Evidence map›Paper›PMID 29735283›Full record

ReviewTrends in genetics : TIG2018

Break-Induced Replication: The Where, The Why, and The How.

J Kramara, B Osia, A Malkova

Abstract readReview
In one paragraph

Review in Trends in genetics : TIG, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 168 papers.

0numbers the graph read from it
0cells of the map it votes in
168citing papers in PubMed
11.0field-weighted citation impact, top 1% 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

168 citing papers in PubMed, 243 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Mechanisms and genomic implications of break-induced replication.Nature structural & molecular biology · 2025
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Monomers and short oligomers of human RAD52 promote single-strand annealing.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  18. Article
  19. Article
  20. Biomedicines · 2025
    Article

108 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

3 authors at 1 institution in 1 country.

J KramaraThese authors contributed equally to this work.
B OsiaThese authors contributed equally to this work.
A MalkovaDepartment of Biology, University of Iowa, Iowa City, IA 52242, USA. Electronic address: anna-malkova@uiowa.edu.
University of Iowa · US

Funding

Viral VectorP30CA086862 · NCI · UNIVERSITY OF IOWA · PI Christopher K Laubenthal · 2000 to 2026
$70.0M
Double strand break repair maelstrom: causes, mechanisms and genome destabilizing consequencesR35GM127006 · NIGMS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Anna L Malkova · 2018 to 2026
$3.8M
Amplification of risk resulting from mis-routing of double-strand break repairR01GM084242 · NIGMS · UNIVERSITY OF IOWA · PI MALKOVA, ANNA L · 2008 to 2017
$2.7M
Suppressors and drivers of long-tract repair DNA synthesisR03ES029306 · NIEHS · UNIVERSITY OF IOWA · PI MALKOVA, ANNA L · 2018 to 2019
$153k
NIEHS NIH HHS R03 ES029306NIGMS NIH HHS R01 GM084242NIGMS NIH HHS R35 GM127006
6 · The paper itself

Abstract

Break-induced replication (BIR) is a pathway that repairs one-ended double-strand breaks (DSBs). For decades, yeast model systems offered the only opportunities to study eukaryotic BIR. These studies described an unusual mode of BIR synthesis that is carried out by a migrating bubble and shows conservative inheritance of newly synthesized DNA, leading to genomic instabilities like those associated with cancer in humans. Yet, evidence of BIR functioning in mammals or during repair of other DNA breaks has been missing. Recent studies have uncovered multiple examples of BIR working in replication restart and repair of eroded telomeres in yeast and mammals, as well as some unexpected findings, including the RAD51 independence of BIR. Strong interest remains in determining the variations in molecular mechanisms that drive and regulate BIR in different genetic backgrounds, across organisms, and particularly in the context of human disease.

Indexed as

AnimalsDNA Breaks, Double-StrandedDNA RepairDNA ReplicationGenomic InstabilityHumansRecombination, GeneticTelomerealternative lengthening of telomeresBreak-induced replicationMMBIRmutation clusterRad51-dependent BIRRAD51-independent BIR

Identifiers

PMID29735283
PMCPMC6469874
OpenAlexW2800503833

What OpenQuestion holds

Textmetadata
LicenceTDM
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.