Frequent detection of hepatitis B virus DNA in hepatocellular carcinoma of patients with sustained virologic response for hepatitis C virus

2009 ◽  
Vol 81 (6) ◽  
pp. 1009-1014 ◽  
Author(s):  
Akihiro Tamori ◽  
Takehiro Hayashi ◽  
Mayumi Shinzaki ◽  
Sawako Kobayashi ◽  
Shuji Iwai ◽  
...  
2000 ◽  
Vol 118 (4) ◽  
pp. A1005
Author(s):  
Akihiro Tamori ◽  
Shuhei Nishiguchi ◽  
Shoji Kubo ◽  
Susumu Shiomi ◽  
Shuichi Seki ◽  
...  

2005 ◽  
Vol 100 (8) ◽  
pp. 1748-1753 ◽  
Author(s):  
Akihiro Tamori ◽  
Shuhei Nishiguchi ◽  
Susumu Shiomi ◽  
Takehiro Hayashi ◽  
Sawako Kobayashi ◽  
...  

2017 ◽  
Vol 05 (03) ◽  
Author(s):  
Jennifer Wu ◽  
Tsivia Hochman ◽  
Judith D Goldberg ◽  
Jafar Al Mondhiry ◽  
Bennal Perkins ◽  
...  

2018 ◽  
Vol 12 (1) ◽  
pp. 26-32 ◽  
Author(s):  
Arnolfo Petruzziello

Introduction:Hepatocellular carcinoma (HCC) is one of the most prevalent primary malignant tumors and accounts for about 90% of all primary liver cancers. Its distribution varies greatly according to geographic location and it is more common in middle and low- income countries than in developed ones especially in Eastern Asia and Sub Saharan Africa (70% of all new HCCs worldwide), with incidence rates of over 20 per 100,000 individuals.Explanation:The most important risk factors for HCC are Hepatitis B Virus (HBV) infection, Hepatitis C Virus (HCV) infection, excessive consumption of alcohol and exposition to aflatoxin B1. Its geographic variability and heterogeneity have been widely associated with the different distribution of HBV and HCV infections worldwide.Chronic HBV infection is one of the leading risk factors for HCC globally accounting for at least 50% cases of primary liver tumors worldwide. Generally, while HBV is the main causative agent in the high incidence HCC areas, HCV is the major etiological factor in low incidence HCC areas, like Western Europe and North America.Conclusion:HBV-induced HCC is a complex, stepwise process that includes integration of HBV DNA into host DNA at multiple or single sites. On the contrary, the cancerogenesis mechanism of HCV is not completely known and it still remains controversial as to whether HCV itself plays a direct role in the development of tumorigenic progression.


2011 ◽  
Vol 140 (5) ◽  
pp. S-924-S-925 ◽  
Author(s):  
Hillary Lin ◽  
Nghiem B. Ha ◽  
Deawodi Ladzekpo ◽  
Aijaz Ahmed ◽  
Walid Ayoub ◽  
...  

2019 ◽  
Vol 71 (3) ◽  
pp. 664-666 ◽  
Author(s):  
Adeel A Butt ◽  
Peng Yan ◽  
Samia Aslam ◽  
Abdul-Badi Abou-Samra ◽  
Kenneth E Sherman ◽  
...  

Abstract For persons with baseline Fibrosis-4 1.46–3.25, cirrhosis incidence/1000 patient-years was 49.3 among hepatitis B virus (HBV)/hepatitis C virus (HCV) coinfected and 18.2 among HCV monoinfected (P = .03). Cirrhosis risk was numerically higher but statistically nonsignificant among HBV/HCV coinfected (hazards ratio [HR] 1.51; 95% confidence intervals [CI], .37–6.05) but lower among those who attained sustained virologic response (HR, .52; 95% CI, .42–.63).


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