Evidence map›Paper›PMID 28125801›Full record

ArticleOncotarget2017

Genome-wide copy number aberrations and HER2 and FGFR1 alterations in primary breast cancer by molecular inversion probe microarray.

Hui Chen, Rajesh R Singh, Xinyan Lu, Lei Huo, Hui Yao, Kenneth Aldape, Ronald Abraham, Shumaila Virani, Meenakshi Mehrotra, Bal Mukund Mishra and 11 more

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

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

8 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Oncotarget · 2018
    Article
  8. Survival Outcomes byJCO precision oncology · 2018
    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

21 authors at 2 institutions in 2 countries.

Hui ChenDepartments of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Rajesh R SinghDepartment of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Xinyan LuDepartment of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Lei HuoDepartments of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Hui YaoDepartment of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Kenneth AldapeDepartments of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Ronald AbrahamDepartment of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Shumaila ViraniDepartment of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Meenakshi MehrotraDepartment of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Bal Mukund MishraDepartment of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Alex BousamraDepartments of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Constance AlbarracinDepartments of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Yun WuDepartments of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Sinchita Roy-ChowdhuriDepartments of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Rashmi Kanagal-ShamannaDepartment of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Mark J RoutbortDepartment of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
L Jeffrey MedeirosDepartment of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Keyur P PatelDepartment of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Russell BroaddusDepartments of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Aysegul SahinDepartments of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Rajyalakshmi LuthraDepartment of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
The University of Texas MD Anderson Cancer Center · USUniversity Health Network · CA

Funding

Targeting the PI3K Signaling Pathway in Endometrial CarcinomaP50CA098258 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BODURKA, DIANE · 2003 to 2020
$32.0M
NCI NIH HHS P50 CA098258
6 · The paper itself

Abstract

Breast cancer remains the second leading cause of cancer-related death in women despite stratification based on standard hormonal receptor (HR) and HER2 testing. Additional prognostic markers are needed to improve breast cancer treatment. Chromothripsis, a catastrophic genome rearrangement, has been described recently in various cancer genomes and affects cancer progression and prognosis. However, little is known about chromothripsis in breast cancer. To identify novel prognostic biomarkers in breast cancer, we used molecular inversion probe (MIP) microarray to explore genome-wide copy number aberrations (CNA) and breast cancer-related gene alterations in DNA extracted from formalin-fixed paraffin-embedded tissue. We examined 42 primary breast cancers with known HR and HER2 status assessed via immunohistochemistry and FISH and analyzed MIP microarray results for correlation with standard tests and survival outcomes. Global genome-wide CNA ranged from 0.2% to 65.7%. Chromothripsis-like patterns were observed in 23/38 (61%) cases and were more prevalent in cases with ≥10% CNA (20/26, 77%) than in cases with <10% CNA (3/12, 25%; p<0.01). Most frequently involved chromosomal segment was 17q12-q21, the HER2 locus. Chromothripsis-like patterns involving 17q12 were observed in 8/19 (42%) of HER2-amplified tumors but not in any of the tumors without HER2 amplification (0/19; p<0.01). HER2 amplification detected by MIP microarray was 95% concordant with conventional testing (39/41). Interestingly, 21% of patients (9/42) had fibroblast growth factor receptor 1 (FGFR1)amplification and had a 460% higher risk for mortality than those without FGFR1 amplification (p<0.01). In summary, MIP microarray provided a robust assessment of genomic CNA of breast cancer.

Indexed as

DNA Copy Number VariationsAdultAgedBreast NeoplasmsBreast Neoplasms, MaleChromosomes, Human, Pair 17ChromothripsisErb-b2 Receptor Tyrosine KinasesFemaleGene AmplificationGenome-Wide Association StudyHigh-Throughput Nucleotide SequencingHumansImmunohistochemistryIn Situ Hybridization, FluorescenceMaleERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesFGFR1 protein, humanMolecular ProbesReceptor, Fibroblast Growth Factor, Type 1breast cancerchromothripsisHER2molecular inversion probe microarrayPathology SectionSNP microarray

Identifiers

PMID28125801
PMCPMC5355228
OpenAlexW2581525749

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.