Evidence map›Paper›PMID 30515767›Full record

ArticleInternational journal of cancer2019

Genetic variations in human papillomavirus and cervical cancer outcomes.

Janet S Rader, Shirng-Wern Tsaih, Daniel Fullin, Miriam W Murray, Marissa Iden, Michael T Zimmermann, Michael J Flister

Abstract read
In one paragraph

Article in International journal of cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 2 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

28 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
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  15. HPV positivity status in males is related to the acquisition of HPV infection in females in heterosexual couples.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 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.

Janet S RaderDepartment of Obstetrics and Gynecology, Medical College of Wisconsin, Milwaukee, WI, USA.
Shirng-Wern TsaihDepartment of Physiology, Medical College of Wisconsin, Milwaukee, WI, USA.
Daniel FullinDepartment of Obstetrics and Gynecology, Medical College of Wisconsin, Milwaukee, WI, USA.
Miriam W MurrayDepartment of Obstetrics and Gynecology, Medical College of Wisconsin, Milwaukee, WI, USA.
Marissa IdenDepartment of Obstetrics and Gynecology, Medical College of Wisconsin, Milwaukee, WI, USA.ORCID 0000-0003-3383-1751
Michael T ZimmermannGenomics Sciences and Precision Medicine Center, Medical College of Wisconsin, Milwaukee, WI, USA.
Michael J FlisterDepartment of Physiology, Medical College of Wisconsin, Milwaukee, WI, USA.

Funding

Leveraging genetic mapping for personalized targeting of breast cancer microenvironmentR01CA193343 · NCI · MEDICAL COLLEGE OF WISCONSIN · PI Amit Joshi · 2015 to 2026
$3.5M
Genetic Susceptibility to Cervical CancerR01CA095713 · NCI · WASHINGTON UNIVERSITY · PI RADER, JANET S. · 2003 to 2009
$1.8M
NCI NIH HHS R01 CA095713NCI NIH HHS R01 CA193343
6 · The paper itself

Abstract

Cervical cancer is driven by persistent infection of human papillomavirus (HPV), which is influenced by HPV type and intratypic variants, yet the impact of HPV type and intratypic variants on patient outcomes is far less understood. Here, we examined the association of cervical cancer stage and survival with HPV type, clade, lineage, and intratypic variants within the HPV E6 locus. Of 1,028 HPV-positive cases recruited through the CerGE study, 301 were in-situ and 727 were invasive cervical cancer (ICC), with an average post-diagnosis follow-up of 4.8 years. HPV sequencing was performed using tumor-isolated DNA to assign HPV type, HPV 16 lineage, clade, and intratypic variants within the HPV 16 E6 locus, of which nonsynonomous variants were functionally annotated by molecular modeling. HPV 18-related types were more prevalent in ICC compared to in-situ disease and associated with significantly worse recurrence-free survival (RFS) compared to HPV 16-related types. The HPV 16 Asian American lineage D3 and Asian lineage A4 associated more frequently with ICC than with in situ disease and women with an intratypic HPV 16 lineage B exhibited a trend toward worse RFS than those with A, C, or D lineages. Participants with intratypic E6 variants predicted to stabilize the E6-E6AP-p53 complex had worse RFS. Variants within the highly immunogenic HPV 16 E6 region (E14-I34) were enriched in ICC compared to in-situ lesions but were not associated with survival. Collectively, our results suggest that cervical cancer outcome is associated with HPV variants that affect virus-host interactions.

Indexed as

AdultBase SequenceDNA-Binding ProteinsDNA, ViralFemaleGenetic VariationHuman papillomavirus 16Human papillomavirus 18HumansOncogene Proteins, ViralPapillomavirus InfectionsProtein BindingRepressor ProteinsSequence Analysis, DNAUterine Cervical NeoplasmsDNA-Binding ProteinsDNA, ViralE6 protein, Human papillomavirus type 16E6 protein, Human papillomavirus type 18Oncogene Proteins, ViralRepressor Proteinscancer riskcervical cancerE6 oncoproteinHPV typesHPV variantshuman papillomavirus (HPV)patient outcome

Identifiers

PMID30515767
PMCPMC6450540

What OpenQuestion holds

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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.