ArticleHuman genetics1996
Proportion of the GSTM1 0/0 genotype in some Slavic populations and its correlation with cystic fibrosis and some multifactorial diseases.
Article in Human genetics, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 3 of them syntheses that pooled it.
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Who cites it
19 citing papers in PubMed, 3 syntheses or guidelines pooled it, 106 citations in OpenAlex.
- Null genotypes of GSTM1 and GSTT1 and endometriosis risk: a meta-analysis of 25 case-control studies.PloS one · 2014Pooled it
- Assessment of cumulative evidence for the association between glutathione S-transferase polymorphisms and lung cancer: application of the Venice interim guidelines.Pharmacogenetics and genomics · 2010Pooled it
- Genetic variation and gene expression in antioxidant related enzymes and risk of COPD: a systematic review.Thorax · 2008Pooled it
- GSTM1 suppresses cardiac fibrosis post-myocardial infarction through inhibiting lipid peroxidation and ferroptosis.Military Medical Research · 2025Article
- Detection ofJournal of clinical medicine · 2023Article
- Cancer driver mutations in endometriosis: Variations on the major theme of fibrogenesis.Reproductive medicine and biology · 2018Review
- Increased Expression of Plasma-Induced ABCC1 mRNA in Cystic Fibrosis.International journal of molecular sciences · 2017Article
- Association between glutathione S-transferase M1/T1 gene polymorphisms and susceptibility to endometriosis: A systematic review and meta-analysis.Experimental and therapeutic medicine · 2016Article
- Association study of Glutathione S-Transferase polymorphisms and risk of endometriosis in an Iranian population.International journal of reproductive biomedicine · 2016Article
- Polymorphisms in the glutathione pathway modulate cystic fibrosis severity: a cross-sectional study.BMC medical genetics · 2014Article
- Genetic interaction of GSH metabolic pathway genes in cystic fibrosis.BMC medical genetics · 2013Article
- Genetic influences on cystic fibrosis lung disease severity.Frontiers in pharmacology · 2013Article
- No association of GSTM1 null polymorphism with endometriosis in women from central and southern Iran.Iranian journal of reproductive medicine · 2012Article
- Update on gene modifiers in cystic fibrosis.Current opinion in pulmonary medicine · 2008Review
- Recombinant Saccharomyces cerevisiae strain expressing a model cytochrome P450 in the rat digestive environment: viability and bioconversion activity.Applied and environmental microbiology · 2007Article
- Strategies for identifying modifier genes in cystic fibrosis.Proceedings of the American Thoracic Society · 2007Review
- Disease modifying genes in cystic fibrosis: therapeutic option or one-way road?Naunyn-Schmiedeberg's archives of pharmacology · 2006Review
- The GCC repeat length in the 5'UTR of MRP1 gene is polymorphic: a functional characterization of its relevance for cystic fibrosis.BMC medical genetics · 2006Article
- Review
Corrections and comments
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Authors and funding
20 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A homozygous gene deletion at the glutathione S-transferase M1 (GSTM1) locus of genomic DNA from blood spots was studied by PCR in the group of Slavic populations from the north-western and central-eastern regions of European Russia and in patients with lung cancer (LC), other tumors (OT), endometriosis (E), alcoholic cirrhosis (AC), cystic fibrosis (CF) and chronic bronchitis (CB). The frequencies of the GSTM1 0/0 genotype were 38.8% and 67.5% for both population groups, respectively. The proportion of the GSTM1 gene deletion genotype was estimated as significantly increased in LC (81%), OT (65%), E (81%), AC (77.3%), and in CB (73.6%) patients with symptoms of CB confirmed by X-ray but not in CB patients without X-ray evidence of disease (40.9%). A definite preponderance of GSTM1-0 homozygotes (51.1%) has been registered in CF patients of the pancreatic sufficient group with clear-cut pulmonological manifestations but not in those of the pancreatic insufficient group with predominantly intestinal or mixed clinical symptoms (41.2% and 37.5%, respectively). Earlier clinical manifestations and death before the age of 5 years are typical for GSTM1-deleted CF patients. These data support the notion that GSTM1 deletion should be considered as a convenient genetic marker for the early detection of groups at higher risk of many diseases caused by environmental and genetic factors, where manifestation depends on the lack of detoxification. High levels of GSTM1 0/0 genotypes in E patients favor the substantial contribution of certain environmental toxins in the pathogenesis of this widespread disease.
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