Evidence map›Paper›PMID 24705290›Full record

ArticleGenes2014

Mechanisms of base substitution mutagenesis in cancer genomes.

Albino Bacolla, David N Cooper, Karen M Vasquez

Open access · goldAbstract read
In one paragraph

Article in Genes, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

34 citing papers in PubMed, 60 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Histone mutations in cancer.Biochemical Society transactions · 2023
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. *K-means and cluster models for cancer signatures.Biomolecular detection and quantification · 2017
    Article
  20. Base Excision Repair Variants in Cancer.Methods in enzymology · 2017
    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

3 authors at 2 institutions in 2 countries.

Albino BacollaDell Pediatric Research Institute, Division of Pharmacology and Toxicology, College of Pharmacy, The University of Texas at Austin, 1400 Barbara Jordan Blvd., Austin, TX 78723, USA. albino.bacolla@austin.utexas.edu.
David N CooperInstitute of Medical Genetics, School of Medicine, Cardiff University, Cardiff CF14 4XN, UK. cooperDN@cardiff.ac.uk.
Karen M VasquezDell Pediatric Research Institute, Division of Pharmacology and Toxicology, College of Pharmacy, The University of Texas at Austin, 1400 Barbara Jordan Blvd., Austin, TX 78723, USA. karen.vasquez@austin.utexas.edu.
The University of Texas at Austin · USCardiff University · GB

Funding

Recognition and processing of complex lesions by components from multiple DNAP01CA097175 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI WOOD, RICHARD D · 2004 to 2014
$15.3M
REPAIR OF GENOME DESTABILIZING DNA STRUCTURESR01CA093729 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Karen M Vasquez · 2002 to 2026
$8.2M
NCI NIH HHS P01 CA097175NCI NIH HHS R01 CA093729
6 · The paper itself

Abstract

Cancer genome sequence data provide an invaluable resource for inferring the key mechanisms by which mutations arise in cancer cells, favoring their survival, proliferation and invasiveness. Here we examine recent advances in understanding the molecular mechanisms responsible for the predominant type of genetic alteration found in cancer cells, somatic single base substitutions (SBSs). Cytosine methylation, demethylation and deamination, charge transfer reactions in DNA, DNA replication timing, chromatin status and altered DNA proofreading activities are all now known to contribute to the mechanisms leading to base substitution mutagenesis. We review current hypotheses as to the major processes that give rise to SBSs and evaluate their relative relevance in the light of knowledge acquired from cancer genome sequencing projects and the study of base modifications, DNA repair and lesion bypass. Although gene expression data on APOBEC3B enzymes provide support for a role in cancer mutagenesis through U:G mismatch intermediates, the enzyme preference for single-stranded DNA may limit its activity genome-wide. For SBSs at both CG:CG and YC:GR sites, we outline evidence for a prominent role of damage by charge transfer reactions that follow interactions of the DNA with reactive oxygen species (ROS) and other endogenous or exogenous electron-abstracting molecules.

Identifiers

PMID24705290
PMCPMC3978516
OpenAlexW2133226965

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.