ArticleScientific reports2019
DNA damage signalling from the placenta to foetal blood as a potential mechanism for childhood leukaemia initiation.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Impact of near continuous low dose rate neutron irradiation on pregnancy outcomes in mice.NPJ microgravity · 2024Article
- Additive genotoxic effects in cord blood cells upon indirect exposure to chemotherapeutic compounds crossing an in vitro placental barrier.Scientific reports · 2024Article
- The intercellular communications mediating radiation-induced bystander effects and their relevance to environmental, occupational, and therapeutic exposures.International journal of radiation biology · 2023Review
- Infant leukaemia - faithful models, cell of origin and the niche.Disease models & mechanisms · 2021Review
- Review
- Pathogenesis of pediatric B-cell acute lymphoblastic leukemia: Molecular pathways and disease treatments.Oncology letters · 2020Review
- Cortical cells are altered by factors including bone morphogenetic protein released from a placental barrier model under altered oxygenation.Neuronal signaling · 2020Article
- Fetal liver Mll-AF4+ hematopoietic stem and progenitor cells respond directly to poly(I:C), but not to a single maternal immune activation.Experimental hematology · 2019Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 1 country.
Funding
Abstract
For many diseases with a foetal origin, the cause for the disease initiation remains unknown. Common childhood acute leukaemia is thought to be caused by two hits, the first in utero and the second in childhood in response to infection. The mechanism for the initial DNA damaging event are unknown. Here we have used in vitro, ex vivo and in vivo models to show that a placental barrier will respond to agents that are suspected of initiating childhood leukaemia by releasing factors that cause DNA damage in cord blood and bone marrow cells, including stem cells. We show that DNA damage caused by in utero exposure can reappear postnatally after an immune challenge. Furthermore, both foetal and postnatal DNA damage are prevented by prenatal exposure of the placenta to a mitochondrially-targeted antioxidant. We conclude that the placenta might contribute to the first hit towards leukaemia initiation by bystander-like signalling to foetal haematopoietic cells.
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Registered trials
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