Evidence map›Paper›PMID 10027410›Full record

ArticleThe American journal of pathology1999

Specific chromosomal aberrations and amplification of the AIB1 nuclear receptor coactivator gene in pancreatic carcinomas.

B M Ghadimi, E Schröck, R L Walker, D Wangsa, A Jauho, P S Meltzer, T Ried

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The American journal of pathology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
12.0field-weighted citation impact, top 1% 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

47 citing papers in PubMed, 197 citations in OpenAlex.

  1. Trial
  2. Article
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  5. SRC-3, a Steroid Receptor Coactivator: Implication in Cancer.International journal of molecular sciences · 2021
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Molecular Pathways: Targeting Steroid Receptor Coactivators in Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016
    Article
  12. Journal of Cancer · 2016
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
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  19. 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

7 authors at 2 institutions in 1 country.

B M GhadimiNational Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland 20892, USA. bghadimi@nhgri.nih.gov
E Schröck
R L Walker
D Wangsa
A Jauho
P S Meltzer
T Ried
National Human Genome Research Institute · USNational Institutes of Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To screen pancreatic carcinomas for chromosomal aberrations we have applied molecular cytogenetic techniques, including fluorescent in situ hybridization, comparative genomic hybridization, and spectral karyotyping to a series of nine established cell lines. Comparative genomic hybridization revealed recurring chromosomal gains on chromosome arms 3q, 5p, 7p, 8q, 12p, and 20q. Chromosome losses were mapped to chromosome arms 8p, 9p, 17p, 18q, 19p, and chromosome 21. The comparison with comparative genomic hybridization data from primary pancreatic tumors indicates that a specific pattern of chromosomal copy number changes is maintained in cell culture. Metaphase chromosomes from six cell lines were analyzed by spectral karyotyping, a technique that allows one to visualize all chromosomes simultaneously in different colors. Spectral karyotyping identified multiple chromosomal rearrangements, the majority of which were unbalanced. No recurring reciprocal translocation was detected. Cytogenetic aberrations were confirmed using fluorescent in situ hybridization with probes for the MDR gene and the tumor suppressor genes p16 and DCC. Copy number increases on chromosome 20q were validated with a probe specific for the nuclear receptor coactivator AIB1 that maps to chromosome 20q12. Amplification of this gene was identified in six of nine pancreatic cancer cell lines and correlated with increased expression.

Indexed as

Gene AmplificationChromosome AberrationsChromosomes, Human, Pair 20DNA, NeoplasmFemaleHistone AcetyltransferasesHumansIn Situ Hybridization, FluorescenceKaryotypingMaleNuclear Receptor Coactivator 1Pancreatic NeoplasmsReceptors, SteroidRNA, NeoplasmTranscription FactorsTumor Cells, CulturedDNA, NeoplasmHistone AcetyltransferasesNCOA1 protein, humanNuclear Receptor Coactivator 1Receptors, SteroidRNA, NeoplasmTranscription Factors

Identifiers

PMID10027410
PMCPMC1850008
OpenAlexW2134404166

What OpenQuestion holds

Texttitle and abstract
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.