Hepatocellular carcinoma: role of hepatitis B and hepatitis C viruses proteins in hepatocarcinogenesis

[Guest guest]

Journal of Viral Hepatitis

Volume 11 Issue 5 Page 383 - September 2004

doi:10.1111/j.1365-2893.2004.00521.x

REVIEW

Hepatocellular carcinoma: role of hepatitis B and hepatitis C viruses

proteins in hepatocarcinogenesis

M. Anzola

Summary. Hepatocellular carcinoma (HCC) is the most important primary

hepatic cancer, being a common cancer type worldwide. Many aetiological

factors have been related with HCC development, such as cirrhosis, hepatitis

viruses and alcohol. Chronic infection with hepatitis B (HBV) and C viruses

(HCV) often results in cirrhosis and enhances the probability of developing

HCC. The underlying mechanisms that lead to malignant transformation of

infected cells, however, remain unclear. HBV is a DNA virus that integrates

into the host genome, and this integration is believed, in part, to be

carcinogenic. Besides, the virus encodes a 17 kDa protein, HBx, which is

known to be a causative agent in the formation of HCC. On the contrary, HCV

is a RNA virus that does not integrate into the host genome but likely

induces HCC through host protein interactions or via the inflammatory

response to the virus. Products encoded in the HCV genome interfere with and

disturb intracellular signal transduction. Some HCV proteins, such as the

core protein, NS3 and NS5A, have seen to have a regulatory effect on

cellular promoters, to interact with a number of cellular proteins, and to

be involved in programmed-cell death modulation under certain conditions.

The identification of these proteins functions in HCC development and the

subsequent development of strategies to inhibit protein-protein interactions

may be the first step towards reducing the chronicity and/or of the

carcinogenicity of these two viruses.

[Guest guest]

Journal of Viral Hepatitis

Volume 11 Issue 5 Page 383 - September 2004

doi:10.1111/j.1365-2893.2004.00521.x

REVIEW

Hepatocellular carcinoma: role of hepatitis B and hepatitis C viruses

proteins in hepatocarcinogenesis

M. Anzola

Summary. Hepatocellular carcinoma (HCC) is the most important primary

hepatic cancer, being a common cancer type worldwide. Many aetiological

factors have been related with HCC development, such as cirrhosis, hepatitis

viruses and alcohol. Chronic infection with hepatitis B (HBV) and C viruses

(HCV) often results in cirrhosis and enhances the probability of developing

HCC. The underlying mechanisms that lead to malignant transformation of

infected cells, however, remain unclear. HBV is a DNA virus that integrates

into the host genome, and this integration is believed, in part, to be

carcinogenic. Besides, the virus encodes a 17 kDa protein, HBx, which is

known to be a causative agent in the formation of HCC. On the contrary, HCV

is a RNA virus that does not integrate into the host genome but likely

induces HCC through host protein interactions or via the inflammatory

response to the virus. Products encoded in the HCV genome interfere with and

disturb intracellular signal transduction. Some HCV proteins, such as the

core protein, NS3 and NS5A, have seen to have a regulatory effect on

cellular promoters, to interact with a number of cellular proteins, and to

be involved in programmed-cell death modulation under certain conditions.

The identification of these proteins functions in HCC development and the

subsequent development of strategies to inhibit protein-protein interactions

may be the first step towards reducing the chronicity and/or of the

carcinogenicity of these two viruses.

[Guest guest]

Journal of Viral Hepatitis

Volume 11 Issue 5 Page 383 - September 2004

doi:10.1111/j.1365-2893.2004.00521.x

REVIEW

Hepatocellular carcinoma: role of hepatitis B and hepatitis C viruses

proteins in hepatocarcinogenesis

M. Anzola

Summary. Hepatocellular carcinoma (HCC) is the most important primary

hepatic cancer, being a common cancer type worldwide. Many aetiological

factors have been related with HCC development, such as cirrhosis, hepatitis

viruses and alcohol. Chronic infection with hepatitis B (HBV) and C viruses

(HCV) often results in cirrhosis and enhances the probability of developing

HCC. The underlying mechanisms that lead to malignant transformation of

infected cells, however, remain unclear. HBV is a DNA virus that integrates

into the host genome, and this integration is believed, in part, to be

carcinogenic. Besides, the virus encodes a 17 kDa protein, HBx, which is

known to be a causative agent in the formation of HCC. On the contrary, HCV

is a RNA virus that does not integrate into the host genome but likely

induces HCC through host protein interactions or via the inflammatory

response to the virus. Products encoded in the HCV genome interfere with and

disturb intracellular signal transduction. Some HCV proteins, such as the

core protein, NS3 and NS5A, have seen to have a regulatory effect on

cellular promoters, to interact with a number of cellular proteins, and to

be involved in programmed-cell death modulation under certain conditions.

The identification of these proteins functions in HCC development and the

subsequent development of strategies to inhibit protein-protein interactions

may be the first step towards reducing the chronicity and/or of the

carcinogenicity of these two viruses.

[Guest guest]

Journal of Viral Hepatitis

Volume 11 Issue 5 Page 383 - September 2004

doi:10.1111/j.1365-2893.2004.00521.x

REVIEW

Hepatocellular carcinoma: role of hepatitis B and hepatitis C viruses

proteins in hepatocarcinogenesis

M. Anzola

Summary. Hepatocellular carcinoma (HCC) is the most important primary

hepatic cancer, being a common cancer type worldwide. Many aetiological

factors have been related with HCC development, such as cirrhosis, hepatitis

viruses and alcohol. Chronic infection with hepatitis B (HBV) and C viruses

(HCV) often results in cirrhosis and enhances the probability of developing

HCC. The underlying mechanisms that lead to malignant transformation of

infected cells, however, remain unclear. HBV is a DNA virus that integrates

into the host genome, and this integration is believed, in part, to be

carcinogenic. Besides, the virus encodes a 17 kDa protein, HBx, which is

known to be a causative agent in the formation of HCC. On the contrary, HCV

is a RNA virus that does not integrate into the host genome but likely

induces HCC through host protein interactions or via the inflammatory

response to the virus. Products encoded in the HCV genome interfere with and

disturb intracellular signal transduction. Some HCV proteins, such as the

core protein, NS3 and NS5A, have seen to have a regulatory effect on

cellular promoters, to interact with a number of cellular proteins, and to

be involved in programmed-cell death modulation under certain conditions.

The identification of these proteins functions in HCC development and the

subsequent development of strategies to inhibit protein-protein interactions

may be the first step towards reducing the chronicity and/or of the

carcinogenicity of these two viruses.