Evidence map›Paper›PMID 19183484›Full record

ArticleBMC genomics2009

Over half of breakpoints in gene pairs involved in cancer-specific recurrent translocations are mapped to human chromosomal fragile sites.

Allison A Burrow, Laura E Williams, Levi C T Pierce, Yuh-Hwa Wang

Open access · goldAbstract read
In one paragraph

Article in BMC genomics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
4.8field-weighted citation impact, top 5% 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

67 citing papers in PubMed, 105 citations in OpenAlex.

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  12. Coordinating DNA Replication and Mitosis through Ubiquitin/SUMO and CDK1.International journal of molecular sciences · 2021
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  17. Review
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7 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

4 authors at 2 institutions in 1 country.

Allison A BurrowDepartment of Biochemistry, Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157-1016, USA. aburrow@wfubmc.edu
Laura E Williams
Levi C T Pierce
Yuh-Hwa Wang
Wake Forest University · USUniversity of Kansas · US

Funding

The Role of Fragile Sites in RET/PTC RearrangementR01CA113863 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI WANG, YUH-HWA · 2006 to 2018
$2.5M
MOLECULAR STUDIES OF CANCER SPECIFIC FRAGILE SITESR01CA085826 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI WANG, YUH-HWA · 2000 to 2008
$2.0M
Structural and Computational Biophysics Training ProgramT32GM095440 · NIGMS · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI HOLLIS, THOMAS J, LYLES, DOUGLAS S. · 2011 to 2020
$1.7M
NCI NIH HHS CA113863NCI NIH HHS CA85826NCI NIH HHS R01 CA085826NCI NIH HHS R01 CA113863NIGMS NIH HHS T32 GM095440
6 · The paper itself

Abstract

backgroundGene rearrangements such as chromosomal translocations have been shown to contribute to cancer development. Human chromosomal fragile sites are regions of the genome especially prone to breakage, and have been implicated in various chromosome abnormalities found in cancer. However, there has been no comprehensive and quantitative examination of the location of fragile sites in relation to all chromosomal aberrations.

resultsUsing up-to-date databases containing all cancer-specific recurrent translocations, we have examined 444 unique pairs of genes involved in these translocations to determine the correlation of translocation breakpoints and fragile sites in the gene pairs. We found that over half (52%) of translocation breakpoints in at least one gene of these gene pairs are mapped to fragile sites. Among these, we examined the DNA sequences within and flanking three randomly selected pairs of translocation-prone genes, and found that they exhibit characteristic features of fragile DNA, with frequent AT-rich flexibility islands and the potential of forming highly stable secondary structures.

conclusionOur study is the first to examine gene pairs involved in all recurrent chromosomal translocations observed in tumor cells, and to correlate the location of more than half of breakpoints to positions of known fragile sites. These results provide strong evidence to support a causative role for fragile sites in the generation of cancer-specific chromosomal rearrangements.

Indexed as

Chromosome BreakageChromosome Fragile SitesTranslocation, GeneticComputational BiologyDatabases, GeneticDNAGenome, HumanHumansNeoplasmsNucleic Acid ConformationSequence Analysis, DNADNA

Identifiers

PMID19183484
PMCPMC2642838
OpenAlexW2131195660

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.