Evidence map›Paper›PMID 26056362›Full record

ReviewPhilosophical transactions of the Royal Society of London. Series B, Biological sciences2015

Maternal-fetal conflict, genomic imprinting and mammalian vulnerabilities to cancer.

David Haig

2 registry-linked trialsAbstract readReview
In one paragraph

Review in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from 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.

2 · The registry

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.

NCT03563443 unknown statusnot on this mapstarted 2017, after this paper: background citation

Evaluation of Genomic Imprinting Testing for Detection and Surveillance of Bladder Cancer Patients

TypeobservationalSponsorChanghai HospitalRan2017 to 2019Enrolled300ConditionsBladder Cancer, Urine Marking, Diagnoses DiseaseArmsGenomic Imprinting Testing
NCT03882684 unknown statusnot on this mapstarted 2017, after this paper: background citation

Role of Genomic Imprinting in Cancer Diagnosis

TypeobservationalSponsorChinese Alliance Against Lung CancerRan2017 to 2020Enrolled1,500ConditionsEarly Diagnosis, Cancer, Biomarker, Genomic ImprintingArmsIn-situ imprinting detection
3 · Its place in the literature

Who cites it

22 citing papers in PubMed.

  1. Review
  2. Evidence for coopetition at the maternal-fetal interface shaping placental invasion.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  3. Article
  4. Brinkmanship in intragenomic conflict.Proceedings. Biological sciences · 2025
    Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Comment on the exchange between BoddyEvolution, medicine, and public health · 2020
    Article
  14. Lifetime cancer prevalence and life history traits in mammals.Evolution, medicine, and public health · 2020
    Article
  15. From humans to hydra: patterns of cancer across the tree of life.Biological reviews of the Cambridge Philosophical Society · 2018
    Review
  16. Article
  17. Cancer cell transmission via the placenta.Evolution, medicine, and public health · 2018
    Review
  18. Lost in translation: The 3'-UTR ofEvolution, medicine, and public health · 2018
    Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author.

David HaigDepartment of Organismic and Evolutionary Biology, Harvard University, Cambridge, MA 02138, USA dhaig@oeb.harvard.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Antagonistic coevolution between maternal and fetal genes, and between maternally and paternally derived genes may have increased mammalian vulnerability to cancer. Placental trophoblast has evolved to invade maternal tissues and evade structural and immunological constraints on its invasion. These adaptations can be co-opted by cancer in intrasomatic selection. Imprinted genes of maternal and paternal origin favour different degrees of proliferation of particular cell types in which they reside. As a result, the set of genes favouring greater proliferation will be selected to evade controls on cell-cycle progression imposed by the set of genes favouring lesser proliferation. The dynamics of stem cell populations will be a particular focus of this intragenomic conflict. Gene networks that are battlegrounds of intragenomic conflict are expected to be less robust than networks that evolve in the absence of conflict. By these processes, maternal-fetal and intragenomic conflicts may undermine evolved defences against cancer.

Indexed as

Genomic ImprintingAnimalsBiological EvolutionFemaleGene Regulatory NetworksHumansMaternal-Fetal ExchangeNeoplasmsPregnancySelection, GeneticTrophoblastscomparative oncologyimprinted gene networkparent–offspring conflictstem cellstrophoblast

Identifiers

PMID26056362
PMCPMC4581023

What OpenQuestion holds

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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.