Evidence map›Paper›PMID 30104284›Full record

ArticleGenome research2018

Noncanonical secondary structures arising from non-B DNA motifs are determinants of mutagenesis.

Ilias Georgakopoulos-Soares, Sandro Morganella, Naman Jain, Martin Hemberg, Serena Nik-Zainal

Abstract read
In one paragraph

Article in Genome research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

99 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. HSeeker: an algorithm for systematic H-DNA sequence identification.bioRxiv : the preprint server for biology · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Topographical archetypes of somatic mutagenesis in cancer.bioRxiv : the preprint server for biology · 2026
    Article
  9. Review
  10. Characterization of Z-DNA dynamics across the tree of life.bioRxiv : the preprint server for biology · 2025
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Assessment and Mitigation of CRISPR-Cas9-Induced Nontargeted Translocations.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  20. Article

39 more citing papers are in PubMed but not listed here.

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

5 authors.

Ilias Georgakopoulos-SoaresWellcome Trust Sanger Institute, Wellcome Genome Campus, Hinxton CB10 1SA, United Kingdom.
Sandro MorganellaWellcome Trust Sanger Institute, Wellcome Genome Campus, Hinxton CB10 1SA, United Kingdom.
Naman JainDepartment of Life Sciences, Imperial College London, London SW7 2AZ, United Kingdom.
Martin HembergWellcome Trust Sanger Institute, Wellcome Genome Campus, Hinxton CB10 1SA, United Kingdom.
Serena Nik-ZainalWellcome Trust Sanger Institute, Wellcome Genome Campus, Hinxton CB10 1SA, United Kingdom.

Funding

Cancer Research UK 22932Cancer Research UK 23433Cancer Research UK 23916Wellcome Trust
6 · The paper itself

Abstract

Somatic mutations show variation in density across cancer genomes. Previous studies have shown that chromatin organization and replication time domains are correlated with, and thus predictive of, this variation. Here, we analyze 1809 whole-genome sequences from 10 cancer types to show that a subset of repetitive DNA sequences, called non-B motifs that predict noncanonical secondary structure formation can independently account for variation in mutation density. Combined with epigenetic factors and replication timing, the variance explained can be improved to 43%-76%. Approximately twofold mutation enrichment is observed directly within non-B motifs, is focused on exposed structural components, and is dependent on physical properties that are optimal for secondary structure formation. Therefore, there is mounting evidence that secondary structures arising from non-B motifs are not simply associated with increased mutation density-they are possibly causally implicated. Our results suggest that they are determinants of mutagenesis and increase the likelihood of recurrent mutations in the genome. This analysis calls for caution in the interpretation of recurrent mutations and highlights the importance of taking non-B motifs that can simply be inferred from the reference sequence into consideration in background models of mutability henceforth.

Indexed as

MutagenesisNucleotide MotifsDNA, B-FormHumansNeoplasmsDNA, B-Form

Identifiers

PMID30104284
PMCPMC6120622

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.