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BioMed Research International
Volume 2015 (2015), Article ID 179867, 7 pages
Research Article

The Effect of CYP, GST, and SULT Polymorphisms and Their Interaction with Smoking on the Risk of Hepatocellular Carcinoma

1Institute of Public Health, Section of Hygiene, Department of Public Health, Università Cattolica del Sacro Cuore, Largo Francesco Vito 1, 00168 Rome, Italy
2IRCCS San Raffaele Pisana, Via della Pisana 235, 00163 Rome, Italy
3Institute of Internal Medicine, Gemelli Hospital, Università Cattolica del Sacro Cuore, Largo Francesco Vito 1, 00168 Rome, Italy
4Internal Medicine and Gastroenterology Unit, Complesso Integrato Columbus, Via Giuseppe Moscati 31-33, 00168 Rome, Italy
5University Clinical-Hospital Center “Dr Dragisa Misovic-Dedinje”, Milana Tepica 1, 11000 Belgrade, Serbia
6Department of Epidemiology, IRCCS Istituto di Ricerche Farmacologiche “Mario Negri”, Via La Masa 19, 20156 Milan, Italy
7Faculty of Medicine, University of Belgrade, Dr Subotica 8, 11000 Belgrade, Serbia
8Internal Medicine and Gastroenterology Division, Gemelli Hospital, Università Cattolica del Sacro Cuore, Largo Francesco Vito 1, 00168 Rome, Italy
9Department of Clinical Sciences and Community Health, Università degli Studi di Milano, Via Festa del Perdono 7, 20122 Milan, Italy

Received 16 April 2014; Revised 19 June 2014; Accepted 19 June 2014

Academic Editor: Paolo Boffetta

Copyright © 2015 Stefania Boccia et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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 CYP2E15B variant allele (OR: 0.23; 95% CI: 0.06-0.71) and CYP2E16 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 CYP1A12A 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. CYP2E15B and CYP2E16 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.