Evidence map›Paper›PMID 25008999›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2014

MGMT gene silencing by promoter hypermethylation in gastric cancer in a high incidence area.

Adfar Yousuf, Mohammad Younis Bhat, Arshad A Pandith, Dil Afroze, Nighat P Khan, Khursheed Alam, Parveen Shah, M Amin Shah, Syed Mudassar

Abstract read
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 3 pooled it
2.8field-weighted citation impact, top 9% 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

23 citing papers in PubMed, 3 syntheses or guidelines pooled it, 32 citations in OpenAlex.

  1. Pooled it
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  3. Pooled it
  4. Review
  5. Review
  6. Article
  7. OWorld journal of gastrointestinal oncology · 2022
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  8. Article
  9. Review
  10. Article
  11. Article
  12. Aberrant gene promoter methylation of E-cadherin, p16Medical oncology (Northwood, London, England) · 2017
    Article
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  14. Article
  15. Article
  16. Article
  17. Relationships betweenOncoTargets and therapy · 2016
    Article
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  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

9 authors at 1 institution in 1 country.

Adfar YousufDepartment of Clinical Biochemistry, Sher-I-Kashmir Institute of Medical Sciences, Soura, Srinagar, Kashmir, 190011, India.
Mohammad Younis Bhat
Arshad A Pandith
Dil Afroze
Nighat P Khan
Khursheed Alam
Parveen Shah
M Amin Shah
Syed Mudassar
Sher-i-Kashmir Institute of Medical Sciences · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeInactivation of tumor suppressor and DNA repair genes by promoter hypermethylation does commonly occur in human cancers. O(6)-methylguanine-DNA methyltransferase (MGMT) is a DNA repair enzyme that removes methyl groups as well as larger adducts at the O(6) position of guanine. In the absence of MGMT activity, O(6)-methylguanine mispairs with thymine during DNA replication, resulting in G:C to A:T transitions. Promoter hypermethylation of the MGMT gene has been observed in various cancers, including gastric cancer. Here, we aimed at assessing the promoter hypermethylation, mutation and expression status of the MGMT gene in patients from a geographic region with a high incidence of gastric cancer (Kashmir, North India) and to investigate their association with various clinicopathological characteristics.

methodsIn this study 82 gastric cancer samples and adjacent normal tissues were included. Mutations in the MGMT gene were detected by single stranded conformational polymorphism (SSCP) analysis and direct sequencing. Methylation-specific polymerase chain reaction (MS-PCR) and Western blot analyses were performed to detect promoter hypermethylation and concomitant (loss of) expression of the MGMT gene.

resultsPromoter hypermethylation of the MGMT gene was found in 52.44% (43 of 82) of the tumor samples and loss of MGMT protein expression was detected in 45.12% (37 of 82) of the tumor samples. Hypermethylation and loss of expression were significantly associated with higher tumor grades (moderately/poorly differentiated) (P < 0.05) and higher tumor stages (III/IV) (P < 0.05). In addition, MGMT hypermethylation and loss of expression were found to be significantly associated with high salt tea consumption (P < 0.05).

conclusionsOur results indicate that MGMT promoter hypermethylation and concomitant loss of MGMT protein expression may play an important role in the development of gastric cancer in the Kashmiri population. High salt tea consumption may be a risk factor.

Indexed as

DNA MethylationDNA Modification MethylasesDNA Repair EnzymesFemaleGene SilencingHumansIndiaIn Vitro TechniquesMaleMiddle AgedPolymorphism, Single-Stranded ConformationalPromoter Regions, GeneticRisk FactorsStomach NeoplasmsTumor Suppressor ProteinsDNA Modification MethylasesDNA Repair EnzymesMGMT protein, humanTumor Suppressor Proteins

Identifiers

PMID25008999
PMCPMC13004438
OpenAlexW2081991237

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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.