Evidence map›Paper›PMID 28036379›Full record

ArticlePloS one2016

Different Association of Human Papillomavirus 16 Variants with Early and Late Presentation of Cervical Cancer.

Ana Alfaro, Eligia Juárez-Torres, Ingrid Medina-Martínez, Norma Mateos-Guerrero, Maura Bautista-Huerta, Edgar Román-Bassaure, Nicolás Villegas-Sepúlveda, Jaime Berumen

Abstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
–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.

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

8 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  4. Review
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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

8 authors.

Ana AlfaroUnidad de Medicina Genómica, Facultad de Medicina, Universidad Nacional Autónoma de México / Hospital General de México, México City, México.
Eligia Juárez-TorresUnidad de Medicina Genómica, Facultad de Medicina, Universidad Nacional Autónoma de México / Hospital General de México, México City, México.
Ingrid Medina-MartínezUnidad de Medicina Genómica, Facultad de Medicina, Universidad Nacional Autónoma de México / Hospital General de México, México City, México.
Norma Mateos-GuerreroUnidad de Medicina Genómica, Facultad de Medicina, Universidad Nacional Autónoma de México / Hospital General de México, México City, México.
Maura Bautista-HuertaUnidad de Medicina Genómica, Facultad de Medicina, Universidad Nacional Autónoma de México / Hospital General de México, México City, México.
Edgar Román-BassaureServicio de Oncología, Hospital General de México, México City, México.
Nicolás Villegas-SepúlvedaDepartamento de Biomedicina Molecular, Centro de Investigación y Estudios Avanzados del Instituto Politécnico Nacional, México City, México.
Jaime BerumenUnidad de Medicina Genómica, Facultad de Medicina, Universidad Nacional Autónoma de México / Hospital General de México, México City, México.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The median age of cervical cancer (CC) presentation coincides with the mean age of menopause presentation (49 years) in Mexico. Here, we investigated the association between different HPV16 variants and early (≤ 49 years) or delayed (≥ 50 years) CC presentation. We conducted a case-case study that included 462 CCs, 386 squamous cell carcinomas (SCC), 63 adenocarcinomas (ACC), and 13 additional cell types. Variants were identified by PCR and DNA sequencing. The risk conferred by each variant for developing CC earlier than 50 years was analyzed using a univariate logistic regression model considering old-aged patients (≥ 50 years) and non-HPV16 cases as the reference variables. Overall, the frequency of HPV16 was 50.9%, and the only identified variants were the European A1/2 (31.2%) and the Asian-American D2 (10.8%), and D3 (8.9%). D2 was mainly associated with ≤ 49-year-old patients (15.9%); A1/2 was uniformly distributed between the two age groups (~31%), whereas D3 increased with age to a frequency of 11.8% in the older group. Only the D2 variant conferred a 3.3-fold increase in the risk of developing CC before 50 years of age (OR = 3.3, 95% CI = 1.7-6.6, p < 0.001) in relation with non-HPV16 cases. Remarkably, this risk was higher for ACC (OR = 6.0, 95% CI = 1.1-33, p < 0.05) than for SCC (OR = 2.8, 95% CI = 1.3-5.9, p < 0.01). Interestingly, when analyzing only the HPV16-positive CC, D2 increases (OR = 2.5, 95% CI = 1.2-5, p < 0.05) and D3 decreases (OR = 0.45, 95% CI 0.2-0.9, p < 0.05) the risk to develop CC before 50 years old in relation with A1/2 variant. These results indicated that D2 variant is associated with early and D3 with delayed CC presentation, whereas A1/2 variant was uniformly distributed between the two age groups.

Indexed as

AdenocarcinomaAdultAgedAged, 80 and overAge FactorsBase SequenceCarcinoma, Squamous CellDNA, ViralFemaleGenetic VariationHuman papillomavirus 16HumansMexicoMiddle AgedPapillomavirus InfectionsRisk FactorsDNA, Viral

Identifiers

PMID28036379
PMCPMC5201311

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Registered trials

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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.