Minjie Wang1, Yuting Wang2, Xiaoshuang Feng3, Ruijun Wang4, Yanmei Wang5, Hongmei Zeng6, Jun Qi7, Hong Zhao8, Ni Li9, Jianqiang Cai10, Chunfeng Qu11. 1. National Cancer Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China. Electronic address: chinaminjie@sina.com. 2. National Cancer Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China. Electronic address: wyt2051@163.com. 3. National Cancer Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China. Electronic address: fengxs2016@163.com. 4. National Cancer Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China. Electronic address: wangruijun21cams@163.com. 5. National Cancer Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China. Electronic address: wangyanmei_cams@163.com. 6. National Cancer Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China. Electronic address: hongmeizeng2011@163.com. 7. National Cancer Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China. Electronic address: qijun5610@126.com. 8. National Cancer Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China. Electronic address: zhaohong@cicams.ac.cn. 9. National Cancer Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China. Electronic address: lini1240@hotmail.com. 10. National Cancer Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China. Electronic address: caijianqiang188@sina.com. 11. National Cancer Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China. Electronic address: quchf@cicams.ac.cn.
Abstract
INTRODUCTION: The aim of this study was to determine the impact of hepatitis B virus (HBV) and/or hepatitis C virus (HCV) on primary liver cancer (PLC) in China north areas. METHODS: A total of 2172 histologically confirmed PLC patients attending the National Cancer Center/Cancer Hospital, Chinese Academy of Medical Sciences during the period January 1, 2003 to December 31, 2014 were enrolled. Details of hepatitis B surface antigen (HBsAg), antibodies against HBV core antigen (anti-HBc), and antibodies against HCV (anti-HCV) status were recorded. Sequencing of the HBV PreS-S gene and the C/E1 and NS5B fragments of HCV was performed and the genotypes were analyzed for some of the patients with hepatocellular carcinoma (HCC). RESULTS: Among the 2172 histologically confirmed PLC cases, 1823 (83.9%) had HCC and 238 (11.0%) had intrahepatic cholangiocarcinoma (iCCA). Among HCC cases, HBV infection alone, indicated by HBsAg-neg/pos+anti-HBc-pos, was found in 1567 (86.0%) cases; of these, 18.2% (331/1823) were HBsAg-neg+anti-HBc-pos. Serum HBV-DNA was detectable in 70% of HBsAg-neg+anti-HBc-pos HCC cases. The dominant HBV genotype was HBV-C2 (94.4%). HCV infection alone, indicated by anti-HCV-pos, was found in 2.5% (46/1823) of cases; HCV-1b (72.1%) was the dominant genotype. HBV+HCV co-infection markers were found in 6.7% (122/1823) of cases. Only 88 (4.8%) cases had no HBV and no HCV markers. Among the 238 iCCA cases, 54 (22.7%) were HBsAg-pos+anti-HBc-pos; none was anti-HCV-pos alone. CONCLUSIONS: HBV remains the major contributor to PLC in China north areas Individuals with occult HBV infection should not be ignored in liver cancer screening.
INTRODUCTION: The aim of this study was to determine the impact of hepatitis B virus (HBV) and/or hepatitis C virus (HCV) on primary liver cancer (PLC) in China north areas. METHODS: A total of 2172 histologically confirmed PLC patients attending the National Cancer Center/Cancer Hospital, Chinese Academy of Medical Sciences during the period January 1, 2003 to December 31, 2014 were enrolled. Details of hepatitis B surface antigen (HBsAg), antibodies against HBV core antigen (anti-HBc), and antibodies against HCV (anti-HCV) status were recorded. Sequencing of the HBV PreS-S gene and the C/E1 and NS5B fragments of HCV was performed and the genotypes were analyzed for some of the patients with hepatocellular carcinoma (HCC). RESULTS: Among the 2172 histologically confirmed PLC cases, 1823 (83.9%) had HCC and 238 (11.0%) had intrahepatic cholangiocarcinoma (iCCA). Among HCC cases, HBV infection alone, indicated by HBsAg-neg/pos+anti-HBc-pos, was found in 1567 (86.0%) cases; of these, 18.2% (331/1823) were HBsAg-neg+anti-HBc-pos. Serum HBV-DNA was detectable in 70% of HBsAg-neg+anti-HBc-pos HCC cases. The dominant HBV genotype was HBV-C2 (94.4%). HCV infection alone, indicated by anti-HCV-pos, was found in 2.5% (46/1823) of cases; HCV-1b (72.1%) was the dominant genotype. HBV+HCV co-infection markers were found in 6.7% (122/1823) of cases. Only 88 (4.8%) cases had no HBV and no HCV markers. Among the 238 iCCA cases, 54 (22.7%) were HBsAg-pos+anti-HBc-pos; none was anti-HCV-pos alone. CONCLUSIONS:HBV remains the major contributor to PLC in China north areas Individuals with occult HBV infection should not be ignored in liver cancer screening.
Authors: Fang Wang; Sumaira Mubarik; Yu Zhang; Lu Wang; Yafeng Wang; Chuanhua Yu; Hao Li Journal: Int J Environ Res Public Health Date: 2019-08-12 Impact factor: 3.390
Authors: Marco Fiore; Sebastiano Leone; Alberto Enrico Maraolo; Emilio Berti; Giovanni Damiani Journal: Biomed Res Int Date: 2018-02-06 Impact factor: 3.411