Evidence map›Paper›PMID 36298660›Full record

ReviewViruses2022

Viral Agents as Potential Drivers of Diffuse Large B-Cell Lymphoma Tumorigenesis.

Esma Bilajac, Lejla Mahmutović, Kenneth Lundstrom, Una Glamočlija, Jasmin Šutković, Abas Sezer, Altijana Hromić-Jahjefendić

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Viruses, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.7field-weighted citation impact, top 28% 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

5 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
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 at 2 institutions in 1 country.

Esma BilajacDepartment of Genetics and Bioengineering, Faculty of Engineering and Natural Sciences, International University of Sarajevo, Hrasnička cesta 15, 71000 Sarajevo, Bosnia and Herzegovina.
Lejla MahmutovićDepartment of Genetics and Bioengineering, Faculty of Engineering and Natural Sciences, International University of Sarajevo, Hrasnička cesta 15, 71000 Sarajevo, Bosnia and Herzegovina.ORCID 0000-0002-7358-5009
Kenneth LundstromPanTherapeutics, Route de Lavaux 49, CH1095 Lutry, Switzerland.
Una GlamočlijaDepartment of Pharmaceutical Biochemistry and Laboratory Diagnostics, University of Sarajevo, Faculty of Pharmacy, Zmaja od Bosne 8, 71 000 Sarajevo, Bosnia and Herzegovina.
Jasmin ŠutkovićDepartment of Genetics and Bioengineering, Faculty of Engineering and Natural Sciences, International University of Sarajevo, Hrasnička cesta 15, 71000 Sarajevo, Bosnia and Herzegovina.ORCID 0000-0001-9962-6908
Abas SezerDepartment of Genetics and Bioengineering, Faculty of Engineering and Natural Sciences, International University of Sarajevo, Hrasnička cesta 15, 71000 Sarajevo, Bosnia and Herzegovina.
Altijana Hromić-JahjefendićDepartment of Genetics and Bioengineering, Faculty of Engineering and Natural Sciences, International University of Sarajevo, Hrasnička cesta 15, 71000 Sarajevo, Bosnia and Herzegovina.
International University of Sarajevo · BAUniversity of Sarajevo · BA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Among numerous causative agents recognized as oncogenic drivers, 13% of total cancer cases occur as a result of viral infections. The intricacy and diversity of carcinogenic processes, however, raise significant concerns about the mechanistic function of viruses in cancer. All tumor-associated viruses have been shown to encode viral oncogenes with a potential for cell transformation and the development of malignancies, including diffuse large B-cell lymphoma (DLBCL). Given the difficulties in identifying single mechanistic explanations, it is necessary to combine ideas from systems biology and viral evolution to comprehend the processes driving viral cancer. The potential for more efficient and acceptable therapies lies in targeted medicines that aim at viral proteins or trigger immune responses to either avoid infection or eliminate infected or cancerous cells. In this review, we aim to describe the role of viral infections and their mechanistic approaches in DLBCL tumorigenesis. To the best of our knowledge, this is the first review summarizing the oncogenic potential of numerous viral agents in DLBCL development.

Indexed as

Epstein-Barr Virus InfectionsLymphoma, Large B-Cell, DiffuseCarcinogenesisHerpesvirus 4, HumanHumansOncogenic VirusesViral ProteinsViral Proteinsdiffuse large B-cell lymphomaEpstein–Barr virushepatitis viruseshuman immunodeficiency virushuman T-cell leukemia virus type 1simian virus 40viral infectionsvirus-induced tumorigenesis

Identifiers

PMID36298660
PMCPMC9610751
OpenAlexW4296826646

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.