Evidence map›Paper›PMID 23975201›Full record

ArticleNucleic acids research2013

Homology-mediated end-capping as a primary step of sister chromatid fusion in the breakage-fusion-bridge cycles.

Michael Marotta, Xiongfong Chen, Takaaki Watanabe, Pieter W Faber, Scott J Diede, Stephen Tapscott, Raymond Tubbs, Anna Kondratova, Robert Stephens, Hisashi Tanaka

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

17 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Palindromes in DNA-A Risk for Genome Stability and Implications in Cancer.International journal of molecular sciences · 2021
    Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. 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

10 authors at 5 institutions in 1 country.

Michael MarottaDepartment of Molecular Genetics, Cleveland Clinic Lerner Research Institute, Cleveland, OH 44195, USA, Advanced Biomedical Computing Center, SAIC-Frederick, Inc., Frederick, MD 21702, USA, Genomics Facility, University of Chicago, Chicago, IL 60637, USA, Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA, Department of Molecular Pathology, Cleveland Clinic, Cleveland, OH 44195, USA and Department of Molecular Medicine, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH 44195, USA.
Xiongfong Chen
Takaaki Watanabe
Pieter W Faber
Scott J Diede
Stephen Tapscott
Raymond Tubbs
Anna Kondratova
Robert Stephens
Hisashi Tanaka
Cleveland Clinic Lerner College of Medicine · USFred Hutch Cancer Center · USCancer Research Center · USCase Western Reserve University · USUniversity of Chicago · US

Funding

TUMOR METABOLISM PROGRAMP30CA043703 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI MARK R CHANCE · 1987 to 2026
$142.3M
Mechanisms of gene amplification in human cancersR01CA149385 · NCI · CLEVELAND CLINIC LERNER COM-CWRU · PI TANAKA, HISASHI · 2010 to 2022
$3.4M
NCI NIH HHS P30 CA043703NCI NIH HHS R01 CA149385NCI NIH HHS R01CA149385
6 · The paper itself

Abstract

Breakage-fusion-bridge (BFB) cycle is a series of chromosome breaks and duplications that could lead to the increased copy number of a genomic segment (gene amplification). A critical step of BFB cycles leading to gene amplification is a palindromic fusion of sister chromatids following the rupture of a dicentric chromosome during mitosis. It is currently unknown how sister chromatid fusion is produced from a mitotic break. To delineate the process, we took an integrated genomic, cytogenetic and molecular approach for the recurrent MCL1 amplicon at chromosome 1 in human tumor cells. A newly developed next-generation sequencing-based approach identified a cluster of palindromic fusions within the amplicon at ∼50-kb intervals, indicating a series of breaks and fusions by BFB cycles. The physical location of the amplicon (at the end of a broken chromosome) further indicated BFB cycles as underlying processes. Three palindromic fusions were mediated by the homologies between two nearby inverted Alu repeats, whereas the other two fusions exhibited microhomology-mediated events. Such breakpoint sequences indicate that homology-mediated fold-back capping of broken ends followed by DNA replication is an underlying mechanism of sister chromatid fusion. Our results elucidate nucleotide-level events during BFB cycles and end processing for naturally occurring mitotic breaks.

Indexed as

Chromosome BreakageCell LineCell Line, TumorChromatidsChromosome BreakpointsGene AmplificationGenomicsHumansInverted Repeat Sequences

Identifiers

PMID23975201
PMCPMC3834830
OpenAlexW2022394720

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.