Evidence map›Paper›PMID 30005627›Full record

ArticleBMC cancer2018

Chromoanasynthesis is a common mechanism that leads to ERBB2 amplifications in a cohort of early stage HER2

George Vasmatzis, Xue Wang, James B Smadbeck, Stephen J Murphy, Katherine B Geiersbach, Sarah H Johnson, Athanasios G Gaitatzes, Yan W Asmann, Farhad Kosari, Mitesh J Borad and 5 more

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.2field-weighted citation impact, top 17% 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

16 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Chromoanagenesis and Beyond: Catastrophic Events Shaping the Genome.Methods in molecular biology (Clifton, N.J.) · 2025
    Review
  5. Chromoanasynthesis.Methods in molecular biology (Clifton, N.J.) · 2025
    Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. The somatic molecular evolution of cancer: Mutation, selection, and epistasis.Progress in biophysics and molecular biology · 2021
    Article
  11. Article
  12. Article
  13. Article
  14. Review
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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

15 authors at 5 institutions in 1 country.

George VasmatzisDepartment of Molecular Medicine, Mayo Clinic, 200 First St., SE, Rochester, MN, 55905, USA. vasm@mayo.edu.ORCID http://orcid.org/0000-0002-3401-3497
Xue WangHealth Sciences Research, Mayo Clinic, Jacksonville, Florida, USA.
James B SmadbeckDepartment of Molecular Medicine, Mayo Clinic, 200 First St., SE, Rochester, MN, 55905, USA.
Stephen J MurphyDepartment of Molecular Medicine, Mayo Clinic, 200 First St., SE, Rochester, MN, 55905, USA.
Katherine B GeiersbachLaboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA.
Sarah H JohnsonDepartment of Molecular Medicine, Mayo Clinic, 200 First St., SE, Rochester, MN, 55905, USA.
Athanasios G GaitatzesDepartment of Molecular Medicine, Mayo Clinic, 200 First St., SE, Rochester, MN, 55905, USA.
Yan W AsmannHealth Sciences Research, Mayo Clinic, Jacksonville, Florida, USA.
Farhad KosariDepartment of Molecular Medicine, Mayo Clinic, 200 First St., SE, Rochester, MN, 55905, USA.
Mitesh J BoradHematology/Oncology, Mayo Clinic, Phoenix, Arizona, USA.
Daniel J SerieDepartment of Molecular Medicine, Mayo Clinic, 200 First St., SE, Rochester, MN, 55905, USA.
Sarah A McLaughlinGeneral Surgery, Mayo Clinic, Jacksonville, Florida, USA.
Jennifer M KachergusCancer Research, Mayo Clinic, Jacksonville, Florida, USA.
Brian M NecelaCancer Research, Mayo Clinic, Jacksonville, Florida, USA.
E Aubrey ThompsonCancer Biology, Mayo Clinic, Griffin Building 214, Jacksonville, Florida, USA. thompson.aubrey@mayo.edu.
Mayo Clinic · USMayo Clinic in Florida · USJacksonville College · USMayo Clinic in Arizona · USWinnMed · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHER2 positive (HER2+) breast cancers involve chromosomal structural alterations that act as oncogenic driver events.

methodsWe interrogated the genomic structure of 18 clinically-defined HER2+ breast tumors through integrated analysis of whole genome and transcriptome sequencing, coupled with clinical information.

resultsERBB2 overexpression in 15 of these tumors was associated with ERBB2 amplification due to chromoanasynthesis with six of them containing single events and the other nine exhibiting multiple events. Two of the more complex cases had adverse clinical outcomes. Chromosomes 8 was commonly involved in the same chromoanasynthesis with 17. In ten cases where chromosome 8 was involved we observed NRG1 fusions (two cases), NRG1 amplification (one case), FGFR1 amplification and ADAM32 or ADAM5 fusions. ERBB3 over-expression was associated with NRG1 fusions and EGFR and ERBB3 expressions were anti-correlated. Of the remaining three cases, one had a small duplication fully encompassing ERBB2 and was accompanied with a pathogenic mutation.

conclusionChromoanasynthesis involving chromosome 17 can lead to ERBB2 amplifications in HER2+ breast cancer. However, additional large genomic alterations contribute to a high level of genomic complexity, generating the hypothesis that worse outcome could be associated with multiple chromoanasynthetic events.

Indexed as

ChromothripsisGene AmplificationBreast NeoplasmsChromosomes, Human, Pair 17Cohort StudiesErb-b2 Receptor Tyrosine KinasesFemaleHumansNeoplasm StagingERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesAmplificationChromoanagenesisChromoanasynthesisChromodesmyChromoplexyChromothripsisNeochromosomeReplication

Identifiers

PMID30005627
PMCPMC6045826
OpenAlexW2884928179

What OpenQuestion holds

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LicenceCC BY
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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.