Evidence map›Paper›PMID 22514011›Full record

ArticleThe Journal of pathology2012

Tandem duplication of chromosomal segments is common in ovarian and breast cancer genomes.

David J McBride, Dariush Etemadmoghadam, Susanna L Cooke, Kathryn Alsop, Joshy George, Adam Butler, Juok Cho, Danushka Galappaththige, Chris Greenman, Karen D Howarth and 12 more

Abstract readComparative Study
In one paragraph

Article in The Journal of pathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing 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

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

  1. Homologous Recombination Deficiency in Pancreatic Cancer: A Systematic Review and Prevalence Meta-Analysis.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2021
    Pooled it
  2. The association of rs25487 of theBiomolecules & biomedicine · 2025
    Article
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  13. Review
  14. Molecular subtypes of pancreatic cancer.Nature reviews. Gastroenterology & hepatology · 2019
    Review
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  16. Article
  17. Article
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  19. Article
  20. Shelterin components mediate genome reorganization in response to replication stress.Proceedings of the National Academy of Sciences of the United States of America · 2017
    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

22 authors.

David J McBrideCancer Genome Project, Wellcome Trust Sanger Institute, Hinxton, Cambridge, UK. david.bowtell@petermac.org
Dariush Etemadmoghadam
Susanna L Cooke
Kathryn Alsop
Joshy George
Adam Butler
Juok Cho
Danushka Galappaththige
Chris Greenman
Karen D Howarth
King W Lau
Charlotte K Ng
Keiran Raine
Jon Teague
David C Wedge
Australian Ovarian Cancer Study Group
Xavier Caubit
Michael R Stratton
James D Brenton
Peter J Campbell
P Andrew Futreal
David Dl Bowtell

Funding

Cancer Research UK 15601Wellcome Trust 077012/Z/05/ZWellcome Trust 088340Wellcome Trust 093867
6 · The paper itself

Abstract

The application of paired-end next generation sequencing approaches has made it possible to systematically characterize rearrangements of the cancer genome to base-pair level. Utilizing this approach, we report the first detailed analysis of ovarian cancer rearrangements, comparing high-grade serous and clear cell cancers, and these histotypes with other solid cancers. Somatic rearrangements were systematically characterized in eight high-grade serous and five clear cell ovarian cancer genomes and we report here the identification of > 600 somatic rearrangements. Recurrent rearrangements of the transcriptional regulator gene, TSHZ3, were found in three of eight serous cases. Comparison to breast, pancreatic and prostate cancer genomes revealed that a subset of ovarian cancers share a marked tandem duplication phenotype with triple-negative breast cancers. The tandem duplication phenotype was not linked to BRCA1/2 mutation, suggesting that other common mechanisms or carcinogenic exposures are operative. High-grade serous cancers arising in women with germline BRCA1 or BRCA2 mutation showed a high frequency of small chromosomal deletions. These findings indicate that BRCA1/2 germline mutation may contribute to widespread structural change and that other undefined mechanism(s), which are potentially shared with triple-negative breast cancer, promote tandem chromosomal duplications that sculpt the ovarian cancer genome.

Indexed as

Adenocarcinoma, Clear CellBRCA1 ProteinBRCA2 ProteinBreast NeoplasmsChromosome DuplicationDNA, NeoplasmFemaleGene RearrangementGenomeHumansMutationNeoplasms, Cystic, Mucinous, and SerousOvarian NeoplasmsTandem Repeat SequencesBRCA1 ProteinBRCA1 protein, humanBRCA2 ProteinBRCA2 protein, humanDNA, Neoplasm

Identifiers

PMID22514011
PMCPMC3428857

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.