Evidence map›Paper›PMID 34071792›Full record

ReviewCancers2021

Virus-Driven Carcinogenesis.

Yuichiro Hatano, Takayasu Ideta, Akihiro Hirata, Kayoko Hatano, Hiroyuki Tomita, Hideshi Okada, Masahito Shimizu, Takuji Tanaka, Akira Hara

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
4.4field-weighted citation impact, top 4% 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

35 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
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  13. Article
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  15. The Pathology according to p53 Pathway.Pathobiology : journal of immunopathology, molecular and cellular biology · 2024
    Review
  16. Article
  17. Article
  18. Article
  19. 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

9 authors at 3 institutions in 1 country.

Yuichiro HatanoDepartment of Tumor Pathology, Gifu University Graduate School of Medicine, Gifu 501-1194, Japan.ORCID 0000-0002-5121-6325
Takayasu IdetaDepartment of Gastroenterology, Gifu University Graduate School of Medicine, Gifu 501-1194, Japan.
Akihiro HirataLaboratory of Veterinary Pathology, Joint Department of Veterinary Medicine, Faculty of Applied Biological Sciences, Gifu University, Gifu 501-1194, Japan.
Kayoko HatanoDepartment of Obstetrics and Gynecology, Gifu University Hospital, Gifu 501-1194, Japan.
Hiroyuki TomitaDepartment of Tumor Pathology, Gifu University Graduate School of Medicine, Gifu 501-1194, Japan.ORCID 0000-0002-3291-0274
Hideshi OkadaDepartment of Emergency and Disaster Medicine, Gifu University Graduate School of Medicine, Gifu 501-1194, Japan.ORCID 0000-0002-7775-4308
Masahito ShimizuDepartment of Gastroenterology, Gifu University Graduate School of Medicine, Gifu 501-1194, Japan.ORCID 0000-0002-1151-2058
Takuji TanakaDepartment of Diagnostic Pathology (DDP) and Research Center of Diagnostic Pathology (RC-DiP), Gifu Municipal Hospital, Gifu 500-8513, Japan.ORCID 0000-0002-1428-1582
Akira HaraDepartment of Tumor Pathology, Gifu University Graduate School of Medicine, Gifu 501-1194, Japan.ORCID 0000-0002-5554-8060
Gifu University · JPGifu Municipal Hospital · JPGifu University Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer arises from the accumulation of genetic and epigenetic alterations. Even in the era of precision oncology, carcinogens contributing to neoplastic process are still an important focus of research. Comprehensive genomic analyses have revealed various combinations of base substitutions, referred to as the mutational signatures, in cancer. Each mutational signature is believed to arise from specific DNA damage and repair processes, including carcinogens. However, as a type of carcinogen, tumor viruses increase the cancer risk by alternative mechanisms, including insertional mutagenesis, viral oncogenes, and immunosuppression. In this review, we summarize virus-driven carcinogenesis to provide a framework for the control of malignant cell proliferation. We first provide a brief overview of oncogenic viruses and describe their implication in virus-related tumors. Next, we describe tumor viruses (HPV, Human papilloma virus; HBV, Hepatitis B virus; HCV, Hepatitis C virus; EBV, Epstein-Barr virus; Kaposi sarcoma herpesvirus; MCV, Merkel cell polyoma virus; HTLV-1, Human T-cell lymphotropic virus, type-1) and tumor virus-related cancers. Lastly, we introduce emerging tumor virus candidates, human cytomegalovirus (CMV), human herpesvirus-6 (HHV-6) and adeno-associated virus-2 (AAV-2). We expect this review to be a hub in a complex network of data for virus-associated carcinogenesis.

Indexed as

EBVHBVHCVHIV-1HPVHTLV-1KSHVMCVtumor virus

Identifiers

PMID34071792
PMCPMC8198641
OpenAlexW3165066172

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.