ArticleFrontiers in cell and developmental biology2021
Cyclophosphamide Exposure Causes Long-Term Detrimental Effect of Oocytes Developmental Competence Through Affecting the Epigenetic Modification and Maternal Factors' Transcription During Oocyte Growth.
Article in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 33 citations in OpenAlex.
- Ovarian puncture alters genes but not follicle growth in cyclophosphamide mice model.Reproduction & fertility · 2026Article
- HucMSC-mediated stromal metabolic reprogramming in reactivating aged ovaries: a single-cell transcriptomic perspective.Cellular & molecular biology letters · 2026Article
- IVF outcomes in cancer survivors: lower ovarian response and early embryo development but comparable success in frozen embryo transfer cycles - a retrospective cohort study.Frontiers in endocrinology · 2026Article
- Oocyte and embryo developmental competence following small multiple cyclophosphamide dose administrations in prepubertal female mice are comparable to adolescents.Scientific reports · 2025Article
- Oxidoreductase delivery by cell therapies in cyclophosphamide-induced premature ovarian insufficiency: a mechanistic insight into ovarian rejuvenation.Journal of ovarian research · 2025Article
- The risk factors, pathogenesis and treatment of premature ovarian insufficiency.Journal of ovarian research · 2025Review
- High-dose estrogen impairs demethylation of H3K27me3 by decreasing Kdm6b expression during ovarian hyperstimulation in mice.Journal of Zhejiang University. Science. B · 2025Article
- Intrinsic differences in mTOR activity mediates lineage-specific responses to cyclophosphamide in mouse and human granulosa cells.Journal of ovarian research · 2025Article
- Comparison of large single and small multiple doses of cyclophosphamide exposure in mice during early prepubertal age on fertility outcome.Scientific reports · 2024Article
- Female fertility preservation for family planning: a position statement of the Italian Society of Fertility and Sterility and Reproductive Medicine (SIFES-MR).Journal of assisted reproduction and genetics · 2024Article
- The effect of L-carnitine in reactive oxygen species reduction and apoptotic gene expression in mice after cyclophosphamide: An experimental study.International journal of reproductive biomedicine · 2024Article
- Review
- Rapamycin prevents cyclophosphamide-induced ovarian follicular loss and potentially inhibits tumour proliferation in a breast cancer xenograft mouse model.Human reproduction (Oxford, England) · 2024Article
- Unveiling the mechanisms and challenges of cancer drug resistance.Cell communication and signaling : CCS · 2024Review
- Insight on cytotoxic NHC gold(I) halide complexes evaluated in multifaceted culture systems.Current research in toxicology · 2024Article
- The EZH2-H3K27me3 axis modulates aberrant transcription and apoptosis in cyclophosphamide-induced ovarian granulosa cell injury.Cell death discovery · 2023Article
- HucMSC-EVs Facilitate In Vitro Development of Maternally Aged Preantral Follicles and Oocytes.Stem cell reviews and reports · 2023Article
- The future of fertility preservation for women treated with chemotherapy.Reproduction & fertility · 2023Article
- Chemotherapy induced oxidative stress in the ovary: drug-dependent mechanisms and potential interventions†.Biology of reproduction · 2023Review
- Effects ofFrontiers in nutrition · 2023Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cyclophosphamide (CTX) is widely used in various cancer therapies and in immunosuppression, and patients can still have babies after CTX chemotherapy. CTX directly causes primordial follicle loss with overactivation and DNA damage-induced apoptosis. Previous studies have shown that maternal exposure to CTX before conception increases the incidence of birth abnormalities and alters the methylation of genes in the oocytes of offspring. Mice were treated with a single dose of CTX (100 mg/kg) at post-natal day 21 and sacrificed 47 days later when primordial follicles surviving chemotherapy developed to the antral stage. Acute DNA damage and acceleration of the activation of primordial follicles after CTX treatment were repaired within several days, but the remaining follicle numbers remarkably decrease. Although partial surviving primordial follicle were developed to mature oocyte, oocyte quality hemostasis was impaired exhibiting aberrant meiosis progression, abnormal spindle and aneuploidy, mitochondrial dysfunction and increased endoplasmic reticulum stress. Thereafter, embryo development competency significantly decreased with fewer blastocyst formation after CTX exposure. CTX treatment resulted in alteration of DNA methylations and histone modifications in fully grown GV oocytes. Single-cell RNA-seq revealed CTX treatment suppressed multiple maternal genes' transcription including many methyltransferases and maternal factor YAP1, which probably accounts for low quality of CTX-repaired oocyte.
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