ArticleGut1993
GSTM1 null polymorphism at the glutathione S-transferase M1 locus: phenotype and genotype studies in patients with primary biliary cirrhosis.
Article in Gut, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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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.
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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.
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Who cites it
14 citing papers in PubMed, 35 citations in OpenAlex.
- Trial
- GSTM1 suppresses cardiac fibrosis post-myocardial infarction through inhibiting lipid peroxidation and ferroptosis.Military Medical Research · 2025Article
- The influence of polymorphic GSTM1 gene on the increased susceptibility of non-viral hepatic cirrhosis: evidence from observational studies.European journal of medical research · 2018Review
- Peripheral blood mononuclear cell traffic plays a crucial role in mother-to-infant transmission of hepatitis B virus.International journal of biological sciences · 2015Article
- Article
- Antioxidant status and GST gene polymorphisms in antitubercular treatment-induced hepatotoxicity patients.Hepatology international · 2013Article
- Asthmatic airway neutrophilia after allergen challenge is associated with the glutathione S-transferase M1 genotype.American journal of respiratory and critical care medicine · 2013Article
- Glutathione-S-Transferase M1 null genotype in autoimmune hepatitis.Digestive diseases and sciences · 2001Article
- Collection of genomic DNA by buccal swabs for polymerase chain reaction-based biomarker assays.Environmental health perspectives · 1999Article
- Article
- High Helicobacter pylori numbers are associated with low eradication rate after triple therapy.Gut · 1995Article
- Mycobacterial granulomatous inflammation in the ulcerated caecum of indomethacin-treated rats.International journal of experimental pathology · 1995Article
- Use of site-directed mutagenesis of allele-specific PCR primers to identify the GSTM1 A, GSTM1 B, GSTM1 A,B and GSTM1 null polymorphisms at the glutathione S-transferase, GSTM1 locus.The Biochemical journal · 1993Article
- GSTP1, GSTM1, and GSTT1 genetic polymorphisms in patients with cryptogenic liver cirrhosis.Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary TractArticle
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Studies were carried out to test the hypothesis that the GSTM1 null phenotype at the mu (mu) class glutathione S-transferase 1 locus is associated with an increased predisposition to primary biliary cirrhosis. Starch gel electrophoresis was used to compare the prevalence of GSTM1 null phenotype 0 in patients with end stage primary biliary cirrhosis and a group of controls without evidence of liver disease. The prevalence of GSTM1 null phenotype in the primary biliary cirrhosis and control groups was similar; 39% and 45% respectively. In the primary biliary cirrhosis group all subjects were of the common GSTM1 0, GSTM1 A, GSTM1 B or GSTM1 A, B phenotypes while in the controls, one subject showed an isoform with an anodal mobility compatible with it being a product of the putative GSTM1*3 allele. As the GSTM1 phenotype might be changed by the disease process, the polymerase chain reaction was used to amplify the exon 4-exon 5 region of GSTM1 and show that in 13 control subjects and 11 patients with primary biliary cirrhosis, GSTM1 positive and negative genotypes were associated with corresponding GSTM1 expressing and non-expressing phenotypes respectively. The control subject with GSTM1 3 phenotype showed a positive genotype.
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Registered trials
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.