Evidence map›Paper›PMID 30954690›Full record

ReviewPapillomavirus research (Amsterdam, Netherlands)2019

Genetic susceptibility to cervical neoplasia.

Matthew A Brown, Paul J Leo

Open access · goldAbstract readReview
In one paragraph

Review in Papillomavirus research (Amsterdam, Netherlands), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 13% of its field
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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Progress in eliminating HPV-associated disease.Papillomavirus research (Amsterdam, Netherlands) · 2019
    Article
  13. Immunotherapy for HPV associated cancer.Papillomavirus research (Amsterdam, Netherlands) · 2019
    Review
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

2 authors at 2 institutions in 1 country.

Matthew A BrownInstitute of Health and Biomedical Innovation, Queensland University of Technology, Translational Research Institute, Princess Alexandra Hospital, Woolloongabba, QLD, 4102, Australia. Electronic address: Matt.brown@qut.edu.au.
Paul J LeoInstitute of Health and Biomedical Innovation, Queensland University of Technology, Translational Research Institute, Princess Alexandra Hospital, Woolloongabba, QLD, 4102, Australia.
Princess Alexandra Hospital · AUQueensland University of Technology · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Twin and family studies suggest that genetic factors play a role in cervical neoplasia susceptibility. Both rare high penetrant and common low penetrant host genetic variants have been shown to influence the risk of HPV persistence, and common variants have been shown to influence the risk of cervical neoplasia. The strongest associations with cervical neoplasia are with HLA genes, with associations having been demonstrated to both reduce and increase the risk of the disease. Fine-mapping using imputed amino-acid sequences of HLA-types has shown that the HLA associations are driven primarily by the HLA-B amino acid position 156 (B156), and HLA-DRB1 amino acid positions 13 and 71. This is informative about the types of peptides that may be useful for peptide vaccines. As cervical neoplasia is at least moderately heritable, genetics may be able to identify those at high or low disease risk. Using the findings of hundreds of disease-associated SNPs to calculate genetic risk scores, it has been shown that women with genetic risk scores in the bottom 10% of the population have very low risk of cervical neoplasia (<0.17%), whereas those in the top 5% have 22% risk of developing the disease. Further large scale genetic studies would be helpful to better define particularly the non-MHC component of genetic risk.

Indexed as

Genetic Predisposition to DiseaseFemaleHLA AntigensHumansImmunologic FactorsPapillomavirus InfectionsPolymorphism, Single NucleotideUterine Cervical NeoplasmsHLA AntigensImmunologic FactorsCervical neoplasiaGenetic risk predictionGenomewide association studyHeritabilityHLA

Identifiers

PMID30954690
PMCPMC6460319
OpenAlexW2928336616

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.