867. Accumulation of Hepatitis B Virus DNA in Hepatocellular Carcinoma of Patients with Sustained Virological Response for Hepatitis C Virus

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867. Accumulation of Hepatitis B Virus DNA in Hepatocellular Carcinoma of

Patients with Sustained Virological Response for Hepatitis C Virus

A. Tamori; T. Hayashi; M. Shinzaki; S. Kobayshi; S. Iwai; H. Morikawa; M.

Enomoto; H. Sakaguchi; S. Shiomi; S. Kubo; N. Kawada

Background and Aim:

Hepatocellular carcinoma (HCC) has been reported in patients in whom hepatitis C

virus (HCV) was eliminated by interferon (IFN) therapy. HBV genome is frequently

detectable in liver tumors in HBsAg-negative patients with HCV. To elucidate the

role of occult HBV infection on HCC in patients with sustained viral response

(SVR HCC), we compared the clinical factors of SVR HCC and those of HCV HCC.

Patients and Methods:

Operable HCC developed in fifteen of 342 patients cured of HCV infection by IFN

monotherapy. We examined 15 patients with SVR HCC and 50 patients with HCV. All

patients were male. No patient abused alcohol or autoimmune hepatitis or primary

biliary cirrhosis. Mean age was 66 years in patients with SVR HCC and 65 years

in patients with HCV HCC. Anti-HBc and anti-HBs in serum were examined with

enzyme-linked immunoassay. HBV-DNA in serum and in liver was examined by nested

polymerase chain reaction (PCR) using primers specific for HBx, HBs, HBc,

cccHBV. In seven samples from SVR HCC, HBV integration sites in human genome

were identified by cassette-ligation-mediated PCR.

Results:

Anti-HBc was positive in 10 (66.7%) of 15 patients with SVR HCC and in 25 (50%)

of 50 patients with HCV HCC. Anti-HBs was positive in six (40%) of 15 SVR HCC

and nine (18%) of 50 HCV HCC. HBV DNA was not amplified in serum samples from

SVR HCC and HCV HCC. Occult HBV infections were twelve (80%) of 15 in SVR HCC

and 20 (40%) of 50 in HCV HCC (p = 0.015). HBV DNA integration was detected in

four of 7 SVR HCC. The liver of SVR HCC with HBV DNA integration had not

progressed to cirrhosis. Three tumors with HBV integration had one integration

site each, located at chromosomes 11q12, 11q22-23, and 22q11, respectively. The

other tumor had two integration sites, situated at chromosomes 11q13 and 14q32.

At chromosome 11q12, HBV DNA was integrated into protein-coding genome, the

function of which remains unclear.

Conclusion:

Occult HBV infection might be one of the most important factors in SVR HCC in

Japan

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http://www.hbvadvocate.org/news/reports/HBV_AASLD_2008/Abstracts/Nov2%20Disease%\

20Progression.htm#Nov2a867

867. Accumulation of Hepatitis B Virus DNA in Hepatocellular Carcinoma of

Patients with Sustained Virological Response for Hepatitis C Virus

A. Tamori; T. Hayashi; M. Shinzaki; S. Kobayshi; S. Iwai; H. Morikawa; M.

Enomoto; H. Sakaguchi; S. Shiomi; S. Kubo; N. Kawada

Background and Aim:

Hepatocellular carcinoma (HCC) has been reported in patients in whom hepatitis C

virus (HCV) was eliminated by interferon (IFN) therapy. HBV genome is frequently

detectable in liver tumors in HBsAg-negative patients with HCV. To elucidate the

role of occult HBV infection on HCC in patients with sustained viral response

(SVR HCC), we compared the clinical factors of SVR HCC and those of HCV HCC.

Patients and Methods:

Operable HCC developed in fifteen of 342 patients cured of HCV infection by IFN

monotherapy. We examined 15 patients with SVR HCC and 50 patients with HCV. All

patients were male. No patient abused alcohol or autoimmune hepatitis or primary

biliary cirrhosis. Mean age was 66 years in patients with SVR HCC and 65 years

in patients with HCV HCC. Anti-HBc and anti-HBs in serum were examined with

enzyme-linked immunoassay. HBV-DNA in serum and in liver was examined by nested

polymerase chain reaction (PCR) using primers specific for HBx, HBs, HBc,

cccHBV. In seven samples from SVR HCC, HBV integration sites in human genome

were identified by cassette-ligation-mediated PCR.

Results:

Anti-HBc was positive in 10 (66.7%) of 15 patients with SVR HCC and in 25 (50%)

of 50 patients with HCV HCC. Anti-HBs was positive in six (40%) of 15 SVR HCC

and nine (18%) of 50 HCV HCC. HBV DNA was not amplified in serum samples from

SVR HCC and HCV HCC. Occult HBV infections were twelve (80%) of 15 in SVR HCC

and 20 (40%) of 50 in HCV HCC (p = 0.015). HBV DNA integration was detected in

four of 7 SVR HCC. The liver of SVR HCC with HBV DNA integration had not

progressed to cirrhosis. Three tumors with HBV integration had one integration

site each, located at chromosomes 11q12, 11q22-23, and 22q11, respectively. The

other tumor had two integration sites, situated at chromosomes 11q13 and 14q32.

At chromosome 11q12, HBV DNA was integrated into protein-coding genome, the

function of which remains unclear.

Conclusion:

Occult HBV infection might be one of the most important factors in SVR HCC in

Japan

[Guest guest]

http://www.hbvadvocate.org/news/reports/HBV_AASLD_2008/Abstracts/Nov2%20Disease%\

20Progression.htm#Nov2a867

867. Accumulation of Hepatitis B Virus DNA in Hepatocellular Carcinoma of

Patients with Sustained Virological Response for Hepatitis C Virus

A. Tamori; T. Hayashi; M. Shinzaki; S. Kobayshi; S. Iwai; H. Morikawa; M.

Enomoto; H. Sakaguchi; S. Shiomi; S. Kubo; N. Kawada

Background and Aim:

Hepatocellular carcinoma (HCC) has been reported in patients in whom hepatitis C

virus (HCV) was eliminated by interferon (IFN) therapy. HBV genome is frequently

detectable in liver tumors in HBsAg-negative patients with HCV. To elucidate the

role of occult HBV infection on HCC in patients with sustained viral response

(SVR HCC), we compared the clinical factors of SVR HCC and those of HCV HCC.

Patients and Methods:

Operable HCC developed in fifteen of 342 patients cured of HCV infection by IFN

monotherapy. We examined 15 patients with SVR HCC and 50 patients with HCV. All

patients were male. No patient abused alcohol or autoimmune hepatitis or primary

biliary cirrhosis. Mean age was 66 years in patients with SVR HCC and 65 years

in patients with HCV HCC. Anti-HBc and anti-HBs in serum were examined with

enzyme-linked immunoassay. HBV-DNA in serum and in liver was examined by nested

polymerase chain reaction (PCR) using primers specific for HBx, HBs, HBc,

cccHBV. In seven samples from SVR HCC, HBV integration sites in human genome

were identified by cassette-ligation-mediated PCR.

Results:

Anti-HBc was positive in 10 (66.7%) of 15 patients with SVR HCC and in 25 (50%)

of 50 patients with HCV HCC. Anti-HBs was positive in six (40%) of 15 SVR HCC

and nine (18%) of 50 HCV HCC. HBV DNA was not amplified in serum samples from

SVR HCC and HCV HCC. Occult HBV infections were twelve (80%) of 15 in SVR HCC

and 20 (40%) of 50 in HCV HCC (p = 0.015). HBV DNA integration was detected in

four of 7 SVR HCC. The liver of SVR HCC with HBV DNA integration had not

progressed to cirrhosis. Three tumors with HBV integration had one integration

site each, located at chromosomes 11q12, 11q22-23, and 22q11, respectively. The

other tumor had two integration sites, situated at chromosomes 11q13 and 14q32.

At chromosome 11q12, HBV DNA was integrated into protein-coding genome, the

function of which remains unclear.

Conclusion:

Occult HBV infection might be one of the most important factors in SVR HCC in

Japan

[Guest guest]

http://www.hbvadvocate.org/news/reports/HBV_AASLD_2008/Abstracts/Nov2%20Disease%\

20Progression.htm#Nov2a867

867. Accumulation of Hepatitis B Virus DNA in Hepatocellular Carcinoma of

Patients with Sustained Virological Response for Hepatitis C Virus

A. Tamori; T. Hayashi; M. Shinzaki; S. Kobayshi; S. Iwai; H. Morikawa; M.

Enomoto; H. Sakaguchi; S. Shiomi; S. Kubo; N. Kawada

Background and Aim:

Hepatocellular carcinoma (HCC) has been reported in patients in whom hepatitis C

virus (HCV) was eliminated by interferon (IFN) therapy. HBV genome is frequently

detectable in liver tumors in HBsAg-negative patients with HCV. To elucidate the

role of occult HBV infection on HCC in patients with sustained viral response

(SVR HCC), we compared the clinical factors of SVR HCC and those of HCV HCC.

Patients and Methods:

Operable HCC developed in fifteen of 342 patients cured of HCV infection by IFN

monotherapy. We examined 15 patients with SVR HCC and 50 patients with HCV. All

patients were male. No patient abused alcohol or autoimmune hepatitis or primary

biliary cirrhosis. Mean age was 66 years in patients with SVR HCC and 65 years

in patients with HCV HCC. Anti-HBc and anti-HBs in serum were examined with

enzyme-linked immunoassay. HBV-DNA in serum and in liver was examined by nested

polymerase chain reaction (PCR) using primers specific for HBx, HBs, HBc,

cccHBV. In seven samples from SVR HCC, HBV integration sites in human genome

were identified by cassette-ligation-mediated PCR.

Results:

Anti-HBc was positive in 10 (66.7%) of 15 patients with SVR HCC and in 25 (50%)

of 50 patients with HCV HCC. Anti-HBs was positive in six (40%) of 15 SVR HCC

and nine (18%) of 50 HCV HCC. HBV DNA was not amplified in serum samples from

SVR HCC and HCV HCC. Occult HBV infections were twelve (80%) of 15 in SVR HCC

and 20 (40%) of 50 in HCV HCC (p = 0.015). HBV DNA integration was detected in

four of 7 SVR HCC. The liver of SVR HCC with HBV DNA integration had not

progressed to cirrhosis. Three tumors with HBV integration had one integration

site each, located at chromosomes 11q12, 11q22-23, and 22q11, respectively. The

other tumor had two integration sites, situated at chromosomes 11q13 and 14q32.

At chromosome 11q12, HBV DNA was integrated into protein-coding genome, the

function of which remains unclear.

Conclusion:

Occult HBV infection might be one of the most important factors in SVR HCC in

Japan