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Research Journal of Applied Biotechnology
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Dabour, S., Abied, M., Badra, G., El-Sayed, I. (2015). Molecular Evaluation of K-Ras Mutation in Egyptian Hepatocellular Carcinoma Patients. Research Journal of Applied Biotechnology, 1(1), 13-20. doi: 10.21608/rjab.2015.53281
Sara M. Dabour; Mohamed E. Abied; Gamal Badra; Ibrahim H. El-Sayed. "Molecular Evaluation of K-Ras Mutation in Egyptian Hepatocellular Carcinoma Patients". Research Journal of Applied Biotechnology, 1, 1, 2015, 13-20. doi: 10.21608/rjab.2015.53281
Dabour, S., Abied, M., Badra, G., El-Sayed, I. (2015). 'Molecular Evaluation of K-Ras Mutation in Egyptian Hepatocellular Carcinoma Patients', Research Journal of Applied Biotechnology, 1(1), pp. 13-20. doi: 10.21608/rjab.2015.53281
Dabour, S., Abied, M., Badra, G., El-Sayed, I. Molecular Evaluation of K-Ras Mutation in Egyptian Hepatocellular Carcinoma Patients. Research Journal of Applied Biotechnology, 2015; 1(1): 13-20. doi: 10.21608/rjab.2015.53281

Molecular Evaluation of K-Ras Mutation in Egyptian Hepatocellular Carcinoma Patients

Article 2, Volume 1, Issue 1, June 2015, Page 13-20  XML PDF (403.94 K)
Document Type: Original Article
DOI: 10.21608/rjab.2015.53281
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Authors
Sara M. Dabour* 1; Mohamed E. Abied email 1; Gamal Badra* 2; Ibrahim H. El-Sayed* 1
1Molecular Biology Department, Genetic Engineering and Biotechnology Research Institute - University of Sadat City, Egypt.
2Internal Medicine Department, National Liver Institute, Minoufiya University.
Abstract
Background. The RAS gene family is among the most studied and best characterized of theknown cancer-related genes. Of the three human ras isoforms, KRAS is the most frequently altered gene, with mutations occurring in 17%–25% of all cancers.
Aim of the study. The purpose of the study was identification of point mutation in codon 12 of K-RAS in Egyptian hepatocellular carcinoma (HCC) patients.
Patients and methods. Blood and urine samples were taken from 100 volunteers: 25 HCC patients, 25 HCC patients with HBV, HCV or schist soma infection and 50 healthy volunteers as control subject.
Mutant allele specific amplification (MASA), which is a highly sensitive method for detecting KRM, was performed, with the DNAS extracted from these samples.
Results. K-Ras mutation detected in 13 (13%) HCC patients from total 100. There was 4 patients with positive KRM among 22 HCC patients with HBV, 5 patients with positive KRM among 22 HCC patients with HCV infection and 3 HCC patients with schist soma have KRM.
Conclusion. The KRM incidence was found to be relatively high for HCC patients especially who combine HBV infection. This result suggests that the detection of KRM by MASA is useful for screening of HCC.
Keywords
K-Ras; codon 12; mutant allele specific amplification and hepatocellular carcinoma
References
Barbacid, M. (1987). Ras genes. Annu. Rev. Biochem 56: 779-827.
• Bos, J. L.; Fearon, E. R.; Hamilton. S. R. et al. (1987). Prevalence of raÃgene mutations in human colorectal cancers. Nature (Lond.). 327: 293-297.
• Diego, F.; Calvisi, Sara ladu, Elizabeth, A. Conner, Daekwan Seo, Jer-Tsong HsiehValentina M. factor , Snorri S. Thorgeirsson. (2011).Inactivation of Ras GTPase-activating proteins promotesunrestrained activity of wild-type Ras in human liver cancer. Journal of Hepatology. 54:311–3 9.
• El-Serag, H.B. and Rudolph, K.L. (2007). Hepatocellular carcinoma: epidemiology and molecular carcinogenesis. Gastroenterology 132: 2557–2576.
• Farr, C. J.; Saiki, R. K.; Erlich, H. A.; McCormic. F. and Marshall, C. J. (1988).Analysis of ras gene mutations in acute myeloid leukemia by polymerase chain reaction and oligonuclcotide probes. Proc. Nati. Acad. Sci. 85: 629- 633
• Hopkins, N.H.; Roberts, J. W.; Steits, J. A. and Weiner, A. M. (1987). The origins of human cancer. Molecular Biology of the Gene 2: 58- 96.
• Jemal, A.; Murray, T.; Ward, E.; Samuels, A.; Tiwari, RC.; Ghafoor, A. et al. (2005). Cancer statistics. CA Cancer J Clin. 55:10–3.
• Kranenburg, O.; Gebbink, M.F. and Voest, E.E. (2004). Stimulation of angiogenesis by Ras proteins. Biochim. Biophys. Acta .1654 :23– 37.
• Qingsu Xia, Ping Yi, De-Jin Zhan, Linda, S.; Von Tungeln, Ronald, W.; Hart, Robert, H.; Heflich, and Peter, P. Fu. (1998). Liver tumors induced in B6C3F1 mice by 7-chlorobenz[a]anthracene and 7-bromobenz[a]anthracene contain K-ras protooncogene mutations. Cancer Letters. 123: 21–25.
• Rodcnhuis, S.; van de Wetering, M. L.; Mooi, W. J.; Evers, S. G.; van Zandwijk, N. and Bos, J. L. (1987).
• Mutational activation of the K-ras oncogene: apossible pathogenetic factor in adenocarcinoma of the lung. N. Engl. J. Med 3 7:929-935.
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