Evidence map›Paper›PMID 25720522›Full record

ArticleMedical oncology (Northwood, London, England)2015

Aberrant gene promoter methylation of p16, FHIT, CRBP1, WWOX, and DLC-1 in Epstein-Barr virus-associated gastric carcinomas.

Dan He, Yi-wang Zhang, Na-na Zhang, Lu Zhou, Jian-ning Chen, Ye Jiang, Chun-kui Shao

Abstract read
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In one paragraph

Article in Medical oncology (Northwood, London, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.4field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

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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

37 citing papers in PubMed, 66 citations in OpenAlex.

  1. Retinoic acid in health and disease.Signal transduction and targeted therapy · 2026
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  5. Gastric Cancer in the Era of Epigenetics.International journal of molecular sciences · 2024
    Review
  6. Integrated analysis ofCell cycle (Georgetown, Tex.) · 2024
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Viral Pathogens in Oesophageal and Gastric Cancer.Pathogens (Basel, Switzerland) · 2022
    Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Review
  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

7 authors at 2 institutions in 1 country.

Dan HeDepartment of Pathology, The Third Affiliated Hospital, Sun Yat-sen University, No. 600 Tianhe Road, Guangzhou, 510630, Guangdong Province, China.
Yi-wang Zhang
Na-na Zhang
Lu Zhou
Jian-ning Chen
Ye Jiang
Chun-kui Shao
Third Affiliated Hospital of Sun Yat-sen University · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alterations in global DNA methylation and specific regulatory gene methylation are frequently found in cancer, but the significance of these epigenetic changes in EBV-associated gastric carcinoma (EBVaGC) remains unclear. We evaluated global DNA methylation status in 49 EBVaGC and 45 EBV-negative gastric carcinoma (EBVnGC) tissue samples and cell lines by 5-methylcytosine immunohistochemical staining and methylation quantification. We determined promoter methylation status and protein expression for the p16, FHIT, CRBP1, WWOX, and DLC-1 genes in tissues and studied the correlation between CpG island methylator phenotype (CIMP) class and clinicopathological characteristics. Changes in gene methylation and mRNA expression in EBVaGC cell line SNU-719 and in EBVnGC cell lines SGC-7901, BGC-823, and AGS were assessed after treatment with 5-aza-2'-deoxycytidine (5-aza-dC), trichostatin A (TSA), or a combination of both, by methylation-specific PCR and quantitative real-time RT-PCR. Global genomic DNA hypomethylation was more pronounced in EBVnGC than in EBVaGC. Promoter methylation of all five genes was more frequent in EBVaGC than in EBVnGC (p < 0.05). p16 and FHIT methylation was reversely correlated with protein expression in EBVaGC. Most (41/49) EBVaGC exhibited CIMP-high (CIMP-H), and the prognosis of CIMP-H patients was significantly worse than that of CIMP-low (p = 0.027) and CIMP-none (p = 0.003) patients. Treatment with 5-aza-dC and/or TSA induced upregulation of RNA expression of all five genes in SNU-719; meanwhile, individual gene expression increased in EBVnGC cell lines. In summary, EBV-induced hypermethylation of p16, FHIT, CRBP1, WWOX, and DLC-1 may contribute to EBVaGC development. Demethylation therapy may represent a novel therapeutic strategy for EBVaGC.

Indexed as

DNA MethylationGene Expression Regulation, NeoplasticAcid Anhydride HydrolasesApoptosisBiomarkers, TumorBis(5'-adenosyl)triphosphataseCell ProliferationCpG IslandsCyclin-Dependent Kinase Inhibitor p16DNA, NeoplasmEpigenesis, GeneticEpstein-Barr Virus InfectionsFemaleFollow-Up StudiesGTPase-Activating ProteinsHerpesvirus 4, HumanAcid Anhydride HydrolasesBiomarkers, TumorBis(5'-adenosyl)triphosphataseCDKN2A protein, humanCyclin-Dependent Kinase Inhibitor p16DLC1 protein, humanDNA, NeoplasmGTPase-Activating ProteinsNeoplasm ProteinsOxidoreductasesReceptors, Retinoic Acidretinoic acid binding protein I, cellularRNA, MessengerTumor Suppressor ProteinsWW Domain-Containing OxidoreductaseWWOX protein, human

Identifiers

PMID25720522
OpenAlexW2000010384

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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.