Evidence map›Paper›PMID 22143801›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2011

PRDM1 is a tumor suppressor gene in natural killer cell malignancies.

Can Küçük, Javeed Iqbal, Xiaozhou Hu, Phillip Gaulard, Laurence De Leval, Gopesh Srivastava, Wing Yan Au, Timothy W McKeithan, Wing C Chan

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
5.9field-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

67 citing papers in PubMed, 122 citations in OpenAlex.

  1. Role of PRDM1 in natural killer cells.Molecular biology reports · 2026
    Review
  2. Clonal selection of somatic mutations shapes NK cell memory.bioRxiv : the preprint server for biology · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Genetic and Epigenetic Aberrations ofCurrent issues in molecular biology · 2025
    Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

7 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

9 authors at 5 institutions in 6 countries.

Can KüçükDepartment of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE 68198, USA.
Javeed Iqbal
Xiaozhou Hu
Phillip Gaulard
Laurence De Leval
Gopesh Srivastava
Wing Yan Au
Timothy W McKeithan
Wing C Chan
University of Nebraska Medical Center · USClinique Saint-Joseph · BEQueen Mary Hospital · CNUniversité Paris-Est Créteil · FRUniversity of Hong Kong · HK

Funding

UNMC/EPPLEY CANCER CENTER SUPPORT GRANTP30CA036727 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI Steven H Caplan · 1985 to 2026
$55.0M
ZINC FINGER-INSPIRED FLUORESCENT CHEMOSENSORSP20RR016469 · NCRR · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI MARLEY, KEVIN · 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
UT M.D. Anderson Cancer Center Lymphoma SPOREP50CA136411 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI GANDHI, VARSHA · 2009 to 2011
$1.5M
NCI NIH HHS 5U01/CA114778NCI NIH HHS CA36727NCI NIH HHS P30 CA036727NCI NIH HHS P50 CA136411NCI NIH HHS P50CA136411-01(NC1)NCI NIH HHS U01 CA114778NCRR NIH HHS P20 RR016469
6 · The paper itself

Abstract

Natural killer cell lymphoma (NKCL) constitutes a rare and aggressive form of non-Hodgkin lymphoma, and there is little insight into its pathogenesis. Here we show that PRDM1 is a tumor suppressor gene in NKCLs that is inactivated by a combination of monoallelic deletion and promoter CpG island hypermethylation. We observed monoallelic deletion of PRDM1 loci in 8 of 18 (44%) NKCL cases. The other allele showed significant promoter methylation in 12 of 17 (71%) cases. In support of its role as a tumor suppressor gene, the reconstitution of PRDM1 in PRDM1-null NK cell lines led to G2/M cell cycle arrest, increased apoptosis, and a strong negative selection pressure with progressive elimination of PRDM1-expressing cells, which was enhanced when IL-2 concentration is limiting. We observed a progressive increase in PRDM1 expression--in particular, PRDM1α--in normal NK cells in response to IL-2 and in normal NK cells activated with an engineered NK cell target, K562-Cl9-mb21, suggesting its role in NK cell homeostasis. In support of this role, knockdown of PRDM1 by shRNA in normal NK cells resulted in the positive selection of these cells. We identified MYC and 4-1BBL as targets of PRDM1 in NK cells. Disruption of homeostatic control by PRDM1 may be an important pathogenetic mechanism for NKCL.

Indexed as

ApoptosisBiopsyCell DivisionCulture MediaDNA Copy Number VariationsDNA MethylationDNA Mutational AnalysisG2 PhaseGene Expression Regulation, NeoplasticGene Knockdown TechniquesGene SilencingHumansInterleukin-2Killer Cells, NaturalLymphoma, Non-HodgkinPositive Regulatory Domain I-Binding Factor 1Culture MediaInterleukin-2Positive Regulatory Domain I-Binding Factor 1PRDM1 protein, humanRepressor ProteinsRNA, Small InterferingTumor Suppressor Proteins

Identifiers

PMID22143801
PMCPMC3250125
OpenAlexW2033522935

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.