Evidence map›Paper›PMID 30694518›Full record

ArticlePathology oncology research : POR2019

Deletion and Single Nucleotide Polymorphisms in Common Glutathione-S Transferases Contribute to Colorectal Cancer Development.

Milica Lj Stojkovic Lalosevic, Vesna M Coric, Tatjana D Pekmezovic, Tatjana P Simic, Marija S Pljesa Ercegovac, Aleksandra R Pavlovic Markovic, Zoran V Krivokapic

Abstract read
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In one paragraph

Article in Pathology oncology research : POR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
0.3field-weighted citation impact, top 45% 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

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Glutathione-Dependent Pathways in Cancer Cells.International journal of molecular sciences · 2024
    Review
  5. Medicina (Kaunas, Lithuania) · 2024
    Article
  6. Review
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 3 institutions in 1 country.

Milica Lj Stojkovic LalosevicClinic of gastroenterology and hepatology, Clinical center of Serbia, Belgrade, 11000, Serbia.
Vesna M CoricInstitute of Medical and Clinical biochemistry, Belgrade, 11000, Serbia.
Tatjana D PekmezovicFaculty of Medicine, University of Belgrade, Belgrade, 11000, Serbia.
Tatjana P SimicInstitute of Medical and Clinical biochemistry, Belgrade, 11000, Serbia.
Marija S Pljesa ErcegovacInstitute of Medical and Clinical biochemistry, Belgrade, 11000, Serbia.
Aleksandra R Pavlovic MarkovicClinic of gastroenterology and hepatology, Clinical center of Serbia, Belgrade, 11000, Serbia.
Zoran V KrivokapicFaculty of Medicine, University of Belgrade, Belgrade, 11000, Serbia. jagodica85@gmail.com.
University of Belgrade · RSCentar za Promociju Nauke · RSInstitute of Physics Belgrade · RS

Funding

Ministarstvo Prosvete, Nauke i Tehnolo?kog Razvoja (RS) OI175030
6 · The paper itself

Abstract

Glutathione-S transferases (GSTs) are xenobiotic-conjugation enzymes involved in the detoxification process of heterocyclic aromatic amines and polycyclic aromatic hydrocarbons, widely recognized risk factors of colorectal cancer (CRC) development. Polymorphism in GSTs often leads to alteration or complete lack of enzyme activity, which might have an effect on CRC carcinogenesis. Aim of this study was to investigate GST gene variants as risk factors in patients with CRC. A total of 523 CRC patients administered for surgical resection and 400 matched controls were included. Deletion polymorphism of GSTs M1 and T1 was investigated by polymerase chain reaction. Single nucleotide polymorphism of GST A1 and P1 was investigated by restriction fragment length polymorphism method. The association between GST genotype and risk of CRC development was found in carriers of GSTT1-null and GSTP1-variant genotypes individually (p = 0.050 and p = 0.016, respectively). Furthermore, statistically significant association was found when combination of GSTP1-variant genotype with any of other three common GST genotypes was analyzed with respect to CRC susceptibility. Additionally, patients with combined GSTM1-null/GSTT1-null/GSTA1 low-activity/GSTP1-variant genotype showed 2.71-fold increased risk of developing CRC (p = 0.037). This study supports hypothesis that GST polymorphisms might have an important role in the process of the CRC development. Additionally, GSTM1-null/ GSTT1-null/ GSTA1 low-activity/ GSTP1-variant genotype could be combination of GST genotypes whose carriers are more prone to CRC development.

Indexed as

Polymorphism, Single NucleotideSequence DeletionBiomarkers, TumorCase-Control StudiesColorectal NeoplasmsFemaleFollow-Up StudiesGenetic Predisposition to DiseaseGenotypeGlutathione S-Transferase piGlutathione TransferaseHumansMaleMiddle AgedPrognosisRisk FactorsBiomarkers, TumorGlutathione S-Transferase piglutathione S-transferase T1Glutathione TransferaseGSTP1 protein, humanCarcinogenesisColorectal cancerColorectal cancer developmentGlutathione-S transferasesGST polymorphism

Identifiers

PMID30694518
OpenAlexW2913073021

What OpenQuestion holds

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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.