermatocytes (13-fold, P < 0.001). Etoposide induced mostly acentric fragments and deletions, types of aberrations expected to result in embryonic lethality, because they represent loss of genetic material. Chromosomal exchanges were rare. Etoposide treatment of pachytene cells induced aneuploidy in both spermatocytes (18-fold, P < 0.01) and zygotes (8-fold, P < 0.05). We know of no other report of an agent for which paternal exposure leads to an increased incidence of aneuploidy in the offspring. Thus, we found that therapeutic doses of etoposide affect primarily meiotic germ cells, producing unstable structural aberrations and aneuploidy, effects that are transmitted to the progeny. This finding suggests that individuals who undergo chemotherapy with etoposide may be at a higher risk for abnormal reproductive outcomes especially within the 2 months after chemotherapy.
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