Evidence map›Paper›PMID 9006325›Full record

ArticleThe American journal of pathology1997

Gain of chromosome 17 is the most frequent abnormality detected in neuroblastoma by comparative genomic hybridization.

D Plantaz, G Mohapatra, K K Matthay, M Pellarin, R C Seeger, B G Feuerstein

Registry-linked trialAbstract read
In one paragraph

Article in The American journal of pathology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01728155 (European Low and Intermediate Risk Neuroblastoma Protocol), which is not on this map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
–field-weighted citation impact
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.

NCT01728155 phase3completednot on this mapstarted 2011, after this paper: background citation

European Low and Intermediate Risk Neuroblastoma Protocol

TypeinterventionalSponsorInstituto de Investigacion Sanitaria La FeRan2011Enrolled685ConditionsLOW AND INTERMEDIATE PAEDIATRIC NEUROBLASTOMA AND NEONATAL SUPRARENAL MASSESArmschemotherapy
3 · Its place in the literature

Who cites it

52 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. miR-15a and miR-15b modulate natural killer and CD8Molecular therapy oncolytics · 2022
    Article
  5. Review
  6. Article
  7. Cancers · 2021
    Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Non-Coding RNA Networks in ALK-Positive Anaplastic-Large Cell Lymphoma.International journal of molecular sciences · 2019
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

6 authors.

D PlantazDepartment of Laboratory Medicine, Division of Molecular Cytometry, University of California, San Francisco 94143-0808, USA.
G Mohapatra
K K Matthay
M Pellarin
R C Seeger
B G Feuerstein

Funding

CHILDRENS CANCER STUDY GROUP CHAIRMAN'S GRANTU10CA013539 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI REAMAN, GREGORY H · 1985 to 2002
$43.1M
TREATMENT OF MALIGNANT BRAIN TUMORSP01CA013525 · NCI · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI DEEN, DENNIS F. · 1985 to 1999
–
MOLECULAR CYTOGENETIC MARKERS IN GLIOMA PROGNOSISR01CA061147 · NCI · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI FEUERSTEIN, BURT G · 1994 to 1996
–
NCI NIH HHS CA13525NCI NIH HHS CA13539NCI NIH HHS CA61147
6 · The paper itself

Abstract

Neuroblastoma behavior is variable and outcome partially depends on genetic factors. However, tumors that lack high-risk factors such as MYCN amplification or 1p deletion may progress, possibly due to other genetic aberrations. Comparative genomic hybridization summarizes DNA copy number abnormalities in a tumor by mapping them to their positions on normal metaphase chromosomes. We analyzed 29 tumors from nearly equal proportions of children with stage I, II, III, IV, and IV-S disease by comparative genomic hybridization. We found two classes of copy number abnormalities: whole chromosome and partial chromosome. Whole chromosome losses were frequent at 11, 14, and X. The most frequent partial chromosome losses were on 1p and 11q. Gains were most frequent on chromosome 17 (72% of cases). The two patterns of gain for this chromosome were whole 17 gain and 17q gain, with 17q21-qter as a minimal common region of gain. Other common gains were on chromosomes 7, 6, and 18. High level amplifications were detected at 2p23-25 (MYCN region), at 4q33-35, and at 6p11-22. Chromosome 17q gains were associated with 1p and/or 11q deletions and advanced stage. The high frequency of chromosome 17 gain and its association with bad prognostic factors suggest an important role for this chromosome in the development of neuroblastoma.

Indexed as

Chromosomes, Human, Pair 17In Situ Hybridization, FluorescenceChild, PreschoolChromosome AberrationsChromosome DisordersChromosomes, Human, Pair 2Gene DeletionGenes, mycHumansInfantMaleNeuroblastoma

Identifiers

PMID9006325
PMCPMC1858505

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Registered trials

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.