Evidence map›Paper›PMID 19194464›Full record

ArticleLeukemia2009

Genomic analyses reveal global functional alterations that promote tumor growth and novel tumor suppressor genes in natural killer-cell malignancies.

J Iqbal, C Kucuk, R J Deleeuw, G Srivastava, W Tam, H Geng, D Klinkebiel, J K Christman, K Patel, K Cao and 8 more

Abstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.

0numbers the graph read from it
0cells of the map it votes in
97citing papers in PubMed
5.8field-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

97 citing papers in PubMed, 195 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Role of PRDM1 in natural killer cells.Molecular biology reports · 2026
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Genetic and Epigenetic Aberrations ofCurrent issues in molecular biology · 2025
    Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Observational
  18. Article
  19. Article
  20. Review

37 more citing papers are in PubMed but not listed here.

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

18 authors at 6 institutions in 4 countries.

J IqbalDepartment of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE 68198, USA.
C Kucuk
R J Deleeuw
G Srivastava
W Tam
H Geng
D Klinkebiel
J K Christman
K Patel
K Cao
L Shen
K Dybkaer
I F L Tsui
H Ali
N Shimizu
W Y Au
W L Lam
W C Chan
University of Nebraska Medical Center · USUniversity of Hong Kong · HKUniversity of Nebraska at Omaha · USAalborg University Hospital · DKCornell University · USTokyo Medical and Dental University · JP

Funding

ZINC FINGER-INSPIRED FLUORESCENT CHEMOSENSORSP20RR016469 · NCRR · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI TURPEN, JAMES B · 2001 to 2011
$36.2M
Molecular Signatures to Improve Diagnosis and Outcome PrU01CA114778 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI CHAN, WING C. · 2005 to 2009
$8.7M
NCI NIH HHS 5 U01 CA114778NCRR NIH HHS P20 RR016469
6 · The paper itself

Abstract

Natural killer (NK)-cell malignancies are among the most aggressive lymphoid neoplasms with very poor prognosis. We performed array comparative genomic hybridization analysis on a number of NK cell lines and primary tumors to gain better understanding of the pathogenesis and tumor biology of these malignancies. We also obtained transcriptional profiles of genes residing in these regions and compared them with normal and activated NK cells. Only 30-50% of the genes residing in the gained or deleted regions showed corresponding increased or decreased expression. However, many of the upregulated genes in regions of gain are functionally important for the proliferation and growth of the neoplastic population. Genes downregulated in regions of loss included many transcription factors or repressors, tumor suppressors or negative regulators of the cell cycle. The minimal common region of deletion in 6q21 included three known genes (PRDM1, ATG5 and AIM1) showing generally low expression. Mutations resulting in truncated PRDM1 and changes in conserved amino-acid sequences of AIM1 were detected. Highly methylated CpG islands 5' of PRDM1 and AIM1 correlated with low expression of the transcripts. Reversal of methylation by Decitabine induced expression of PRDM1 and cell death. In conclusion, we have shown a general tumor-promoting effect of genetic alterations and have identified PRDM1 as the most likely target gene in del6q21. ATG5, an essential gene for autophagy and AIM1, a gene implicated in melanoma, may also participate in the functional abnormalities.

Indexed as

Comparative Genomic HybridizationGene Expression Regulation, NeoplasticGenes, Tumor SuppressorAdultAgedAutophagy-Related Protein 5Cell ProliferationChromosomes, Human, Pair 6CrystallinsGene Expression ProfilingHumansKiller Cells, NaturalLymphomaMembrane ProteinsMicrotubule-Associated ProteinsMiddle AgedATG5 protein, humanAutophagy-Related Protein 5CRYBG1 protein, humanCrystallinsMembrane ProteinsMicrotubule-Associated ProteinsPositive Regulatory Domain I-Binding Factor 1PRDM1 protein, humanRepressor Proteins

Identifiers

PMID19194464
OpenAlexW2058194048

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.