Evidence map›Paper›PMID 17675364›Full record

ArticleGenome research2007

Architectures of somatic genomic rearrangement in human cancer amplicons at sequence-level resolution.

Graham R Bignell, Thomas Santarius, Jessica C M Pole, Adam P Butler, Janet Perry, Erin Pleasance, Chris Greenman, Andrew Menzies, Sheila Taylor, Sarah Edkins and 10 more

Open access · bronzeAbstract read
In one paragraph

Article in Genome research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers.

0numbers the graph read from it
0cells of the map it votes in
117citing papers in PubMed
–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

117 citing papers in PubMed, 199 citations in OpenAlex.

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57 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

20 authors at 3 institutions in 1 country.

Graham R BignellWellcome Trust Sanger Institute, Hinxton, Cambridge, CB10 1SA, United Kingdom.
Thomas Santarius
Jessica C M Pole
Adam P Butler
Janet Perry
Erin Pleasance
Chris Greenman
Andrew Menzies
Sheila Taylor
Sarah Edkins
Peter Campbell
Michael Quail
Bob Plumb
Lucy Matthews
Kirsten McLay
Paul A W Edwards
Jane Rogers
Richard Wooster
P Andrew Futreal
Michael R Stratton
Wellcome Sanger Institute · GBUniversity of Cambridge · GBInstitute of Cancer Research · GB

Funding

Wellcome Trust 088340
6 · The paper itself

Abstract

For decades, cytogenetic studies have demonstrated that somatically acquired structural rearrangements of the genome are a common feature of most classes of human cancer. However, the characteristics of these rearrangements at sequence-level resolution have thus far been subject to very limited description. One process that is dependent upon somatic genome rearrangement is gene amplification, a mechanism often exploited by cancer cells to increase copy number and hence expression of dominantly acting cancer genes. The mechanisms underlying gene amplification are complex but must involve chromosome breakage and rejoining. We sequenced 133 different genomic rearrangements identified within four cancer amplicons involving the frequently amplified cancer genes MYC, MYCN, and ERBB2. The observed architectures of rearrangement were diverse and highly distinctive, with evidence for sister chromatid breakage-fusion-bridge cycles, formation and reinsertion of double minutes, and the presence of bizarre clusters of small genomic fragments. There were characteristic features of sequences at the breakage-fusion junctions, indicating roles for nonhomologous end joining and homologous recombination-mediated repair mechanisms together with nontemplated DNA synthesis. Evidence was also found for sequence-dependent variation in susceptibility of the genome to somatic rearrangement. The results therefore provide insights into the DNA breakage and repair processes operative in somatic genome rearrangement and illustrate how the evolutionary histories of individual cancers can be reconstructed from large-scale cancer genome sequencing.

Indexed as

DNA DamageDNA, NeoplasmDNA RepairGene RearrangementGenome, HumanBase PairingCell Line, TumorCell Transformation, NeoplasticChromosome AberrationsChromosomes, Artificial, BacterialChromosomes, HumanFemaleGene DosageGenetic VariationHumansIn Situ Hybridization, FluorescenceDNA, Neoplasm

Identifiers

PMID17675364
PMCPMC1950898
OpenAlexW2164291580

What OpenQuestion holds

Textmetadata
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.