Evidence map›Paper›PMID 35141704›Full record

ArticleFrontiers in virology (Lausanne, Switzerland)2021

Oncogenic Viruses as Entropic Drivers of Cancer Evolution.

Italo Tempera, Paul M Lieberman

Open access · goldAbstract read
In one paragraph

Article in Frontiers in virology (Lausanne, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
6.6field-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

31 citing papers in PubMed, 46 citations in OpenAlex.

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  7. [Clinical Progress and Prospects of mRNA Tumor Drugs].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2026
    Review
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  20. High Risk of Heart Tumors after COVID-19.Life (Basel, Switzerland) · 2023
    Article
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

2 authors at 1 institution in 1 country.

Italo TemperaProgram in Gene Expression and Regulation, The Wistar Institute, Philadelphia, PA, United States.
Paul M LiebermanProgram in Gene Expression and Regulation, The Wistar Institute, Philadelphia, PA, United States.
The Wistar Institute · US

Funding

Regulation of Epstein-Barr Virus LatencyR01CA093606 · NCI · WISTAR INSTITUTE · PI LIEBERMAN, PAUL M. · 2002 to 2022
$6.7M
Epigenetic Regulation of Epstein-Barr Virus Latency ProgramsR01DE017336 · NIDCR · WISTAR INSTITUTE · PI PAUL M. LIEBERMAN · 2005 to 2026
$6.5M
Regulation of KSHV LatencyR01CA117830 · NCI · WISTAR INSTITUTE · PI PAUL M. LIEBERMAN · 2006 to 2026
$6.4M
Regulation of Viral Chromatin Architecture During EBV LatencyR01AI130209 · NIAID · WISTAR INSTITUTE · PI Italo Tempera · 2018 to 2026
$3.8M
Regulation of EBV Latency by Purine Metabolism and SignalingR01AI153508 · NIAID · WISTAR INSTITUTE · PI TEMPERA, ITALO · 2021 to 2025
$2.3M
Regulation of PRC2 functions by PARP1R01GM124449 · NIGMS · WISTAR INSTITUTE · PI TEMPERA, ITALO · 2017 to 2021
$1.8M
Role of Nuclear Lamina in the epigenetic regulation of Epstein-Barr Virus InfectionR21AI122035 · NIAID · TEMPLE UNIV OF THE COMMONWEALTH · PI TEMPERA, ITALO · 2016 to 2017
$429k
NCI NIH HHS R01 CA093606NCI NIH HHS R01 CA117830NIAID NIH HHS R01 AI130209NIAID NIH HHS R01 AI153508NIAID NIH HHS R21 AI122035NIDCR NIH HHS R01 DE017336NIGMS NIH HHS R01 GM124449
6 · The paper itself

Abstract

Viral infection is an indisputable causal factor for nearly 17% of all human cancers. However, the diversity and complexity of oncogenic mechanisms raises new questions as to the mechanistic role of viruses in cancer. Classical viral oncogenes have been identified for all tumor-associated viruses. These oncogenes can have multiple oncogenic activities that may or may not be utilized in a particular tumor cell. In addition, stochastic events, like viral mutation and integration, as well as heritable host susceptibilities and immune deficiencies are also implicated in tumorigenesis. A more contemporary view of tumor biology highlights the importance of evolutionary forces that select for phenotypes better adapted to a complex and changing environment. Given the challenges of prioritizing singular mechanistic causes, it may be necessary to integrate concepts from evolutionary theory and systems biology to better understand viral cancer-driving forces. Here, we propose that viral infection provides a biological "entropy" that increases genetic variation and phenotypic plasticity, accelerating the main driving forces of cancer cell evolution. Viruses can also influence the evolutionary selection criteria by altering the tumor microenvironment and immune signaling. Utilizing concepts from cancer cell evolution, population genetics, thermodynamics, and systems biology may provide new perspectives on viral oncogenesis and identify novel therapeutic strategies for treating viruses and cancer.

Indexed as

cancerEBV–Epstein-Barr virusepigenetichepatitis B virusHPV–human papillomavirusKSHVMerkel cancerplasticity

Identifiers

PMID35141704
PMCPMC8822580
OpenAlexW3211777932

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.