Evidence map›Paper›PMID 15380028›Full record

ArticleBMC genomics2004

cDNA array-CGH profiling identifies genomic alterations specific to stage and MYCN-amplification in neuroblastoma.

Qing-Rong Chen, Sven Bilke, Jun S Wei, Craig C Whiteford, Nicola Cenacchi, Alexei L Krasnoselsky, Braden T Greer, Chang-Gue Son, Frank Westermann, Frank Berthold and 3 more

Open access · goldAbstract read
In one paragraph

Article in BMC genomics, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
7.5field-weighted citation impact, top 2% 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

32 citing papers in PubMed, 90 citations in OpenAlex.

  1. Article
  2. Article
  3. MYCN in Neuroblastoma: "Old Wine into New Wineskins".Diseases (Basel, Switzerland) · 2021
    Review
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  6. Review
  7. The neuroblastoma and ganglion components of nodular ganglioneuroblastoma are genetically similar: evidence against separate clonal origins.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2015
    Article
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  16. Review
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  18. High-risk neuroblastoma tumors with 11q-deletion display a poor prognostic, chromosome instability phenotype with later onset.Proceedings of the National Academy of Sciences of the United States of America · 2010
    Article
  19. Article
  20. 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

13 authors at 7 institutions in 4 countries.

Qing-Rong ChenOncogenomics Section, Pediatric Oncology Branch, Advanced Technology Center, National Cancer Institute, 8717 Grovemont Circle, Gaithersburg, MD 20877, USA. chenqi@mail.nih.gov
Sven Bilke
Jun S Wei
Craig C Whiteford
Nicola Cenacchi
Alexei L Krasnoselsky
Braden T Greer
Chang-Gue Son
Frank Westermann
Frank Berthold
Manfred Schwab
Daniel Catchpoole
Javed Khan
National Cancer Institute · USChildren's Hospital at Westmead · AUDaejeon University · KREpigenomics (Germany) · DEGerman Cancer Research Center · DEHeidelberg University · DEZentrum für Kinderheilkunde · DE

Funding

Comparative Genomic Hybridization of NeuroblastomaZIABC010592 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI KHAN, JAVED · 2009 to 2013
$416k
Comparative Genomic Hybridization of NeuroblastomaZ01BC010592 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI KHAN, JAVED · 2004 to 2008
$334k
6 · The paper itself

Abstract

backgroundRecurrent non-random genomic alterations are the hallmarks of cancer and the characterization of these imbalances is critical to our understanding of tumorigenesis and cancer progression.

resultsWe performed array-comparative genomic hybridization (A-CGH) on cDNA microarrays containing 42,000 elements in neuroblastoma (NB). We found that only two chromosomes (2p and 12q) had gene amplifications and all were in the MYCN amplified samples. There were 6 independent non-contiguous amplicons (10.4-69.4 Mb) on chromosome 2, and the largest contiguous region was 1.7 Mb bounded by NAG and an EST (clone: 757451); the smallest region was 27 Kb including an EST (clone: 241343), NCYM, and MYCN. Using a probabilistic approach to identify single copy number changes, we systemically investigated the genomic alterations occurring in Stage 1 and Stage 4 NBs with and without MYCN amplification (stage 1-, 4-, and 4+). We have not found genomic alterations universally present in all (100%) three subgroups of NBs. However we identified both common and unique patterns of genomic imbalance in NB including gain of 7q32, 17q21, 17q23-24 and loss of 3p21 were common to all three categories. Finally we confirm that the most frequent specific changes in Stage 4+ tumors were the loss of 1p36 with gain of 2p24-25 and they had fewer genomic alterations compared to either stage 1 or 4-, indicating that for this subgroup of poor risk NB requires a smaller number of genomic changes are required to develop the malignant phenotype.

conclusionscDNA A-CGH analysis is an efficient method for the detection and characterization of amplicons. Furthermore we were able to detect single copy number changes using our probabilistic approach and identified genomic alterations specific to stage and MYCN amplification.

Indexed as

Gene AmplificationCell Line, TumorChildChild, PreschoolChromosome AberrationsFemaleGene DosageGenome, HumanHumansInfantMaleNeoplasm StagingNeuroblastomaN-Myc Proto-Oncogene ProteinNuclear ProteinsOligonucleotide Array Sequence AnalysisMYCN protein, humanN-Myc Proto-Oncogene ProteinNuclear ProteinsOncogene Proteins

Identifiers

PMID15380028
PMCPMC520814
OpenAlexW2145477362

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LicenceCC BY
Read underepoch 390

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.