Evidence map›Paper›PMID 19691111›Full record

ArticleGenes, chromosomes & cancer2009

Integrative genomics reveals mechanisms of copy number alterations responsible for transcriptional deregulation in colorectal cancer.

Jordi Camps, Quang Tri Nguyen, Hesed M Padilla-Nash, Turid Knutsen, Nicole E McNeil, Danny Wangsa, Amanda B Hummon, Marian Grade, Thomas Ried, Michael J Difilippantonio

Open access · greenAbstract read
In one paragraph

Article in Genes, chromosomes & cancer, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
3.9field-weighted citation impact, top 7% 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

57 citing papers in PubMed, 84 citations in OpenAlex.

  1. Trial
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  7. Mutational Status ofCancers · 2022
    Article
  8. Review
  9. LncRNAAnnals of translational medicine · 2021
    Article
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  15. The m6A readersAmerican journal of cancer research · 2020
    Article
  16. Article
  17. Article
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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

10 authors at 4 institutions in 2 countries.

Jordi CampsGenetics Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Quang Tri Nguyen
Hesed M Padilla-Nash
Turid Knutsen
Nicole E McNeil
Danny Wangsa
Amanda B Hummon
Marian Grade
Thomas Ried
Michael J Difilippantonio
National Cancer Institute · USNational Institutes of Health · USCenter for Cancer Research · USUniversity of Göttingen · DE

Funding

Identification and functional characterization of colorectal cancer genesZIABC010833 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI RIED, THOMAS · 2009 to 2022
$12.1M
Prediction of Therapy Response in Colorectal CancerZIABC010837 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI RIED, THOMAS · 2009 to 2022
$8.9M
Consequences of Genomic Instability and Aneuploidy on the Colorectal Cancer TranZIABC010835 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI RIED, THOMAS · 2009 to 2016
$6.8M
Cancer GenomicsZIABC010836 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI RIED, THOMAS · 2009 to 2011
$1.8M
Intramural NIH HHS Z99 CA999999
6 · The paper itself

Abstract

To evaluate the mechanisms and consequences of chromosomal aberrations in colorectal cancer (CRC), we used a combination of spectral karyotyping, array comparative genomic hybridization (aCGH), and array-based global gene expression profiling on 31 primary carcinomas and 15 established cell lines. Importantly, aCGH showed that the genomic profiles of primary tumors are recapitulated in the cell lines. We revealed a preponderance of chromosome breakpoints at sites of copy number variants (CNVs) in the CRC cell lines, a novel mechanism of DNA breakage in cancer. The integration of gene expression and aCGH led to the identification of 157 genes localized within high-level copy number changes whose transcriptional deregulation was significantly affected across all of the samples, thereby suggesting that these genes play a functional role in CRC. Genomic amplification at 8q24 was the most recurrent event and led to the overexpression of MYC and FAM84B. Copy number dependent gene expression resulted in deregulation of known cancer genes such as APC, FGFR2, and ERBB2. The identification of only 36 genes whose localization near a breakpoint could account for their observed deregulated expression demonstrates that the major mechanism for transcriptional deregulation in CRC is genomic copy number changes resulting from chromosomal aberrations.

Indexed as

DNA Copy Number VariationsGene Expression Regulation, NeoplasticCell Line, TumorChromosome BreakpointsChromosomes, Human, Pair 8Colorectal NeoplasmsComparative Genomic HybridizationGene DeletionGene Expression ProfilingGene Regulatory NetworksHumansNeoplasm ProteinsOligonucleotide Array Sequence AnalysisProto-Oncogene Proteins c-mycReceptors, VirusSpectral KaryotypingFAM89B protein, humanNeoplasm ProteinsProto-Oncogene Proteins c-mycReceptors, Virus

Identifiers

PMID19691111
PMCPMC4721599
OpenAlexW2094969209

What OpenQuestion holds

Textmetadata
LicenceTDM
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.