The Association between EPHX1 Gene Polymorphisms and Lung Cancer among Jordanian People.
| Autor: | Alqudah TE; Department of Physiology and Biochemistry, School of Medicine, University of Jordan, Amman, Jordan., Ismail S; Department of Physiology and Biochemistry, School of Medicine, University of Jordan, Amman, Jordan., Abdeen D; Department of Physiology and Biochemistry, School of Medicine, University of Jordan, Amman, Jordan., Ababneh NA; Department of Pathology, School of Medicine, University of Jordan, Amman, Jordan., Khatib F; Department of Physiology and Biochemistry, School of Medicine, University of Jordan, Amman, Jordan., Al-Essa MK; Department of Physiology and Biochemistry, School of Medicine, University of Jordan, Amman, Jordan., Hawari F; Cancer Control Office, King Hussein Cancer Center, Amman, Jordan., Obeidat N; Department of Internal Medicine, School of Medicine, University of Jordan, Amman, Jordan., Alkayed NJ; Department of Physiology and Biochemistry, School of Medicine, University of Jordan, Amman, Jordan.; Department of Anesthesiology and Perioperative Medicine, Knight Cardiovascular Institute, Oregon Health and Science University, Portland, OR, USA., Shafagoj Y; Department of Physiology and Biochemistry, School of Medicine, University of Jordan, Amman, Jordan. |
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| Jazyk: | angličtina |
| Zdroj: | Asian Pacific journal of cancer prevention : APJCP [Asian Pac J Cancer Prev] 2024 Nov 01; Vol. 25 (11), pp. 3913-3919. Date of Electronic Publication: 2024 Nov 01. |
| DOI: | 10.31557/APJCP.2024.25.11.3913 |
| Abstrakt: | Objective: Genetic susceptibility to lung cancer is the subject of extensive research. We investigated whether polymorphisms in the microsomal epoxide hydrolase (EPHX1) gene is linked to lung cancer susceptibility in Jordanian patients. Methods: In this case-control study a total of 218 subjects from Jordan University Hospital and King Hussein Cancer Center were screened (108 lung cancer patients and 110 matched controls). Polymerase chain reaction-restriction fragment-length polymorphism (PCR-RFLP) was used to detect the two common polymorphisms in EPXH1 located in exons 3 and 4; namely, amino acid substitution from tyrosine to histidine at residue 113 of exon 3 (Tyr113His; low activity allele) and amino acid substitution from histidine to arginine at residue 139 of exon 4 (His139Arg; high activity allele). Results: There was no significant difference in genotype distribution between control subjects and lung cancer patients. In addition, no differences were found when evaluated according to age, gender or tobacco consumption. For exon 3 the adjusted OR was 0.970 (95% CI 0.473 - 1.991) for the Tyr113/His113 genotype and 0.692 (95% CI 0.301 - 1.590) for the Tyr113/Tyr113 genotype, respectively. For exon 4 the adjusted OR was 0.596 (95% CI 0.297-1.197) for the His139/Arg139 genotype and 0.882 (95% CI 0.117- 6.660) for the Arg139/Arg139 genotype, respectively. Logistic regression analysis did not show differences in EPXH1 distributions between patients and controls when categorized according to predicted microsomal epoxide hydrolase activity. Therefore, common polymorphisms within EPHX1 do not appear to be significant risk factors for lung cancer development in the Jordanian population. Conclusion: No associations were observed between lung cancer risk and EPXH1 polymorphisms in the Jordanian population. |
| Databáze: | MEDLINE |
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