Evidence map›Paper›PMID 21539681›Full record

ArticleCancer science2011

Validation of the histone methyltransferase EZH2 as a therapeutic target for various types of human cancer and as a prognostic marker.

Masashi Takawa, Ken Masuda, Masaki Kunizaki, Yataro Daigo, Katsunori Takagi, Yukiko Iwai, Hyun-Soo Cho, Gouji Toyokawa, Yuka Yamane, Kazuhiro Maejima and 9 more

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In one paragraph

Article in Cancer science, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed, 5 pooled it
7.3field-weighted citation impact, top 2% 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

99 citing papers in PubMed, 5 syntheses or guidelines pooled it, 191 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  4. Pooled it
  5. Pooled it
  6. Article
  7. Review
  8. Article
  9. The therapeutic potential of RNA m(6)A in lung cancer.Cell communication and signaling : CCS · 2024
    Review
  10. Article
  11. Article
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  13. Article
  14. Article
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  16. Article
  17. Critical Roles of Polycomb Repressive Complexes in Transcription and Cancer.International journal of molecular sciences · 2022
    Review
  18. Article
  19. Article
  20. Article

39 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

19 authors at 7 institutions in 3 countries.

Masashi TakawaLaboratory of Genome Technology, Human Genome Center, Institute of Medical Science, The University of Tokyo, Minato-ku, Tokyo, Japan.
Ken Masuda
Masaki Kunizaki
Yataro Daigo
Katsunori Takagi
Yukiko Iwai
Hyun-Soo Cho
Gouji Toyokawa
Yuka Yamane
Kazuhiro Maejima
Helen I Field
Takaaki Kobayashi
Takayuki Akasu
Masanori Sugiyama
Eijyu Tsuchiya
Yutaka Atomi
Bruce A J Ponder
Yusuke Nakamura
Ryuji Hamamoto
The University of Tokyo · JPKyorin University · JPUniversity of Cambridge · GBNagasaki University · JPKanagawa Prefectural Hospital Organization · JPNational Cancer Center · USShiga University of Medical Science · JP

Funding

Cancer Research UK 19275
6 · The paper itself

Abstract

The emphasis in anticancer drug discovery has always been on finding a drug with great antitumor potential but few side-effects. This can be achieved if the drug is specific for a molecular site found only in tumor cells. Here, we find the enhancer of zeste homolog 2 (EZH2) to be highly overexpressed in lung and other cancers, and show that EZH2 is integral to proliferation in cancer cells. Quantitative real-time PCR analysis revealed higher expression of EZH2 in clinical bladder cancer tissues than in corresponding non-neoplastic tissues (P < 0.0001), and we confirmed that a wide range of cancers also overexpress EZH2, using cDNA microarray analysis. Immunohistochemical analysis showed positive staining for EZH2 in 14 of 29 cases of bladder cancer, 135 of 292 cases of non-small-cell lung cancer (NSCLC), and 214 of 245 cases of colorectal cancer, whereas no significant staining was observed in various normal tissues. We found elevated expression of EZH2 to be associated with poor prognosis for patients with NSCLC (P = 0.0239). In lung and bladder cancer cells overexpressing EZH2, suppression of EZH2 using specific siRNAs inhibited incorporation of BrdU and resulted in significant suppression of cell growth, even though no significant effect was observed in the normal cell strain CCD-18Co, which has undetectable EZH2. Because EZH2 expression was scarcely detectable in all normal tissues we examined, EZH2 shows promise as a tumor-specific therapeutic target. Furthermore, as elevated levels of EZH2 are associated with poor prognosis of patients with NSCLC, its overexpression in resected specimens could prove a useful molecular marker, indicating the necessity for a more extensive follow-up in some lung cancer patients after surgical treatment.

Indexed as

AdolescentAdultAgedAged, 80 and overBiomarkers, TumorCell ProliferationColorectal NeoplasmsDNA-Binding ProteinsEnhancer of Zeste Homolog 2 ProteinFemaleHumansLung NeoplasmsMaleMiddle AgedNeoplasmsPolycomb Repressive Complex 2Biomarkers, TumorDNA-Binding ProteinsEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanPolycomb Repressive Complex 2Transcription Factors

Identifiers

PMID21539681
PMCPMC11159278
OpenAlexW1980009033

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.