Evidence map›Paper›PMID 30344308›Full record

ArticleBritish journal of cancer2018

Human papillomavirus type 16 genomic variation in women with subsequent in situ or invasive cervical cancer: prospective population-based study.

Laila Sara Arroyo-Mühr, Camilla Lagheden, Emilie Hultin, Carina Eklund, Hans-Olov Adami, Joakim Dillner, Karin Sundström

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 2 pooled it
1.1field-weighted citation impact, top 21% 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

14 citing papers in PubMed, 2 syntheses or guidelines pooled it, 21 citations in OpenAlex.

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  6. Human papillomavirus negative high grade cervical lesions and cancers: Suggested guidance for HPV testing quality assurance.Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology · 2024
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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

7 authors at 3 institutions in 2 countries.

Laila Sara Arroyo-MührDepartment of Laboratory Medicine, Karolinska Institutet, Stockholm, Sweden.
Camilla LaghedenDepartment of Laboratory Medicine, Karolinska Institutet, Stockholm, Sweden.
Emilie HultinDepartment of Laboratory Medicine, Karolinska Institutet, Stockholm, Sweden.
Carina EklundDepartment of Laboratory Medicine, Karolinska Institutet, Stockholm, Sweden.
Hans-Olov AdamiDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
Joakim DillnerDepartment of Laboratory Medicine, Karolinska Institutet, Stockholm, Sweden.
Karin SundströmDepartment of Laboratory Medicine, Karolinska Institutet, Stockholm, Sweden. Karin.sundstrom@ki.se.ORCID http://orcid.org/0000-0002-6865-0224
Karolinska Institutet · SEKarolinska University Hospital · SEUniversity of Oslo · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHPV genomic variation may be involved in viral carcinogenesis.

methodsIn a national register-based nested case-control study, we retrieved archival smears from baseline cytologically normal women who later developed cancer in situ (CIS), squamous cervical cancer (SCC) or remained free of disease. These smears were previously HPV tested by PCR and HPV16 was the strongest risk factor. We now used the Illumina NextSeq platform to sequence HPV16 genomes in cervical smears from 242 women who later developed CIS/CIN3 (n = 134), SCC (n = 92) or remained healthy (n = 16).

resultsThe median sequence depth per sample was high (11,288×). For 218/242 samples (>90%), we covered ≥80% of the complete HPV16 genome with sequencing median depths of >200×. We identified a wide range of unique isolates and 147 novel SNPs across the 218 samples. Most women (97%) had HPV16 lineage A infection, with the sublineages being A1 (66.1%), A2 (28.9%) and A4 (1.8%), respectively. The least variable gene was the E7 (3.4% variability), where 170/204 case women (83%) displayed a fully conserved sequence. There were no obvious differences by disease outcome (CIS or SCC).

conclusionsWe found a high number of novel SNPs. The E7 gene was hypovariable both among women later developing CIN3/CIS, and SCC, respectively.

Indexed as

Genome, ViralNeoplasm InvasivenessAdolescentAdultCarcinoma in SituCase-Control StudiesFemaleHuman papillomavirus 16HumansINDEL MutationMiddle AgedPolymorphism, Single NucleotideProspective StudiesRegistriesSwedenUterine Cervical Neoplasms

Identifiers

PMID30344308
PMCPMC6219482
OpenAlexW2897576230

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.