ReviewOpen biology2018
Exploring the links between cancer and placenta development.
Review in Open biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
102 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- A meta-analysis of pre-pregnancy maternal body mass index and placental DNA methylation identifies 27 CpG sites with implications for mother-child health.Communications biology · 2022Pooled it
- microRNA signatures associated with fetal growth restriction: a systematic review.European journal of clinical nutrition · 2022Pooled it
- Review
- Temporal changes in circulating miRNAs following gestational diabetes diagnosis: a pilot longitudinal study.Journal of clinical & translational endocrinology · 2026Article
- Conserved and divergent DNA methylation features of extraembryonic tissues between human, mouse and chicken.BMC genomics · 2026Article
- Replication stress primes a trophectoderm fate in embryonic stem cells.Cell death discovery · 2026Article
- BPGM as an intrinsic brake to constrain metastasis through phospho-epigenetic-mediated carnitine biosynthesis suppression.Neoplasia (New York, N.Y.) · 2026Article
- Chronic replication stress-mediated genomic instability disrupts placenta development in mice.PLoS genetics · 2026Article
- Pregnancy Associated Melanoma: Diagnostic and Therapeutic Challenges.Medicina (Kaunas, Lithuania) · 2026Review
- Epigenetic Deregulation of Transposable Elements Links Developmental Processes and Tumorigenesis.International journal of molecular sciences · 2026Review
- Repurposing statins for choriocarcinoma: targeting the mevalonate pathway to disrupt mechanosignaling and overcome therapeutic resistance.Clinical & experimental metastasis · 2026Review
- Nanotechnology in placental cancers: advances in targeted therapy and non-invasive diagnostics.Medical oncology (Northwood, London, England) · 2025Review
- ACVR2A facilitates trophoblast cell invasion through TCF7/c-JUN pathway in pre-eclampsia progression.eLife · 2025Article
- Profiling (placental) DNA methylation in cell-free DNA across gestation: the Rotterdam Periconception Cohort.Molecular human reproduction · 2025Article
- Genome-wide methylation profiling of maternal cell-free DNA using methylated DNA sequencing (MeD-seq) indicates a placental and immune-cell signature.European journal of clinical investigation · 2025Article
- The duality of microchimerism and cancer in parous women: a review and evolutionary perspective.Seminars in immunopathology · 2025Review
- Prenatal stress alters mouse offspring dorsal striatal development and placental function in sex-specific ways.Journal of psychiatric research · 2025Article
- Gestational trophoblastic disease: understanding the molecular mechanisms of placental tumours.Disease models & mechanisms · 2025Review
- Proximate and ultimate causes of pregnancy sickness.Evolution, medicine, and public health · 2025Review
- Spatial multiomic landscape of the human placenta at molecular resolution.Nature medicine · 2024Article
42 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
The development of metastatic cancer is a multistage process, which often requires decades to complete. Impairments in DNA damage control and DNA repair in cancer cell precursors generate genetically heterogeneous cell populations. However, despite heterogeneity most solid cancers have stereotypical behaviours, including invasiveness and suppression of immune responses that can be unleashed with immunotherapy targeting lymphocyte checkpoints. The mechanisms leading to the acquisition of stereotypical properties remain poorly understood. Reactivation of embryonic development processes in cells with unstable genomes might contribute to tumour expansion and metastasis formation. However, it is unclear whether these events are linked to immune response modulation. Tumours and embryos have non-self-components and need to avoid immune responses in their microenvironment. In mammalian embryos, neo-antigens are of paternal origin, while in tumour cells DNA mismatch repair and replication defects generate them. Inactivation of the maternal immune response towards the embryo, which occurs at the placental-maternal interface, is key to ensuring embryonic development. This regulation is accomplished by the trophoblast, which mimics several malignant cell features, including the ability to invade normal tissues and to avoid host immune responses, often adopting the same cancer immunoediting strategies. A better understanding as to whether and how genotoxic stress promotes cancer development through reactivation of programmes occurring during early stages of mammalian placentation could help to clarify resistance to drugs targeting immune checkpoint and DNA damage responses and to develop new therapeutic strategies to eradicate cancer.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.