Journals / Eurasian Journal of Medicine and Oncology / 2019 / Cilt: 3 - Sayı: 4

Polymorphisms in COMT and SULT1A1 Genes and Chronic Lymphocytic Leukemia Risk in Estonia

Pages
281–288
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Conclusion: Further large-scale studies are highly needed to confirm or disprove the findings of the present study and determine genetic risk factors for chronic lymphocytic leukemia.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Objectives: Studies investigating associations between common polymorphisms in phase II metabolic enzymes COMT and SULT1A1 and the risk of various cancer types have revealed inconsistent and controversial results, with no attention turned to date to the most common adult leukemia type, i.e., chronic lymphocytic leukemia.
📊
Key Findings & Data:Methods: In this small case-control study with 47 cases and 50 controls, the role of two functional polymorphisms, Val158Met in COMT gene and Arg213His in SULT1A1 gene affecting the activity level of respective enzymes, was studied on the susceptibility to chronic lymphocytic leukemia in an Estonian cohort.
💡
Conclusion & Impact:Conclusion: Further large-scale studies are highly needed to confirm or disprove the findings of the present study and determine genetic risk factors for chronic lymphocytic leukemia.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Özet

Objectives: Studies investigating associations between common polymorphisms in phase II metabolic enzymes COMT and SULT1A1 and the risk of various cancer types have revealed inconsistent and controversial results, with no attention turned to date to the most common adult leukemia type, i.e., chronic lymphocytic leukemia. Methods: In this small case-control study with 47 cases and 50 controls, the role of two functional polymorphisms, Val158Met in COMT gene and Arg213His in SULT1A1 gene affecting the activity level of respective enzymes, was studied on the susceptibility to chronic lymphocytic leukemia in an Estonian cohort. Results: Although statistically non-significant (p>0.05), the suggestive reduction in disease risk observed with low activity enzyme variants could indicate the involvement of O-methylation and sulfation of various endogenous and exogenous substances in the process of leukemogenesis. The odds ratio (OR) for Met158Met genotype of COMT was 0.60 with 95% confidence interval (95% CI) 0.20-1.82 compared to the wild type Val158Val genotype and the OR for His213His genotype of SULT1A1 was 0.58 with 95% CI 0.20-1.71 compared to the wild type Arg213Arg genotype. Conclusion: Further large-scale studies are highly needed to confirm or disprove the findings of the present study and determine genetic risk factors for chronic lymphocytic leukemia.

🔖

Cite This Article

SAK, K., KASEMAA, K., EVERAUS, H. (2019). Polymorphisms in COMT and SULT1A1 Genes and Chronic Lymphocytic Leukemia Risk in Estonia. Eurasian Journal of Medicine and Oncology, Cilt: 3 - Sayı: 4, 281–288. https://ajindex.com/articles/125941

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (16)

  1. Voorhies BN, Stephens DM. What is optimal front-line therapy for chronic lymphocytic leukemia in 2017? Curr Treat Options Oncol 2017
  2. [CrossRef] 2. Janroziak K, Pula B, Walewski J. Current treatment of chronic lymphocytic leukemia. Curr Treat Options Oncol 2017
  3. Robak T, Jamroziak K, Robak P. Current and emerging treatments for chronic lymphocytic leukaemia. Drugs 2009
  4. 2415–49. [CrossRef] 4. Parker H, Strefford JC. The mutational signature of chronic lymphocytic leukemia. Biochem J 2016
  5. 3725–40. [CrossRef] 5. Sak K, Everaus H. Sulfotransferase 1A1 as a biomarker for susceptibility to carcinogenesis: from molecular genetics to the role of dietary flavonoids. Curr Drug Metab 2016
  6. 528–41. 6. Sak K. The Val158Met polymorphism in COMT gene and cancer risk: role of endogenous and exogenous catechols. Drug Metab Rev 2017
  7. 56–83. [CrossRef] 7. Axelrod J, Senoh S, Witkop B. O-Methylation of catechol amines in vivo. J Biol Chem 1958
  8. 697–701. 8. Tian C, Liu L, Yang X, et al. The Val158Met polymorphism in the COMT gene is associated with increased cancer risks in Chinese population. Tumour Biol 2014
  9. 3003–8. [CrossRef] 9. Zhang H, Zhang Z, Wu J, et al. Lack of association between COMT Val158Met polymorphism and prostate cancer susceptibility. Urol Int 2013
  10. 213–9. [CrossRef] 10. Zou LW, Xu XJ, Liu T, et al. No association between COMT Val158Met polymorphism and prostate cancer risk: a metaanalysis. Genet Test Mol Biomarkers 2013
  11. 78–84. [CrossRef] 11. Zhou Q, Wang Y, Chen A, et al. Association between the COMT Val158Met polymorphism and risk of cancer: evidence from 99 case-control studies. Onco Targets Ther 2015
  12. 2791–803. 12. Matos A, Castelao C, Pereira da Silva A, et al. Epistatic interaction of CYP1A1 and COMT polymorphisms in cervical cancer. Oxid Med Cell Longev 2016
  13. 2769804. [CrossRef] 13. Naushad SM, Pavani A, Rupasree Y, et al. Modulatory effect of plasma folate and polymorphisms in one-carbone metabolism on catecholamine methyltransferase (COMT) H108L associated oxidative DNA damage and breast cancer risk. Indian J Biochem Biophys 2011
  14. 283–9. 14. Moreno-Galvan M, Herrera-Gonzalez NE, Robles-Perez V, et al. Impact of CYP1A1 and COMT genotypes on breast cancer risk in Mexican women: a pilot study. Int J Biol Markers 2010
  15. 157–63. [CrossRef] 15. Yager JD. Catechol-O-methyltransferase: characteristics, polymorphisms and role in breast cancer. Drug Discov Today Dis Mech 2012
  16. e41–6. [CrossRef] 16. Doyle AE, Yager JD.