Evidence map›Paper›PMID 28393355›Full record

ArticleCancer2017

Reduced rate of human papillomavirus infection and genetic overtransmission of TP53 72C polymorphic variant lower cervical cancer incidence.

Ghazi A Alsbeih, Najla M Al-Harbi, Sara S Bin Judia, Hatim A Khoja, Mohamed M Shoukri, Asma M Tulbah

Open access · hybridAbstract read
In one paragraph

Article in Cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 2 pooled it
1.4field-weighted citation impact, top 19% 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

16 citing papers in PubMed, 2 syntheses or guidelines pooled it, 20 citations in OpenAlex.

  1. Pooled it
  2. Association between theFrontiers in oncology · 2025
    Pooled it
  3. Article
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  5. Article
  6. Article
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  8. Article
  9. Bimodal Age Distribution in Cancer Incidence.World journal of oncology · 2022
    Review
  10. Review
  11. Article
  12. Article
  13. Cancer Prevention in Low-Resource Countries: An Overview of the Opportunity.American Society of Clinical Oncology educational book. American Society of Clinical Oncology. Annual Meeting · 2020
    Article
  14. Article
  15. Article
  16. Exploring the Causes of the Low Incidence of Cervical Cancer in Western AsiaAsian Pacific journal of cancer prevention : APJCP · 2018
    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

6 authors at 1 institution in 1 country.

Ghazi A AlsbeihBiomedical Physics, King Faisal Specialist Hospital & Research Centre, Riyadh, Saudi Arabia.ORCID http://orcid.org/0000-0002-2128-6293
Najla M Al-HarbiBiomedical Physics, King Faisal Specialist Hospital & Research Centre, Riyadh, Saudi Arabia.
Sara S Bin JudiaBiomedical Physics, King Faisal Specialist Hospital & Research Centre, Riyadh, Saudi Arabia.
Hatim A KhojaPathology & Laboratory Medicine, King Faisal Specialist Hospital & Research Centre, Riyadh, Saudi Arabia.
Mohamed M ShoukriNational Biotechnology Centre, King Faisal Specialist Hospital & Research Centre, Riyadh, Saudi Arabia.
Asma M TulbahPathology & Laboratory Medicine, King Faisal Specialist Hospital & Research Centre, Riyadh, Saudi Arabia.
King Faisal Specialist Hospital & Research Centre · SA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCervical cancer is a predominantly human papillomavirus (HPV)-driven disease worldwide. However, its incidence is unexplainably low in western Asia, including Saudi Arabia. Using this paradigm, we investigated the role of HPV infection rate and host genetic predisposition in TP53 G72C single nucleotide polymorphism (SNP) presumed to affect cancer incidence.

methodsPatients treated between 1990 and 2012 were reviewed, and a series of 232 invasive cervical cancer cases were studied and compared with 313 matched controls without cancer. SNP was genotyped by way of direct sequencing. HPV linear array analysis was used to detect and genotype HPV in tumor samples.

resultsThe incidence of cervical cancer revealed bimodal peaks at 42.5 years, with a slighter rebound at 60.8 years. Among all cases, 77% were HPV-positive and 16 HPV genotypes were detected-mostly genotypes 16 (75%) and 18 (9%)-with no difference by age, histology, or geographical region. Although the TP53 G72C genotype was not associated with overall cervical cancer risk, it was significantly associated with HPV positivity (odds ratio, 0.57; 95% confidence interval, 0.36-0.90; P = .016). Furthermore, the variant C allele was significantly overtransmitted in the population (P < .0003).

conclusionCervical cancer incidence displays bimodal curve peaking at a young age with secondary rebound at older age. The combination of relative low HPV infection and variant TP53 72C allele overtransmission provide a plausible explanation for the low incidence of cervical cancer in our population. Therefore, HPV screening and host SNP genotyping may provide more relevant biomarkers to gauge the risk of developing cervical cancer. Cancer 2017;123:2459-66. © 2017 American Cancer Society.

Indexed as

AdenocarcinomaAdultAgedAge DistributionAllelesCarcinoma, Squamous CellFemaleGenetic Predisposition to DiseaseGenotypeHumansIncidenceMiddle AgedOdds RatioPapillomaviridaePapillomavirus InfectionsPolymorphism, Single NucleotideTP53 protein, humanTumor Suppressor Protein p53cancer predispositioncervical cancerHPV genotypinghuman papillomavirussingle nucleotide polymorphismTP53 polymorphism

Identifiers

PMID28393355
PMCPMC5485004
OpenAlexW2607070109

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.