ArticlePrenatal diagnosis2016
Placental transcriptomes in the common aneuploidies reveal critical regions on the trisomic chromosomes and genome-wide effects.
Article in Prenatal diagnosis, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.
- Current approaches and developments in transcript profiling of the human placenta.Human reproduction update · 2020Pooled it
- REST deficiency and neurogenic-to-gliogenic shift in down syndrome human cerebral organoids.Molecular brain · 2026Article
- The placental effects of trisomy for human chromosome 21 orthologs in four mouse models of Down syndrome.Biology open · 2025Article
- Consequences of chromosome gain: A new view on trisomy syndromes.American journal of human genetics · 2022Review
- Down-syndrome-induced senescence disrupts the nuclear architecture of neural progenitors.Cell stem cell · 2022Article
- Network analysis of Down syndrome and SARS-CoV-2 identifies risk and protective factors for COVID-19.Scientific reports · 2021Article
- Trisomy 21 is Associated with Caspase-2 Upregulation in Cytotrophoblasts at the Maternal-Fetal Interface.Reproductive sciences (Thousand Oaks, Calif.) · 2020Article
- Review
- Comprehensive chromosome screening and gene expression analysis from the same biopsy in human preimplantation embryos.Molecular human reproduction · 2017Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
Abstract
objectiveChromosomal aberrations are frequently associated with birth defects and pregnancy losses. Trisomy 13, Trisomy 18 and Trisomy 21 are the most common, clinically relevant fetal aneusomies. This study used a transcriptomics approach to identify the molecular signatures at the maternal-fetal interface in each aneuploidy.
methodsWe profiled placental gene expression (13-22 weeks) in T13 (n = 4), T18 (n = 4) and T21 (n = 8), and in euploid pregnancies (n = 4).
resultsWe found differentially expressed transcripts (≥2-fold) in T21 (n = 160), T18 (n = 80) and T13 (n = 125). The majority were upregulated and most of the misexpressed genes were not located on the relevant trisomic chromosome, suggesting genome-wide dysregulation. A smaller number of the differentially expressed transcripts were encoded on the trisomic chromosome, suggesting gene dosage. In T21, <10% of the genes were transcribed from the Down syndrome critical region (21q21-22), which contributes to the clinical phenotype. In T13, 15% of the upregulated genes were on the affected chromosome (13q11-14), and in T18, the percentage increased to 24% (18q11-22 region).
conclusionThe trisomic placental (and possibly fetal) phenotypes are driven by the combined effects of genome-wide phenomena and increased gene dosage from the trisomic chromosome. © 2016 John Wiley & Sons, Ltd.
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