Evidence map›Paper›PMID 19669596›Full record

ArticleMolecular biology reports2010

Investigation of glutathione S-transferase M1 and T1 deletions in lung cancer.

Julide Altinisik, Zinnet B Balta, Gunay Aydin, Turgut Ulutin, Nur Buyru

Abstract read
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In one paragraph

Article in Molecular biology reports, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 3 pooled it
1.6field-weighted citation impact, top 18% 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

12 citing papers in PubMed, 3 syntheses or guidelines pooled it, 28 citations in OpenAlex.

  1. Association between glutathione S-transferase T1 null genotype and risk of lung cancer: a meta-analysis of 55 studies.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
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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

5 authors at 1 institution in 1 country.

Julide AltinisikCerrahpasa Medical Faculty, Department of Medical Biology, Istanbul University, Temel Bilimler Binasi Kat:2 Tibbi Biyoloji ABD., Kocamustafapasa, Istanbul, Turkey.
Zinnet B Balta
Gunay Aydin
Turgut Ulutin
Nur Buyru
Istanbul University · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glutathione S-transferases (GSTs) M1 and T1 are known to be polymorphic in humans. Both polymorphisms are due to gene deletions which are responsible for the existence of null genotypes. Previous studies have suggested that GST genotypes may play a role in determining susceptibility to a number of unrelated cancers, including lung cancer. The GSTM1 and GSTT1 polymorphisms were determined by PCR-based analysis in 75 lung cancer patients and 55 controls. The unconditional logistic regression analysis was used to calculate ORs and 95% CI. The frequencies of GSTM1 and GSTT1 null genotypes were 37.3 and 22.7% in lung cancer patients and 27.3 and 16.4% in controls, respectively. When analyzed by histology the GSTM1 null genotype was more prevalent in squamous-cell carcinoma and adenocarcinoma patients. Whereas, GSTT1 null genotype frequency was lower in small-cell lung cancer patients than controls. But these differences were not statistically significant. According to smoking status, null genotype for both gene are associated with an increase in risk for lung cancer. Our results suggest that GSTM1 and GSTT1 polymorphisms may play a role in the development of lung cancer for some histological subtypes and modifies the risk of smoking-related lung cancer.

Indexed as

Gene DeletionAdultAgedAged, 80 and overFemaleGenetic Predisposition to DiseaseGlutathione TransferaseHumansLung NeoplasmsMaleMiddle AgedSmokingglutathione S-transferase T1Glutathione Transferase

Identifiers

PMID19669596
OpenAlexW2007950744

What OpenQuestion holds

Textmetadata
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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.