Evidence map›Paper›PMID 23696333›Full record

ReviewJournal of cellular physiology2013

Transcriptional mutagenesis and its potential roles in the etiology of cancer and bacterial antibiotic resistance.

Jordan F Morreall, Lucy Petrova, Paul W Doetsch

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of cellular physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

23 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Microbiology and molecular biology reviews : MMBR · 2024
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Genomic sites hypersensitive to ultraviolet radiation.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  8. Review
  9. Article
  10. Article
  11. Accurate RNA consensus sequencing for high-fidelity detection of transcriptional mutagenesis-induced epimutations.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. 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

3 authors at 1 institution in 1 country.

Jordan F MorreallDepartment of Biochemistry, Emory University School of Medicine, Atlanta, Georgia; Graduate Program in Genetics and Molecular Biology, Emory University, Atlanta, Georgia.
Lucy Petrova
Paul W Doetsch
Emory University · US

Funding

Resistance to UV Damage: Role of Gene RegulationP01ES011163 · NIEHS · EMORY UNIVERSITY · PI DOETSCH, PAUL WILLIAM · 2002 to 2012
$12.6M
PREDOCTORAL TRAINING PROGRAM IN GENETICST32GM008490 · NIGMS · EMORY UNIVERSITY · PI BOSS, JEREMY M. · 1993 to 2022
$8.0M
Radiation-induced DNA Damage and Transcriptional Mutagenesis in Tumor DevelopmentR01CA120288 · NCI · EMORY UNIVERSITY · PI DOETSCH, PAUL WILLIAM · 2007 to 2011
$1.4M
NCI NIH HHS CA120288NCI NIH HHS R01 CA120288NIEHS NIH HHS ES011163NIEHS NIH HHS P01 ES011163NIGMS NIH HHS T32 GM008490
6 · The paper itself

Abstract

Most cells do not undergo continuous cell division and DNA replication, yet they can still acquire novel RNA mutations that can result in the production of mutant proteins and induce a phenotypic change. All cells are frequently subjected to genotoxic insults that give rise to damaged nucleotides which, similarly to DNA replication, can undergo base mispairing during transcription. This mutagenic lesion bypass by RNA polymerase, transcriptional mutagenesis (TM), has been studied in a variety of systems and organisms, and may be involved in diverse pathogenic processes, such as tumorigenesis and the acquisition of bacterial antibiotic resistance. Tumor cells and bacteria within the human body are subject to especially high levels of oxidative stress, which can damage DNA and consequently drive TM. Mutagenesis at the level of transcription may allow cells to escape growth arrest and undergo replication that could permanently establish mutations in DNA in a process called retromutagenesis (RM). Here, we review the broad range of DNA damages which may result in TM including a variety of non-bulky lesions and some bulky lesions, which recent studies indicate may not completely block transcription, and emerging evidence supporting the RM concept in the context of tumorigenesis and antibiotic resistance.

Indexed as

DNA DamageDrug Resistance, BacterialMutagenesisTranscription, GeneticAnimalsCarcinogenesisHumansNeoplasms

Identifiers

PMID23696333
PMCPMC3963475
OpenAlexW1603777453

What OpenQuestion holds

Textmetadata
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.