ArticleNature communications2025
Chromosomal instability in human trophoblast stem cells and placentas.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- CHD8-Dependent Chromatin Licensing Sustains Trophoblast Stem Cell Transcriptional Programs.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Patient-specific trophoblast stem cells for placental medicine.Trends in molecular medicine · 2026Review
- Technological Advances in Molecular Diagnostic Methods for Hereditary Diseases in Preconception and Prenatal Settings.Current issues in molecular biology · 2026Review
- Chronic replication stress-mediated genomic instability disrupts placenta development in mice.PLoS genetics · 2026Article
- Studies of post-partum placentas provide insights into the origin of structural chromosomal aberrations.Human reproduction (Oxford, England) · 2026Article
- Chromosomal structural abnormalities and tissue-specific mosaicism: insights into false-negative noninvasive prenatal testing.Frontiers in genetics · 2026Article
- Divergent roles of DNA methylation, TRIM28, and p53 surveillance in human embryonic and trophoblast stem cells.bioRxiv : the preprint server for biology · 2025Article
- Exploring and validating the marmoset as a primate model for chromosomal instability in early development.Molecular human reproduction · 2025Article
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Authors and funding
9 authors.
Funding
Abstract
The human placenta, a unique tumor-like organ, is thought to exhibit rare aneuploidy associated with adverse pregnancy outcomes. Discrepancies in reported aneuploidy prevalence in placentas stem from limitations in modeling and detection methods. Here, we use isogenic trophoblast stem cells (TSCs) derived from both naïve and primed human pluripotent stem cells (hPSCs) to reveal the spontaneous occurrence of aneuploidy, suggesting chromosomal instability (CIN) as an inherent feature of the trophoblast lineage. We identify potential pathways contributing to the occurrence and tolerance of CIN, such as autophagy, which may support the survival of aneuploid cells. Despite extensive chromosomal abnormalities, TSCs maintain their proliferative and differentiation capacities. These findings are further validated in placentas, where we observe a high prevalence of heterogeneous aneuploidy across trophoblasts, particularly in invasive extravillous trophoblasts. Our study challenges the traditional view of aneuploidy in the placenta and provides insights into the implications of CIN in placental function.
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Registered trials
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