Evidence map›Paper›PMID 26160881›Full record

ArticleJournal of the National Cancer Institute2015

Interactions Between High- and Low-Risk HPV Types Reduce the Risk of Squamous Cervical Cancer.

Karin Sundström, Alexander Ploner, Lisen Arnheim-Dahlström, Sandra Eloranta, Juni Palmgren, Hans-Olov Adami, Nathalie Ylitalo Helm, Pär Sparén, Joakim Dillner

Abstract read
In one paragraph

Article in Journal of the National Cancer Institute, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing 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.

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

25 citing papers in PubMed.

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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

9 authors.

Karin SundströmDepartment of Laboratory Medicine (KS, JD), Department of Medical Epidemiology and Biostatistics (AP, LAD, JP, HOA, PS, JD), and Department of Medicine, Clinical Epidemiology Unit (SE), Karolinska Institutet, Stockholm, Sweden; Swedish eScience Research Center, Stockholm, Sweden (JP); Institute for Molecular Medicine Finland, Helsinki University, Helsinki, Finland (JP); Department of Epidemiology, Harvard School of Public Health, Boston, MA (HOA); Division of Clinical Cancer Epidemiology, Department of Oncology, Sahlgrenska University Hospital, Gothenburg, Sweden (NYH). karin.sundstrom@ki.se.
Alexander PlonerDepartment of Laboratory Medicine (KS, JD), Department of Medical Epidemiology and Biostatistics (AP, LAD, JP, HOA, PS, JD), and Department of Medicine, Clinical Epidemiology Unit (SE), Karolinska Institutet, Stockholm, Sweden; Swedish eScience Research Center, Stockholm, Sweden (JP); Institute for Molecular Medicine Finland, Helsinki University, Helsinki, Finland (JP); Department of Epidemiology, Harvard School of Public Health, Boston, MA (HOA); Division of Clinical Cancer Epidemiology, Department of Oncology, Sahlgrenska University Hospital, Gothenburg, Sweden (NYH). karin.sundstrom@ki.se.
Lisen Arnheim-DahlströmDepartment of Laboratory Medicine (KS, JD), Department of Medical Epidemiology and Biostatistics (AP, LAD, JP, HOA, PS, JD), and Department of Medicine, Clinical Epidemiology Unit (SE), Karolinska Institutet, Stockholm, Sweden; Swedish eScience Research Center, Stockholm, Sweden (JP); Institute for Molecular Medicine Finland, Helsinki University, Helsinki, Finland (JP); Department of Epidemiology, Harvard School of Public Health, Boston, MA (HOA); Division of Clinical Cancer Epidemiology, Department of Oncology, Sahlgrenska University Hospital, Gothenburg, Sweden (NYH).
Sandra ElorantaDepartment of Laboratory Medicine (KS, JD), Department of Medical Epidemiology and Biostatistics (AP, LAD, JP, HOA, PS, JD), and Department of Medicine, Clinical Epidemiology Unit (SE), Karolinska Institutet, Stockholm, Sweden; Swedish eScience Research Center, Stockholm, Sweden (JP); Institute for Molecular Medicine Finland, Helsinki University, Helsinki, Finland (JP); Department of Epidemiology, Harvard School of Public Health, Boston, MA (HOA); Division of Clinical Cancer Epidemiology, Department of Oncology, Sahlgrenska University Hospital, Gothenburg, Sweden (NYH).
Juni PalmgrenDepartment of Laboratory Medicine (KS, JD), Department of Medical Epidemiology and Biostatistics (AP, LAD, JP, HOA, PS, JD), and Department of Medicine, Clinical Epidemiology Unit (SE), Karolinska Institutet, Stockholm, Sweden; Swedish eScience Research Center, Stockholm, Sweden (JP); Institute for Molecular Medicine Finland, Helsinki University, Helsinki, Finland (JP); Department of Epidemiology, Harvard School of Public Health, Boston, MA (HOA); Division of Clinical Cancer Epidemiology, Department of Oncology, Sahlgrenska University Hospital, Gothenburg, Sweden (NYH).
Hans-Olov AdamiDepartment of Laboratory Medicine (KS, JD), Department of Medical Epidemiology and Biostatistics (AP, LAD, JP, HOA, PS, JD), and Department of Medicine, Clinical Epidemiology Unit (SE), Karolinska Institutet, Stockholm, Sweden; Swedish eScience Research Center, Stockholm, Sweden (JP); Institute for Molecular Medicine Finland, Helsinki University, Helsinki, Finland (JP); Department of Epidemiology, Harvard School of Public Health, Boston, MA (HOA); Division of Clinical Cancer Epidemiology, Department of Oncology, Sahlgrenska University Hospital, Gothenburg, Sweden (NYH).
Nathalie Ylitalo HelmDepartment of Laboratory Medicine (KS, JD), Department of Medical Epidemiology and Biostatistics (AP, LAD, JP, HOA, PS, JD), and Department of Medicine, Clinical Epidemiology Unit (SE), Karolinska Institutet, Stockholm, Sweden; Swedish eScience Research Center, Stockholm, Sweden (JP); Institute for Molecular Medicine Finland, Helsinki University, Helsinki, Finland (JP); Department of Epidemiology, Harvard School of Public Health, Boston, MA (HOA); Division of Clinical Cancer Epidemiology, Department of Oncology, Sahlgrenska University Hospital, Gothenburg, Sweden (NYH).
Pär SparénDepartment of Laboratory Medicine (KS, JD), Department of Medical Epidemiology and Biostatistics (AP, LAD, JP, HOA, PS, JD), and Department of Medicine, Clinical Epidemiology Unit (SE), Karolinska Institutet, Stockholm, Sweden; Swedish eScience Research Center, Stockholm, Sweden (JP); Institute for Molecular Medicine Finland, Helsinki University, Helsinki, Finland (JP); Department of Epidemiology, Harvard School of Public Health, Boston, MA (HOA); Division of Clinical Cancer Epidemiology, Department of Oncology, Sahlgrenska University Hospital, Gothenburg, Sweden (NYH).
Joakim DillnerDepartment of Laboratory Medicine (KS, JD), Department of Medical Epidemiology and Biostatistics (AP, LAD, JP, HOA, PS, JD), and Department of Medicine, Clinical Epidemiology Unit (SE), Karolinska Institutet, Stockholm, Sweden; Swedish eScience Research Center, Stockholm, Sweden (JP); Institute for Molecular Medicine Finland, Helsinki University, Helsinki, Finland (JP); Department of Epidemiology, Harvard School of Public Health, Boston, MA (HOA); Division of Clinical Cancer Epidemiology, Department of Oncology, Sahlgrenska University Hospital, Gothenburg, Sweden (NYH).

Funding

Prospective study on viral load of cervical cancerR01CA093378 · NCI · KAROLINSKA INSTITUTE · PI ADAMI, HANS-OLOV · 2002 to 2005
$1.5M
Molecular epidemiology of cervical adenocarcinomaR01CA111720 · NCI · KAROLINSKA INSTITUTE · PI ADAMI, HANS-OLOV · 2005 to 2007
$1.2M
NCI NIH HHS 1R01CA093378-01A1NCI NIH HHS 5R01CA111720-03
6 · The paper itself

Abstract

backgroundThe clinical significance of co-infections with high-risk (HR) and low-risk (LR) human papillomavirus (HPV) in the etiology of cervical cancer is debated, as prospective evidence on this issue is limited. However, the question is of increasing relevance in relation to HPV-based cancer prevention.

methodsIn two population-based nested case-control studies among women participating in cervical screening with baseline normal smears, we collected 4659 smears from women who later developed cancer in situ (CIS; n = 524) or squamous cervical cancer (SCC; n = 378) and individually matched control subjects who remained free of disease during study follow-up. The median follow-up until diagnosis was 6.4 to 7.8 years. All smears were tested for HPV. We used conditional logistic regression models with two-way interaction terms to estimate relative risks (RRs) for CIS and SCC, respectively. All statistical tests were two-sided.

resultsCompared with women who were infected with HRHPV only, women who were also infected with LRHPV had a lower risk for SCC (RR = 0.2, 95% confidence interval [CI] = 0.04 to 0.99, P = .049). This interaction was not shown for CIS (RR = 1.1, 95% CI = 0.4 to 3.6). Women who were positive for both HRHPV and LRHPV had, on average, a 4.8 year longer time to diagnosis of SCC than women who were positive for HRHPV only (P = .006). Results were highly robust in sensitivity analyses.

conclusionCo-infection with LRHPV is associated with a lower risk of future invasive disease and longer time to diagnosis than infection with HRHPV alone. We propose that co-infection with LRHPV interferes with the rate of progression to invasive cervical cancer.

Indexed as

AdolescentAdultAgedAged, 80 and overCarcinoma in SituCarcinoma, Squamous CellCase-Control StudiesDNA, ViralFemaleFollow-Up StudiesHumansMiddle AgedPapillomaviridaePapillomavirus InfectionsPolymerase Chain ReactionRegistriesDNA, Viral

Identifiers

PMID26160881
PMCPMC5964715

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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.