Hepatitis B and C virus infections as possible risk factor for pancreatic adenocarcinoma

2012 ◽  
Vol 79 (5) ◽  
pp. 678-697 ◽  
Author(s):  
S. Fiorino ◽  
S. Lorenzini ◽  
M. Masetti ◽  
G. Deleonardi ◽  
A.G. Grondona ◽  
...  
2021 ◽  
Vol 5.3 (3) ◽  
pp. 22-26
Author(s):  
Folly Anyovi ◽  
Akomola Sabi ◽  
Yoan Amekoudi ◽  
Mawufemo Tsevi ◽  
Reham Soliman ◽  
...  

2020 ◽  
Vol 101 ◽  
pp. 328-329
Author(s):  
A. Lawal ◽  
A. Alhaji Abubakar ◽  
S. Muawiyya ◽  
Babale ◽  
A. Abayomi. Olorukooba ◽  
...  

2017 ◽  
Vol 84 (5) ◽  
pp. 525-530 ◽  
Author(s):  
Marco Sebastiani ◽  
Fabiola Atzeni ◽  
Laura Milazzo ◽  
Luca Quartuccio ◽  
Carlo Scirè ◽  
...  

1997 ◽  
Vol 88 (2) ◽  
pp. 87-90 ◽  
Author(s):  
Kevin W. Glasgow ◽  
Richard Schabas ◽  
David C. Williams ◽  
Evelyn Wallace ◽  
Lee Ann Nalezyty

2008 ◽  
Vol 89 (11) ◽  
pp. 2882-2890 ◽  
Author(s):  
Zhong-Liao Fang ◽  
Caroline A. Sabin ◽  
Bai-Qing Dong ◽  
Shao-Chao Wei ◽  
Qin-Yan Chen ◽  
...  

A matched nested case–control study of 33 paired cases and controls was conducted, based on a study cohort in Long An county, Guangxi, China, to determine whether infection with hepatitis B virus (HBV) with pre-S deletions is independently associated with the development of hepatocellular carcinoma (HCC), without the confounding effects of basal core promoter (BCP) double mutations. The prevalence of pre-S deletions was significantly higher in HCC (45.5 %, 15 of 33) than the controls (18.2 %, 6 of 33) (P<0.01), under the control of the influence of BCP double mutations. Most of the pre-S deletions occurred in, or involved, the 5′ half of the pre-S2 region and the difference between HCC (93.3 %, 14 of 15) and controls (66.7 %, four of six) was significant for this region (P=0.015). There was no significant difference in pre-S deletions between the BCP mutant group and BCP wild-type group (P>0.05), nor was the prevalence of pre-S deletions significantly different between genotypes B and C (P>0.1). These results suggest that pre-S deletions constitute an independent risk factor for HCC and their emergence and effect are independent of BCP mutations. The 5′ terminus of pre-S2 is the favoured site for the deletion mutations, especially in HCC cases. Further prospective studies are required to confirm the role of these mutations in the development of HCC.


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