Cumulative Risk of Hepatocellular Carcinoma in Hepatitis C Virus Carriers: Statistical Estimations from Cross‐sectional Data

Abstract

The probability of developing hepatocellular carcinoma (HCC) among hepatitis C virus (HCV) carriers during their life‐time is unknown. This paper addresses the estimation of the cumulative risk of HCC among HCV carriers using cross‐sectional data. Age‐specific prevalences of HCV carriers among the general population were estimated according to 5‐year age group, based on the data of 2nd‐generation anti‐HCV assay in blood donors resident in Osaka (33,226 males and 29,054 females). Seropositivity of anti‐HCV among 422 HCC cases, and the Osaka Cancer Registry data on HCC were used in the estimations of 5‐year age‐specific incidence rates of HCV‐linked HCC. Using these data, the cumulative risk, i.e., the probability of contracting HCC within the following 15 years in 50‐year‐old HCV carriers, was estimated as 28% for males and 6% for females.

Factors predictive of response to interferon‐α therapy in hepatitis C virus type 1b infection

“…HCV-induced hepatitis develops as an acute post-transfusion hepatitis in more than 50% of the cases over a 1-year period, while cirrhosis occurs in about 20% of HCV-infected patients after 10 to 20 years [Di Bisceglie et al, 1991;Takahashi et al, 1993]. It is also known that HCV is related to the pathogenesis of hepatocellular carcinoma [Bruix et al, 1989;Kiyosawa et al, 1990;Tanaka et al, 1994].…”

“…Thus, many studies have been carried out to determine the predictive factors of interferon therapy. It has been suggested that different responses to IFN-a treatment in HCV infection might be in¯u-enced by the HCV genotype [Tanaka et al, 1994;Tsubota et al, 1994;Nagayama et al, 2000], by HCV RNA titer at the beginning of IFN-a therapy [Naito et al, 1994;Yoon et al, 1995], by the complexity of quasispecies in the HVR 1 Koizumi et al, 1995;Yuki et al, 1997;Farci et al, 2000], or by the sequences of the interferon sensitivity determining region (ISDR) of nonstructural 5A (NS5A) Kurosaki et al, 1997]. In contrast, other reports have shown opposite results concerning the complexity of quasispecies and ISDR sequences [Herion and Hoofnagle, 1997;Frangeul et al, 1998].…”

Generation of Hepatitis C Virus-Like Particles by Use of a Recombinant Vesicular Stomatitis Virus Vector

“…Mice immunized with VSV-HCV-C/E1/E2 generated cell-mediated immune responses to all of the HCV structural proteins, and humoral responses, particularly to E2, were also readily evident. Our data collectively indicate that engineered VSVs expressing HCV Core, E1, and E2 and/or HCV-LPs represent useful tools in vaccine and immunotherapeutic strategies designed to address HCV infection.Hepatitis C virus (HCV), a hepatotropic, positive-stranded RNA virus of the Flaviviridae family, is estimated to infect at least 400 million people worldwide and is a major etiologic agent of liver failure and hepatocellular carcinoma (11,66,70). HCV comprises a 9.6-kb genome with a conserved 5Ј untranslated region that functions as an internal ribosome entry site (33, 69).…”

“…Hepatitis C virus (HCV), a hepatotropic, positive-stranded RNA virus of the Flaviviridae family, is estimated to infect at least 400 million people worldwide and is a major etiologic agent of liver failure and hepatocellular carcinoma (11,66,70). HCV comprises a 9.6-kb genome with a conserved 5Ј untranslated region that functions as an internal ribosome entry site (33, 69).…”

Activation of human Kupffer cells by thymostimulin (TP-1) to produce cytotoxicity against human hepatocellular cancer

“…Patients with chronic hepatitis B or C virus infection are at high risk of developing HCC (7)(8)(9). In a pilot study of patients with chronic viral hepatitis and HCC, almost 50% of the patients treated with systemic TP-I had reduction in the size of their unresectable liver cancers (10).…”