Evidence map›Paper›PMID 30252041›Full record

ArticleAnnals of oncology : official journal of the European Society for Medical Oncology2018

Mutational mechanisms of amplifications revealed by analysis of clustered rearrangements in breast cancers.

D Głodzik, C Purdie, I H Rye, P T Simpson, J Staaf, P N Span, H G Russnes, S Nik-Zainal

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Annals of oncology : official journal of the European Society for Medical Oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

19 citing papers in PubMed, 50 citations in OpenAlex.

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  18. Whole-genome sequencing reveals clinically relevant insights into the aetiology of familial breast cancers.Annals of oncology : official journal of the European Society for Medical Oncology · 2019
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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

8 authors at 6 institutions in 5 countries.

D GłodzikDivision of Oncology and Pathology, Department of Clinical Sciences Lund, Lund University, Lund, Sweden; Wellcome Trust Sanger Institute, Hinxton, Cambridge.
C PurdieDepartment of Pathology, Ninewells Hospital & Medical School, Dundee, UK.
I H RyeDepartment of Cancer Genetics, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.
P T SimpsonCentre for Clinical Research, Faculty of Medicine, The University of Queensland, Brisbane, Australia.
J StaafDivision of Oncology and Pathology, Department of Clinical Sciences Lund, Lund University, Lund, Sweden.
P N SpanDepartment of Radiation Oncology, Department of Laboratory Medicine, Radboud University Medical Center, Nijmegen, The Netherlands.
H G RussnesDepartment of Cancer Genetics, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway; Department of Pathology, Oslo University Hospital, Oslo, Norway.
S Nik-ZainalWellcome Trust Sanger Institute, Hinxton, Cambridge; Academic Department of Medical Genetics, The Clinical School University of Cambridge, Cambridge, UK. Electronic address: sn206@cam.ac.uk.
Lund University · SEOslo University Hospital · NONinewells Hospital · GBRadboud University Nijmegen · NLThe University of Queensland · AUUniversity of Cambridge · GB

Funding

Cancer Research UK 22932Cancer Research UK 23433Cancer Research UK 23916Cancer Research UK C60100/A23916Wellcome Trust 077012/Z/05/ZWellcome Trust 101126/B/13/Z
6 · The paper itself

Abstract

Background: Complex clusters of rearrangements are a challenge in interpretation of cancer genomes. Some clusters of rearrangements demarcate clear amplifications of driver oncogenes but others are less well understood. A detailed analysis of rearrangements within these complex clusters could reveal new insights into selection and underlying mutational mechanisms. Patients and methods: Here, we systematically investigate rearrangements that are densely clustered in individual tumours in a cohort of 560 breast cancers. Applying an agnostic approach, we identify 21 hotspots where clustered rearrangements recur across cancers. Results: Some hotspots coincide with known oncogene loci including CCND1, ERBB2, ZNF217, chr8:ZNF703/FGFR1, IGF1R, and MYC. Others contain cancer genes not typically associated with breast cancer: MCL1, PTP4A1, and MYB. Intriguingly, we identify clustered rearrangements that physically connect distant hotspots. In particular, we observe simultaneous amplification of chr8:ZNF703/FGFR1 and chr11:CCND1 where deep analysis reveals that a chr8-chr11 translocation is likely to be an early, critical, initiating event. Conclusions: We present an overview of complex rearrangements in breast cancer, highlighting a potential new way for detecting drivers and revealing novel mechanistic insights into the formation of two common amplicons.

Indexed as

Gene AmplificationTranslocation, GeneticAdultAgedAged, 80 and overAge DistributionAlgorithmsBreastBreast NeoplasmsCarrier ProteinsChromosomes, Human, Pair 11Chromosomes, Human, Pair 8Cyclin D1Datasets as TopicFemaleGenetic LociCarrier ProteinsCCND1 protein, humanCyclin D1FGFR1 protein, humanReceptor, Fibroblast Growth Factor, Type 1ZNF703 protein, human

Identifiers

PMID30252041
PMCPMC6290883
OpenAlexW2892516835

What OpenQuestion holds

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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.