Hepatitis B and C virus hepatocarcinogenesis: Lessons learned and future challenges

[Guest guest]

http://www.cancerletters.info/article/PIIS0304383510005495/abstract?rss=yes

CANCER LETTERS

Hepatitis B and C virus hepatocarcinogenesis: Lessons learned and future

challenges

J. Boucharda, Navas-b1

Received 12 August 2010; received in revised form 15 November 2010; accepted 25

November 2010. published online 20 December 2010.

Corrected Proof

Abstract

Worldwide, hepatocellular carcinoma (HCC) is one of the most common cancers. It

is thought that 80% of hepatocellular carcinomas are linked to chronic

infections with the hepatitis B (HBV) or hepatitis C (HCV) viruses. Chronic HBV

and HCV infections can alter hepatocyte physiology in similar ways and may

utilize similar mechanisms to influence the development of HCC. There has been

significant progress towards understanding the molecular biology of HBV and HCV

and identifying the cellular signal transduction pathways that are altered by

HBV and HCV infections. Although the precise molecular mechanisms that link HBV

and HCV infections to the development of HCC are not entirely understood, there

is considerable evidence that both inflammatory responses to infections with

these viruses, and associated destruction and regeneration of hepatocytes, as

well as activities of HBV- or HCV-encoded proteins, contribute to hepatocyte

transformation. In this review, we summarize progress in defining mechanisms

that may link HBV and HCV infections to the development of HCC, discuss the

challenges of directly defining the processes that underlie HBV- and

HCV-associated HCC, and describe areas that remain to be explored.

a Department of Biochemistry and Molecular Biology, Drexel University College of

Medicine, Philadelphia, PA 19102, USA

b Department of Microbiology and Immunology, Center for Molecular Virology and

Translational Neuroscience, Institute for Molecular Medicine and Infectious

Disease, Drexel University College of Medicine, Philadelphia, PA 19102, USA

Corresponding author. Address: Department of Biochemistry and Molecular Biology,

Drexel University College of Medicine, 245N. 15th Street, MS 497, Philadelphia,

PA 19102, USA. Tel.: +1 215 762 1898; fax: +1 215 762 4452.

1 Address: Department of Microbiology and Immunology, Drexel University College

of Medicine, 245N. 15th Street, MS1013A, Philadelphia, PA 19102, USA. Tel.: +1

215 762 7284; fax: +1 215 762 8284.

PII: S0304-3835(10)00549-5

doi:10.1016/j.canlet.2010.11.014

© 2010 Published by Elsevier Inc.

[Guest guest]

http://www.cancerletters.info/article/PIIS0304383510005495/abstract?rss=yes

CANCER LETTERS

Hepatitis B and C virus hepatocarcinogenesis: Lessons learned and future

challenges

J. Boucharda, Navas-b1

Received 12 August 2010; received in revised form 15 November 2010; accepted 25

November 2010. published online 20 December 2010.

Corrected Proof

Abstract

Worldwide, hepatocellular carcinoma (HCC) is one of the most common cancers. It

is thought that 80% of hepatocellular carcinomas are linked to chronic

infections with the hepatitis B (HBV) or hepatitis C (HCV) viruses. Chronic HBV

and HCV infections can alter hepatocyte physiology in similar ways and may

utilize similar mechanisms to influence the development of HCC. There has been

significant progress towards understanding the molecular biology of HBV and HCV

and identifying the cellular signal transduction pathways that are altered by

HBV and HCV infections. Although the precise molecular mechanisms that link HBV

and HCV infections to the development of HCC are not entirely understood, there

is considerable evidence that both inflammatory responses to infections with

these viruses, and associated destruction and regeneration of hepatocytes, as

well as activities of HBV- or HCV-encoded proteins, contribute to hepatocyte

transformation. In this review, we summarize progress in defining mechanisms

that may link HBV and HCV infections to the development of HCC, discuss the

challenges of directly defining the processes that underlie HBV- and

HCV-associated HCC, and describe areas that remain to be explored.

a Department of Biochemistry and Molecular Biology, Drexel University College of

Medicine, Philadelphia, PA 19102, USA

b Department of Microbiology and Immunology, Center for Molecular Virology and

Translational Neuroscience, Institute for Molecular Medicine and Infectious

Disease, Drexel University College of Medicine, Philadelphia, PA 19102, USA

Corresponding author. Address: Department of Biochemistry and Molecular Biology,

Drexel University College of Medicine, 245N. 15th Street, MS 497, Philadelphia,

PA 19102, USA. Tel.: +1 215 762 1898; fax: +1 215 762 4452.

1 Address: Department of Microbiology and Immunology, Drexel University College

of Medicine, 245N. 15th Street, MS1013A, Philadelphia, PA 19102, USA. Tel.: +1

215 762 7284; fax: +1 215 762 8284.

PII: S0304-3835(10)00549-5

doi:10.1016/j.canlet.2010.11.014

© 2010 Published by Elsevier Inc.