Evidence map›Paper›PMID 12841866›Full record

ArticleCancer science2003

Promoter hypermethylation of tumor suppressor and tumor-related genes in non-small cell lung cancers.

Naoki Yanagawa, Gen Tamura, Hiroyuki Oizumi, Nobumasa Takahashi, Yasuhisa Shimazaki, Teiichi Motoyama

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Cancer science, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 11 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 11 pooled it
3.4field-weighted citation impact, top 7% 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

56 citing papers in PubMed, 11 syntheses or guidelines pooled it, 136 citations in OpenAlex.

  1. Pooled it
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  3. The clinicopathological significance and potential drug target of E-cadherin in NSCLC.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Pooled it
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  7. E-cadherin gene methylation in lung cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Pooled it
  8. CDKN2A/p16 inactivation mechanisms and their relationship to smoke exposure and molecular features in non-small-cell lung cancer.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2013
    Pooled it
  9. [Meta-analysis of association between E-cadherin promoter methylation and lung cancer risk].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2013
    Pooled it
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  12. Trial
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  15. The transcription activity ofTranslational cancer research · 2023
    Article
  16. CpG Island Methylator Phenotype-A Hope for the Future or a Road to Nowhere?International journal of molecular sciences · 2022
    Review
  17. Article
  18. Article
  19. Article
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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

6 authors at 1 institution in 1 country.

Naoki YanagawaDepartment of Pathology, Yamagata University School of Medicine, Yamagata 990-9585, Japan.
Gen Tamura
Hiroyuki Oizumi
Nobumasa Takahashi
Yasuhisa Shimazaki
Teiichi Motoyama
Yamagata University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aberrant methylation of promoter CpG islands is known to be a major inactivation mechanism of tumor suppressor and tumor-related genes. To determine the clinicopathological significance of gene promoter methylation in non-small cell lung cancer (NSCLC), we examined the promoter methylation status of the APC, DAP-kinase, E-cadherin, GSTP1, hMLH1, p16, RASSF1A and RUNX3 genes in 75 NSCLCs and corresponding non-neoplastic lung tissues by methylation-specific PCR (MSP). The frequencies of methylation in NSCLCs and corresponding non-neoplastic lung tissues were: 37% (28 of 75) and 48% (36 of 75) for APC, 28% (21 of 75) and 13% (10 of 75) for DAP-kinase, 29% (22 of 75) and 15% (11 of 75) for E-cadherin, 1% (1 of 75) and 0% (0 of 75) for GSTP1, 7% (5 of 75) and 0% (0 of 75) for hMLH1, 31% (23 of 75) and 0% (0 of 75) for p16, 43% (32 of 75) and 4% (3 of 75) for RASSF1A, and 20% (15 of 75) and 3% (2 of 75) for RUNX3, respectively. Methylation of p16 was more frequent in squamous cell carcinomas than in adenocarcinomas (P < 0.05), and was associated with tobacco smoking (P < 0.05). On the contrary, methylation of APC and RUNX3 was more frequent in adenocarcinomas than in squamous cell carcinomas (P < 0.05). Thus, a different set of genes is thought to undergo promoter methylation, which leads to the development of different histologies. In addition, methylation of p16, RASSF1A and RUNX3 was mostly cancer-specific (P < 0.05), and may be utilized as a molecular diagnostic marker of NSCLCs.

Indexed as

DNA MethylationGenes, Tumor SuppressorAdultAgedAge FactorsApoptosis Regulatory ProteinsCalcium-Calmodulin-Dependent Protein KinasesCarcinoma, Non-Small-Cell LungDeath-Associated Protein KinasesDNA, NeoplasmDNA PrimersGenes, APCHumansLungLung NeoplasmsMiddle AgedApoptosis Regulatory ProteinsCalcium-Calmodulin-Dependent Protein KinasesDeath-Associated Protein KinasesDNA, NeoplasmDNA PrimersNeoplasm Proteins

Identifiers

PMID12841866
PMCPMC11160194
OpenAlexW1989585142

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.