The Korean Journal of Physiology and Pharmacology

The Korean Society of Pharmacology (대한약리학회)
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Apo-1/Fas (CD95) Gene Polymorphism in Korean Hepatocellular Carcinoma Patients

  • Kim, Sung-Soo (Department of Pharmacology, College of Medicine, Kangwon National University) ;
  • Hong, Seung-Jae (Division of Rheumatology, Department of Internal Medicine, College of Medicine, KyungHee University) ;
  • Ahn, Yun-Gul (Department of Pharmacology, College of Medicine, Kangwon National University) ;
  • Kim, Bong-Seog (Department of Pharmacology, College of Medicine, Kangwon National University,Division of Hemato- oncology, Department of Internal Medicine, Seoul Veterans Hospital) ;
  • Yuh, Young-Jin (Department of Pharmacology, College of Medicine, Kangwon National University,Department of Internal Medicine, Sanggye Paik Hospital, College of Medicine, Inje University) ;
  • Han, Kye-Young (Department of Orthopaedic Surgery, College of Medicine, Kangwon National University) ;
  • Lee, Hee-Jae (Kohwang Medical Research Institute, College of Medicine, Kyung Hee University) ;
  • Chung, Joo-Ho (Kohwang Medical Research Institute, College of Medicine, Kyung Hee University) ;
  • Yim, Sung-Vin (Department of Pharmacology, College of Medicine, Kangwon National University) ;
  • Cho, Jae-Young (Department of Anatomy, College of Medicine, Seoul National University) ;
  • Park, Yeon-Hee (Division of Medical Oncology, Korea Cancer Center Hospital)
  • Published : 2003.02.21
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Abstract

It is well known that different expression of Apo-1/Fas (CD95) plays important roles in various tumors and hepatocellular carcinoma (HCC) pathogenesis. Apo-1/Fas mediated apoptosis is one of the important pathways of apoptosis and is known to mediate apoptotic cell death by fas ligand (FasL). To examine the possible relationship between Apo-1/Fas gene polymorphism and HCC susceptibility, MvaI restriction fragment length polymorphism (RFLP) of Apo-1/Fas gene was examined in 94 Korean HCC patients and 240 control subjects. No statistically significant difference in the genotypic distribution and allelic frequencies was found between the control and the HCC. It is, therefore, concluded that Apo-1/Fas gene polymorphism is not associated with HCC susceptibility. Further studies are needed in order to clarify the relationships between genotypes of Apo-1/Fas gene and HCC pathogenesis.

Keywords

References

  1. Alameddine FM, Zafari AM. Genetic polymorphisms and oxidative stress in heart failure. Congest Heart Fail 8: 157－164, 2002 https://doi.org/10.1111/j.1527-5299.2002.00719.x
  2. Fan XQ, Guo YJ. Apoptosis in oncoloy. Cell Res 11: 1－7, 2001 https://doi.org/10.1038/sj.cr.7290060
  3. Farker K, Schotte U, Scheele J, Hoffmann A. Assessment of frequencies of lifestyle factors and polymorphisms of drugmetabolizing enzymes (NAT2, CYP2E1) in human hepatocellular carcinoma (HCC) patients in a department of surgical medicine-a pilot investigation. Int J Clin Pharmacol Ther 40: 120－124, 2002 https://doi.org/10.5414/CPP40120
  4. Huang QR, Danis V, Lassere M, Edmonds J, Manolios N. Evaluation of a new Apo-1/Fas promoter polymorphism in rheumatoid arthritis and systemic lupus erythematosus patients. Rheumatology (Oxford) 38: 645－651, 1999 https://doi.org/10.1093/rheumatology/38.7.645
  5. Huang QR, Morris D, Manolios N. Identification and characterization of polymorphisms in the promoter region of the human Apo-1/Fas (CD95) gene. Mol Immunol 34: 577－582, 1997 https://doi.org/10.1016/S0161-5890(97)00081-3
  6. Huang QR, Teutsch SM, Buhler MM, Bennetts BH, Heard RN, Manolios N, Stewart GJ. Evaluation of the apo-1/Fas promoter mva I polymorphism in multiple sclerosis. Mult Scler 6: 14－18, 2000 https://doi.org/10.1191/135245800678827392
  7. Kim SA, Kim YJ, Choe BK, Lee HJ, Kim JW, Park JD, Kim CJ, Park SJ, Jung JC, Chung JH. Assessment of an Apo-1/Fas promoter polymorphism in Korean schizophrenia patients. Korean J Physiol Pharmacol 6: 131－138, 2002
  8. Lee SH, Shin MS, Lee HS, Bae JH, Lee HK, Kim HS, Kim SY, Jang JJ, Joo M, Kang YK, Park WS, Park JY, Oh RR, Han SY, Lee JH, Kim SH, Lee JY, Yoo NJ. Expression of Fas and Fas-related molecules in human hepatocellular carcinoma. Hum Pathol 32: 250－256, 2001 https://doi.org/10.1053/hupa.2001.22769
  9. Lee YH, Ji JD, Sohn J, Song GG. Polymorphsims of CTLA-4 exon 1 +49, CTLA-4 promoter -318 and Fas promoter -670 in spondyloarthropathies. Clin Rheumatol 20: 420－422, 2001 https://doi.org/10.1007/s100670170007
  10. Maeda T, Kamihira S. Apoptosis, Part II: The role of mutated Fas genes in tumorigenesis. Adv Clin Chem 36: 109－137, 2001 https://doi.org/10.1016/S0065-2423(01)36026-2
  11. Montesano R, Hall J. Environmental causes of human cancers. Eur J Cancer 37: S67－S87, 2001
  12. Monto A, Wright TL. The epidemiology and prevention of hepatocellular carcinoma. Semin Oncol 28: 441－449, 2001 https://doi.org/10.1016/S0093-7754(01)90137-X
  13. Müllauer L, Gruber P, Sebinger D, Buch J, Wohlfart S, Chott A. Mutations in apoptosis genes: a pathogenetic factor for human disease. Mutat Res 488: 211－231, 2001 https://doi.org/10.1016/S1383-5742(01)00057-6
  14. Nagata S. Fas ligand-induced apoptosis. Annu Rev Genet 33: 29－ 55, 1999 https://doi.org/10.1146/annurev.genet.33.1.29
  15. Peter ME, Krammer PH. Mechanisms of CD95 (APO-1/Fas)- mediated apoptosis. Curr Opin Immunol 10: 545－551, 1998 https://doi.org/10.1016/S0952-7915(98)80222-7
  16. Rogler CE, Chisari FV. Cellular and molecular mechanisms of hepatocarcinogenesis. Semin Liver Dis 12: 265－278, 1992 https://doi.org/10.1055/s-2007-1007398
  17. Schmitz I, Kirchhoff S, Krammer PH. Regulation of death receptormediated apoptosis pathways. Int J Biochem Cell Biol 32: 1123－1136, 2000 https://doi.org/10.1016/S1357-2725(00)00048-0
  18. Sharma K, Wang RX, Zhang LY, Yin DL, Luo XY, Solomon JC, Jiang RF, Markos K, Davidson W, Scott DW, Shi YF. Death the Fas way: regulation and pathophysiology of CD95 and its ligand. Pharmacol Ther 88: 333－347, 2000 https://doi.org/10.1016/S0163-7258(00)00096-6
  19. Sud R, Wells D, Talbot IC, Delhanty JD. Genetic alterations in gastric cancers from British patients. Cancer Genet Cytogenet 126: 111－119, 2001 https://doi.org/10.1016/S0165-4608(00)00397-6
  20. Thorgeirsson SS, Teramoto T, Factor VM. Dysregulation of apoptosis in hepatocellular carcinoma. Semin Liver Dis 18: 115－ 122, 1998 https://doi.org/10.1055/s-2007-1007148
  21. Tiemersma EW, Omer RE, Bunschoten A, van't Veer P, Kok FJ, Idris MO, Kadaru AM, Fedail SS, Kampman E. Role of genetic polymorphism of glutathione-S-transferase T1 and microsomal epoxide hydrolase in aflatoxin-associated hepatocellular carcinoma. Cancer Epidemiol Biomarkers Prev 10: 785－791, 2001
  22. Yu MW, Chiu YH, Yang SY, Santella RM, Chern HD, Liaw YF, Chen CJ. Cytochrome P450 1A1 genetic polymorphisms and risk of hepatocellular carcinoma among chronic hepatitis B carriers. Br J Cancer 80: 598－603, 1999 https://doi.org/10.1038/sj.bjc.6690397
  23. Yu MW, Pai CI, Yang SY, Hsiao TJ, Chang HC, Lin SM, Liaw YF, Chen PJ, Chen CJ. Role of N-acetyltransferase polymorphisms in hepatitis B related hepatocellular carcinoma: impact of smoking on risk. Gut 47: 703－709, 2000 https://doi.org/10.1136/gut.47.5.703
  24. Zhang YJ, Chen SY, Chen CJ, Santella RM. Polymorphisms in cyclin D1 gene and hepatocellular carcinoma. Mol Carcinog 33: 125－129, 2002 https://doi.org/10.1002/mc.10028