Evidence map›Paper›PMID 34399719›Full record

ArticleBMC cancer2021

Possible role of HPV/EBV coinfection in anoikis resistance and development in prostate cancer.

Javid Sadri Nahand, Khadijeh Khanaliha, Hamed Mirzaei, Mohsen Moghoofei, Hossein Bannazadeh Baghi, Maryam Esghaei, Ali Reza Khatami, Maryam Fatemipour, Farah Bokharaei-Salim

Open access · goldAbstract readMulticenter Study
In one paragraph

Article in BMC cancer, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 2 pooled it
5.4field-weighted citation impact, top 3% 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

32 citing papers in PubMed, 2 syntheses or guidelines pooled it, 56 citations in OpenAlex.

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  17. Serum TLR2 and TLR9 in Prostate Cancer Patients in Relation to EBV Status.International journal of molecular sciences · 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

9 authors at 4 institutions in 1 country.

Javid Sadri NahandDepartment of Virology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Khadijeh KhanalihaResearch Center of Pediatric Infectious Diseases, Institute of Immunology and Infectious Diseases, Iran University of Medical Sciences, Tehran, Iran.
Hamed MirzaeiResearch Center for Biochemistry and Nutrition in Metabolic Diseases, Kashan University of Medical Sciences, Kashan, Iran.
Mohsen MoghoofeiInfectious Diseases Research Center, Kermanshah University of Medical Sciences, Kermanshah, Iran.
Hossein Bannazadeh BaghiInfectious and Tropical Diseases Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Maryam EsghaeiDepartment of Virology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Ali Reza KhatamiDepartment of Virology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Maryam FatemipourDepartment of Virology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Farah Bokharaei-SalimDepartment of Virology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran. bokharaei.f@iums.ac.ir.
Iran University of Medical Sciences · IRKashan University of Medical Sciences · IRKermanshah University of Medical Sciences · IRTabriz University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThis study aimed to evaluate the possible role of human papillomavirus (HPV) and Epstein-Barr virus (EBV) coinfection as an etiological factor for prostate cancer (PCa) development.

methodsThis case-control study was conducted on 67 patients with PCa and 40 control subjects. The expression levels of cellular and viral factors involved in inflammation, tumor progression, and metastasis were quantified, using the enzyme-linked immunosorbent assay (ELISA) and quantitative real-time polymerase chain reaction (qRT-PCR) assay.

resultsThe EBV/HPV coinfection was reported in 14.9% of patients in the case group and 7.5% of the control subjects. The high-risk types of HPV, that is, HPV 16 and HPV 18, were responsible for 50 and 30% of HPV/EBV-coinfected PCa cases (n = 10), respectively. No significant relationship was observed between PCa and HPV/EBV coinfection (OR = 2.9, 95% CI: 0.18-45.2, P = 0.31). However, the highest percentage of HPV genome integration was found in the HPV/EBV-coinfected PCa group (8/10; 80%). Also, the mean expression levels of inflammatory factors (IL-17, IL-6, TNF-α, NF-κB, VEGF, ROS, and RNS), anti-apoptotic mediators (Bcl-2 and survivin), and anti-anoikis factors (Twist and N-cadherin) were significantly higher in the HPV/EBV-coinfected PCa group, compared to the non-coinfected PCa cases. Nevertheless, the tumor-suppressor proteins (p53 and pRb) and E-cadherin (inhibitor of anoikis resistance) showed significant downregulations in the HPV/EBV-coinfected PCa group, compared to the non-coinfected PCa cases.

conclusionThe HPV/EBV coinfection may be an etiological factor for PCa through modulation of cellular behaviors.

Indexed as

AnoikisAlphapapillomavirusCase-Control StudiesCoinfectionEpstein-Barr Virus InfectionsFollow-Up StudiesHerpesvirus 4, HumanHumansIranMaleMiddle AgedPapillomavirus InfectionsPrognosisProstatic NeoplasmsAnoikisCo-infectionEpstein-Barr virusHuman papillomavirusInflammationProstate cancer

Identifiers

PMID34399719
PMCPMC8369687
OpenAlexW3194989849

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.