Evidence map›Paper›PMID 12460459›Full record

ArticleJapanese journal of cancer research : Gann2002

Reduced expression and promoter methylation of p16 gene in Epstein-Barr virus-associated gastric carcinoma.

Toshiya Osawa, Ja-Mun Chong, Makoto Sudo, Kazuya Sakuma, Hiroshi Uozaki, Junji Shibahara, Hideo Nagai, Nobuaki Funata, Masashi Fukayama

Open access · bronzeAbstract read
In one paragraph

Article in Japanese journal of cancer research : Gann, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

12 citing papers in PubMed, 56 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Macrophages of multiple sclerosis patients display deficient SHP-1 expression and enhanced inflammatory phenotype.Laboratory investigation; a journal of technical methods and pathology · 2009
    Article
  7. Review
  8. SHP-1 deficiency and increased inflammatory gene expression in PBMCs of multiple sclerosis patients.Laboratory investigation; a journal of technical methods and pathology · 2008
    Article
  9. Epstein-Barr virus and gastric carcinoma--viral carcinogenesis through epigenetic mechanisms.International journal of clinical and experimental pathology · 2008
    Article
  10. Article
  11. Review
  12. 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

9 authors at 4 institutions in 1 country.

Toshiya OsawaDepartment of Pathology, Graduate School of Medicine, University of Tokyo, Bunkyo-ku, Tokyo 113-0033, Japan.
Ja-Mun Chong
Makoto Sudo
Kazuya Sakuma
Hiroshi Uozaki
Junji Shibahara
Hideo Nagai
Nobuaki Funata
Masashi Fukayama
The University of Tokyo · JPJichi Medical University · JPUniversity of Yamanashi · JPTokyo Metropolitan Komagome Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epstein-Barr virus (EBV)-associated gastric carcinoma (EBVaGC) is a unique type of gastric carcinoma (GC), which is considered to develop in a different pathway from EBV-negative GC. To evaluate a possible role of p16, an inhibitor of G1/S transition of the cell cycle, in the carcinogenesis of EBVaGC, p16-immunohistochemistry and methylation-specific PCR analysis (MSP) were applied to surgically resected gastric carcinomas. When the percentage of p16-positive cells in more than 1000 carcinoma cells was expressed as p16 labeling index (p16-LI), it ranged from 2.5 to 88.1 (mean 42.9+/-24.4) in 70 gastric carcinomas. EBVaGC showed significantly lower values (n=15, 26.1+/ -22.1) than EBV-negative GC (n=55, 47.5+/-23.2) (P=0.0036). Fresh frozen tissues of 55 gastric carcinomas (16 EBVaGC and 39 EBV-negative GC) were further subjected to MSP, to evaluate abnormal methylation of the promoter region of the p16 gene. The frequency of methylation was significantly higher in EBVaGC (14/16) than in EBV-negative GC (9/39) (<0.0001). The methylation-positive carcinomas showed significantly lower p16-LI (35.9+/-21.6) than the unmethylated ones (55.2+/-22.7) (P=0.0014). Thus, a marked decrease of p16 expression, caused by the aberrant methylation of the p16 gene promoter, is closely associated with the development of EBVaGC.

Indexed as

DNA MethylationGenes, p16Promoter Regions, GeneticAdultAgedCpG IslandsCyclin-Dependent Kinase Inhibitor p16Epstein-Barr Virus InfectionsFemaleHumansImmunohistochemistryMaleMiddle AgedStomach NeoplasmsCyclin-Dependent Kinase Inhibitor p16

Identifiers

PMID12460459
PMCPMC5926896
OpenAlexW2029902819

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.