Evidence map›Paper›PMID 10935481›Full record

ArticleNeoplasia (New York, N.Y.)1999

Application of comparative genomic hybridization, spectral karyotyping, and microarray analysis in the identification of subtype-specific patterns of genomic changes in rhabdomyosarcoma.

A Pandita, M Zielenska, P Thorner, J Bayani, R Godbout, M Greenberg, J A Squire

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
8.3field-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

24 citing papers in PubMed, 89 citations in OpenAlex.

  1. Gene Amplification in Rhabdomyosarcoma: Lessons from a Rare Cancer.International journal of molecular sciences · 2026
    Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Genomic and clinical analysis of amplification of the 13q31 chromosomal region in alveolar rhabdomyosarcoma: a report from the Children's Oncology Group.Clinical cancer research : an official journal of the American Association for Cancer Research · 2011
    Article
  11. Article
  12. Review
  13. Advantage of FISH analysis using FKHR probes for an adjunct to diagnosis of rhabdomyosarcomas.Virchows Archiv : an international journal of pathology · 2008
    Article
  14. Diagnostic and prognostic sarcoma signatures.Molecular diagnosis & therapy · 2008
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Molecular genetics of pediatric soft tissue tumors: clinical application.The Journal of molecular diagnostics : JMD · 2003
    Review
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

7 authors at 5 institutions in 2 countries.

A PanditaDepartment of Medical Biophysics and Laboratory Medicine and Pathobiology, University of Toronto, Ontario, Canada.
M Zielenska
P Thorner
J Bayani
R Godbout
M Greenberg
J A Squire
Hospital for Sick Children · CAUniversity of Toronto · CACancer Institute (WIA) · INOntario Institute for Cancer Research · CASickKids Foundation · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rhabdomyosarcoma (RMS) in children occurs predominantly as two major histologically defined subtypes called embryonal RMS (RMS-E) and the prognostically less favorable alveolar RMS (RMS-A). Comparative genomic hybridization (CGH) was performed on 21 RMS and identified consistent gains affecting chromosomes 2 (8/10), 5 (5/10), 6 (3/10), 7 (7/10), 8 (9/10), 11 (6/ 10), and 12 (5/10) in RMS-E. Losses/deletions involved chromosomes 19 (2/10) and chromosomes 4, 9, 10, 17, 21 (1/10 each). High copy number amplification, involving the 2p24 region (5/11) and less frequently, the 12q13-21 (2/11), 9p22 (1/11), and 17q22-25 (1/11) regions, was detected in RMS-A. Gene amplification at band 2p24 was present in 6/12 alveolar tumors, and in each case, MYCN was amplified, together with the distally placed DDX1 gene. For these patients there was a shorter disease free interval and a higher mortality than patients with tumors without amplification. Detailed spectral karyotype analysis (SKY) was performed on two RMS cell lines (one of each subtype) and identified a surprisingly high level of structural change. Gene expression studies with the Atlas Human Cancer Array (588 genes) showed that 153 genes generated a signal of similar intensity in both cell lines, and 45 genes appeared to have subtype-specific expression. The chromosomal location of differentially expressed genes was compared to the pattern of genomic alteration in RMS as determined by CGH in this study and the literature.

Indexed as

Chromosome AberrationsChromosome BandingChromosome MappingDNA, ComplementaryGene AmplificationHumansKaryotypingNucleic Acid HybridizationRhabdomyosarcomaDNA, Complementary

Identifiers

PMID10935481
PMCPMC1508078
OpenAlexW1978423911

What OpenQuestion holds

Textmetadata
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.