Evidence map›Paper›PMID 11965547›Full record

ArticleOncogene2002

Inactivation of p57KIP2 by regional promoter hypermethylation and histone deacetylation in human tumors.

Takefumi Kikuchi, Minoru Toyota, Fumio Itoh, Hiromu Suzuki, Toshiro Obata, Hiroyuki Yamamoto, Hideki Kakiuchi, Masanobu Kusano, Jean-Pierre J Issa, Takashi Tokino and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

43 citing papers in PubMed, 116 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Functional Versatility of the CDK Inhibitor p57Frontiers in cell and developmental biology · 2020
    Review
  6. Article
  7. Article
  8. Review
  9. Dual Inhibition of EZH2 and EZH1 Sensitizes PRC2-Dependent Tumors to Proteasome Inhibition.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017
    Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
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  18. Article
  19. Cellular histone modification patterns predict prognosis and treatment response in resectable pancreatic adenocarcinoma: results from RTOG 9704.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2010
    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

11 authors at 2 institutions in 2 countries.

Takefumi KikuchiFirst Department of Internal Medicine, Sapporo Medical University, Sapporo 060-8543, Japan.
Minoru Toyota
Fumio Itoh
Hiromu Suzuki
Toshiro Obata
Hiroyuki Yamamoto
Hideki Kakiuchi
Masanobu Kusano
Jean-Pierre J Issa
Takashi Tokino
Kohzoh Imai
Sapporo Medical University · JPThe University of Texas MD Anderson Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To clarify the role of DNA methylation in the silencing of the expression of cyclin-dependent kinase inhibitor p57KIP2 seen in certain tumors, we investigated the methylation status of its 5' CpG island in various tumor cell lines and primary cancers. Dense methylation of the region around the transcription start site was detected in 1 out of 10 colorectal, 2 out of 8 gastric, and 6 out of 14 hematopoietic tumor cell lines and in 5 out of 35 (14%) gastric, 6 out of 20 (30%) hepatocellular, and 2 out of 18 (11%) pancreatic cancers; 7 out of 25 (28%) acute myeloid leukemia cases also showed methylation of the p57KIP2 gene, which strongly correlated with the CpG island methylator phenotype (P<0.001). Detailed mapping revealed that dense methylation of the region around the transcription start site (-300 to +400), but not of the edges of the CpG island, was closely associated with gene silencing. 5-aza-2'-deoxycytidine, a methyltransferase inhibitor, restored expression of p57KIP2, and chromatin immunoprecipitation using anti-histone H3 and H4 antibodies showed histone to be deacetylated in cell lines where p57KIP2 was methylated at the transcription start site. Regional methylation and histone deacetylation thus appear to be crucially involved in the silencing of p57KIP2 expression in human tumors.

Indexed as

DNA MethylationGene SilencingAcetylationChromatinCpG IslandsCyclin-Dependent Kinase Inhibitor p57DNA, NeoplasmDNA PrimersGene Expression Regulation, NeoplasticHistonesHumansNeoplasmsNuclear ProteinsPromoter Regions, GeneticReverse Transcriptase Polymerase Chain ReactionRNACDKN1C protein, humanChromatinCyclin-Dependent Kinase Inhibitor p57DNA, NeoplasmDNA PrimersHistonesNuclear ProteinsRNA

Identifiers

PMID11965547
OpenAlexW2019511770

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.