ArticleBioMed research international2015
The effect of CYP, GST, and SULT polymorphisms and their interaction with smoking on the risk of hepatocellular carcinoma.
Article in BioMed research international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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.
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.
Who cites it
7 citing papers in PubMed, 21 citations in OpenAlex.
- Single Nucleotide Polymorphisms ofBioMed research international · 2019Trial
- Hepatocellular Carcinoma: A Comprehensive Review.Diseases (Basel, Switzerland) · 2025Review
- Astragalus Injection Modulates the Pharmacokinetics of Doxorubicin and CYP450 Enzymes.Current pharmaceutical design · 2025Article
- Human Cytochrome P450 Cancer-Related Metabolic Activities and Gene Polymorphisms: A Review.Cells · 2024Review
- The Role of Sulfotransferases in Liver Diseases.Drug metabolism and disposition: the biological fate of chemicals · 2020Review
- GSTM1 and GSTT1 null genotype increase the risk of hepatocellular carcinoma: evidence based on 46 studies.Cancer cell international · 2019Article
- The Interaction of Smoking with Gene Polymorphisms on Four Digestive Cancers: A Systematic Review and Meta-Analysis.Journal of Cancer · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aim. The aim of our study was to assess whether selected single nucleotide polymorphisms of CYP1A1 and 2E1, GSTM1, GSTT1, and SULT1A1 influence susceptibility towards HCC, considering their interaction with cigarette smoking. Methods. We recruited HCC cases and controls among patients admitted to the hospital "Agostino Gemelli," from January 2005 until July 2010. Odds ratios (OR) of HCC were derived from unconditional multiple logistic regression. Gene-gene and gene-smoking interaction were quantified by computing the attributable proportion (AP) due to biological interaction. Results. The presence of any CYP2E1 (*) 5B variant allele (OR: 0.23; 95% CI: 0.06-0.71) and CYP2E1 (*) 6 variant allele (OR: 0.08; 95% CI: 0.01-0.33) was inversely related to HCC. There was a borderline increased risk among carriers of combined CYP1A1 (*) 2A and SULT1A1 variant alleles (OR: 1.67; 95% CI: 0.97-3.24). A significant biological interaction was observed between GSTT1 and smoking (AP = 0.48; 95% CI: 0.001-0.815), with an OR of 3.13 (95% CI: 1.69-5.82), and borderline significant interaction was observed for SULT1A1 and smoking (AP = 0.36; 95% CI: -0.021-0.747), with an OR of 3.05 (95% CI: 1.73-5.40). Conclusion. CYP2E1 (*) 5B and CYP2E1 (*) 6 polymorphisms have a favourable effect on the development of HCC, while polymorphisms of GSTT1 and SULT1A1 might play role in increasing the susceptibility among smokers.
Indexed as
Identifiers
What OpenQuestion holds
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.