Evidence map›Paper›PMID 17667943›Full record

ArticleOncogene2008

Expression and sequence analysis of candidates for the 1p36.31 tumor suppressor gene deleted in neuroblastomas.

E R Okawa, T Gotoh, J Manne, J Igarashi, T Fujita, K A Silverman, H Xhao, Y P Mosse, P S White, G M Brodeur

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
6.4field-weighted citation impact, top 3% 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

54 citing papers in PubMed, 100 citations in OpenAlex.

  1. The TAZ-CAMTA1 Fusion Protein Promotes Tumorigenesis via Connective Tissue Growth Factor and Ras-MAPK Signaling in Epithelioid Hemangioendothelioma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022
    Trial
  2. Trial
  3. Review
  4. Article
  5. Article
  6. Clinical value ofFrontiers in oncology · 2023
    Article
  7. Pan-Cancer Analysis Identifies CHD5 as a Potential Biomarker for Glioma.International journal of molecular sciences · 2022
    Article
  8. Article
  9. Article
  10. Article
  11. An overview of neuroblastoma cell lineage phenotypes andExperimental biology and medicine (Maywood, N.J.) · 2020
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  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

10 authors at 2 institutions in 1 country.

E R OkawaDivision of Oncology, The Children's Hospital of Philadelphia, Department of Pediatrics, The University of Pennsylvania, Philadelphia, PA 19104-4318, USA.
T Gotoh
J Manne
J Igarashi
T Fujita
K A Silverman
H Xhao
Y P Mosse
P S White
G M Brodeur
Children's Hospital of Philadelphia · USUniversity of Pennsylvania · US

Funding

MOLECULAR GENETIC ANALYSIS OF NEUROBLASTOMAR01CA039771 · NCI · WASHINGTON UNIVERSITY · PI BRODEUR, GARRETT M · 1985 to 2013
$4.2M
NCI NIH HHS R01-CA039771
6 · The paper itself

Abstract

Neuroblastomas are characterized by 1p deletions, suggesting that a tumor suppressor gene (TSG) resides in this region. We have mapped the smallest region of deletion (SRD) to a 2 Mb region of 1p36.31 using microsatellite and single nucleotide polymorphisms. We have identified 23 genes in this region, and we have analysed these genes for mutations and RNA expression patterns to identify candidate TSGs. We sequenced the coding exons of these genes in 30 neuroblastoma cell lines. Although rare mutations were found in 10 of the 23 genes, none showed a pattern of genetic change consistent with homozygous inactivation. We examined the expression of these 23 genes in 20 neuroblastoma cell lines, and most showed readily detectable expression, and no correlation with 1p deletion. However, 7 genes showed uniformly low expression in the lines, and 2 genes (CHD5, RNF207) had virtually absent expression, consistent with the expected pattern for a TSG. Our mutation and expression analysis in neuroblastoma cell lines, combined with expression analysis in normal tissues, putative function and prior implication in neuroblastoma pathogenesis, suggests that the most promising TSG deleted from the 1p36 SRD is CHD5, but TNFRSF25, CAMTA1 and AJAP1 are also viable candidates.

Indexed as

Genes, Tumor SuppressorCell Line, TumorChromosomes, Human, Pair 1Expressed Sequence TagsGene DeletionGene ExpressionHumansMicrosatellite RepeatsNeuroblastomaPolymorphism, Single NucleotideSequence Analysis, DNA

Identifiers

PMID17667943
OpenAlexW2090014102

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.