Evidence map›Paper›PMID 16791592›Full record

ArticleJournal of cancer research and clinical oncology2006

Aberrant promoter hypermethylation of p16 and MGMT genes in oral squamous cell carcinomas and the surrounding normal mucosa.

Keizo Kato, Akira Hara, Toshiya Kuno, Hideki Mori, Tomomi Yamashita, Makoto Toida, Toshiyuki Shibata

Open access · greenAbstract readComparative Study
In one paragraph

Article in Journal of cancer research and clinical oncology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.2field-weighted citation impact, top 14% 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

35 citing papers in PubMed, 105 citations in OpenAlex.

  1. Review
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  9. Review
  10. Analysis of DNA methylation of E-cadherin and p16Clinical and experimental dental research · 2021
    Article
  11. Review
  12. Article
  13. Current Insights into Oral Cancer Epigenetics.International journal of molecular sciences · 2018
    Review
  14. Aberrant DNA methylation of theJournal of Cancer · 2018
    Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
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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

7 authors at 1 institution in 1 country.

Keizo KatoDepartment of Oral and Maxillofacial Sciences, Graduate School of Medicine, Gifu University, 1-1 Yanagido, Gifu, 501-1194, Japan. keizo@cc.gifu-u.ac.jp
Akira Hara
Toshiya Kuno
Hideki Mori
Tomomi Yamashita
Makoto Toida
Toshiyuki Shibata
Gifu University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeSeveral genetic alterations have been reported to contribute to the development of oral squamous cell carcinoma (OSCC). Recent studies have shown roles of promoter hypermethylation of tumor suppressor genes, including p16 and MGMT, in several types of cancers. The purpose of this study is to examine the hypermethylation status of p16 and MGMT genes in both oral cancers and normal mucosa, surrounding the cancers.

methodsPromoter hypermethylation status of p16 and MGMT genes were examined by the methylation-specific PCR (MSP) in OSCC (n = 51), verrucous carcinoma (n = 2), and carcinoma in situ (n = 2) tissues. Moreover, normal mucosa surrounding the cancers were also examined in 22 cases out of the 51 OSCCs. As a normal control, oral mucosa from healthy volunteers (n = 18) was used.

resultsAberrant promoter hypermethylation of p16 and MGMT genes was detected in 50.9% (28 of 55) and 56.4% (31 of 55) of the total malignant cases, respectively. As for the 22 OSCC cases, in which paired cancerous tissues and the surrounding normal mucosa were examined simultaneously, promoter hypermethylation of p16 and MGMT genes was confirmed in 72.73% (16 of 22) and 68.18% (15 of 22), respectively. In contrast, as for the surrounding normal mucosa, promoter hypermethylation of p16 and MGMT genes was recognized in 27.27% (6 of 22) cases and 40.91% (9 of 22), respectively.

conclusionsHypermethylation of both p16 and MGMT genes was frequently detected in not only OSCC tissues, but also the surrounding normal mucosa around the cancerous tissues. Thus promoter hypermethylation of p16 and MGMT genes are an important, probably early event in oral carcinogenesis.

Indexed as

DNA MethylationAdultAgedAged, 80 and overCarcinoma in SituCarcinoma, Squamous CellCarcinoma, VerrucousCase-Control StudiesCyclin-Dependent Kinase Inhibitor p16DNAFemaleHumansMaleMiddle AgedMouth MucosaMouth NeoplasmsCyclin-Dependent Kinase Inhibitor p16DNAO(6)-Methylguanine-DNA Methyltransferase

Identifiers

PMID16791592
PMCPMC12161033
OpenAlexW2046217395

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.