Evidence map›Paper›PMID 25595865›Full record

ArticleClinical oral investigations2015

The impact of GSTM1/GSTT1 polymorphism for the risk of oral cancer.

Maximilian Krüger, Andreas Max Pabst, Benjamin Mahmoodi, Burkhard Becker, Peer Wolfgang Kämmerer, Felix Peter Koch

Abstract read
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In one paragraph

Article in Clinical oral investigations, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 24% 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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.

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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 3 institutions in 1 country.

Maximilian KrügerDepartment of Oral and Maxillofacial Surgery-Plastic Surgery, University Medical Center of the Johannes Gutenberg-University Mainz, Augustusplatz 2, 55131, Mainz, Germany.
Andreas Max PabstDepartment of Oral and Maxillofacial Surgery-Plastic Surgery, University Medical Center of the Johannes Gutenberg-University Mainz, Augustusplatz 2, 55131, Mainz, Germany.
Benjamin MahmoodiDepartment of Restorative Dentistry, University Medical Center of the Johannes Gutenberg-University Mainz, Augustusplatz 2, 55131, Mainz, Germany.
Burkhard BeckerDepartment of Oral and Maxillofacial Surgery-Plastic Surgery, University Medical Center of the Johannes Gutenberg-University Mainz, Augustusplatz 2, 55131, Mainz, Germany.
Peer Wolfgang KämmererDepartment of Oral and Maxillofacial Surgery, Plastic Facial Surgery, University Medical Center Rostock, Schillingallee 35, 18055, Rostock, Germany.
Felix Peter KochDepartment of Oral and Maxillofacial Surgery, Plastic Facial Surgery, University Medical Center Frankfurt am Main, Theodor-Stern-Kai 7, 60596, Frankfurt am Main, Germany. Koch@facialplastics.de.
Johannes Gutenberg University Mainz · DEUniversity Medical Center of the Johannes Gutenberg University Mainz · DEUniversity of Rostock · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesSince development of oral squamous cell cancer (OSCC) is triggered by various noxa, different variants of the antioxidant glutathione S-transferases (GSTs) can counteract toxic compounds (e.g., tobacco smoke). Because different polymorphisms of GST are known to have an increased sensitivity to carcinogenic agents, the aim of this study was to analyze whether GSTM1 or GSTT1 polymorphisms increase the risk for the development of OSCC. MATERIALS AND

methodsGSTM1 and GSTT1 polymorphism was examined in healthy volunteers (n = 93) and in patients with OSCC (n = 100) by PCR after brush biopsy of oral mucosa. Odds ratio (OR) was calculated to evaluate the risk of oral cancer development.

resultsGSTM1 and GSTT1 deletion was found in 57% (53/93) and 18% (17/93), respectively, in healthy patients, while the OSCC group showed 57% (57/100) for GSTM1 deletion and 22% (22/100) with a deletion of GSTT1. Odds ratio for GSTM1 polymorphism was 1.00 and for GSTT1 1.26. Comparing smokers and nonsmokers with GSTM1 deletion polymorphism, OR was 4.35, while smokers without GSTM1 deletion showed an OR of 1.45. Adapting these data to the smoking habits of the general population in Germany, the OR was 9.25 for smokers with a GSTM1 deletion and OR 6.68 for smokers without a GSTM1 deletion. In smokers with GSTT1 deletion polymorphism, OR was 1.6 (adapted to the smoking habits of the general population: OR 6.16) and 3.16 (OR 8.56) in smokers without deletion in GSTT1 gene.

conclusionsAnalysis of GST-M1 polymorphism in smokers could help to identify patients with a higher risk for the development of oral cancer. CLINICAL RELEVANCE: Early detection of OSCC due to a close meshed monitoring program for patients with GST-M1 polymorphism could help to improve the patient outcome. For polymorphism investigations, the oral brush biopsy is a sufficient method to gain DNA material.

Indexed as

Polymorphism, GeneticFemaleGlutathione TransferaseHumansMaleMouth NeoplasmsNeoplasm ProteinsNeoplasms, Squamous CellRisk FactorsSmokingglutathione S-transferase T1Glutathione TransferaseNeoplasm ProteinsBrush biopsyCancer geneticsGST polymorphismOral squamous cell cancerRisk evaluation

Identifiers

PMID25595865
OpenAlexW2009342011

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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.