کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
8646284 1570079 2016 4 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Hepatitis C virus and schistosomiasis as a causative factor for hTERT amplification in hepatocellular carcinoma
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی ژنتیک
پیش نمایش صفحه اول مقاله
Hepatitis C virus and schistosomiasis as a causative factor for hTERT amplification in hepatocellular carcinoma
چکیده انگلیسی
Telomere abnormalities appear to play a role in carcinogenesis. hTERT is the catalytic component of the telomerase complex. It is regulates telomerase activity in cancers such as hepatocellular carcinoma (HCC). Amplification of the hTERT gene have been detected in about 21% of HCC. HCC occurs frequently in patients with chronic viral hepatitis or liver cirrhosis. Hepatitis B virus (HBV) or hepatitis C virus (HCV) induce HCC. The schistosomal parasite plays a role in the development of HCC through modify the course of hepatitis C accelerating progression to hepatitis C-associated fibrosis and thus quicker progression to HCC. The present study was conducted to evaluate hTERT amplification in HCC in association with HCV and schistosomiasis. Fifteen surgically resected HCC (Grade two) and fourteen cirrhotic resected liver were examined using FISH technique. Amplification of hTERT gene were found in 80% (12/15) of HCC which is much higher than the previously reported data. Eight samples were HCV and schistosomiasis positive, 4 were HCV positive, 2 were schistosomiasis positive and one was HCV and schistosomiasis negative. Amplification of the hTERT gene was not observed in cirrhotic tissues except two cases which is probably due to extension of adjacent HCC. From our results, the coexistence of HCV and/or schistosomiasis with hTERT amplification, we can conclude that the HCV and schistosomiasis may play an important role in upregulation of this gene. Consequently, this may lead to the development of HCC rather than just a marker for cancer development. However this conclusion might need further investigation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Gene Reports - Volume 5, December 2016, Pages 108-111
نویسندگان
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