Strategies for the Management of Hepatocellular Carcinoma
Hepatocellular carcinoma (HCC) generally develops as a consequence of underlying liver disease, most commonly viral hepatitis. The development of HCC follows an orderly progression from cirrhosis to dysplastic nodules to early cancer development, which can be reliably cured if discovered before the development of vascular invasion (typically occurring at a tumor diameter of approximately 2 cm). The identifiable population at risk makes screening a realistic possibility, and liver imaging is recommended every 6 months for patients with cirrhosis. For patients with preserved liver function and no portal hypertension who develop HCC that is confined to one region of the liver, resection is the preferred treatment. If resection is not possible because of poor liver function, and the HCC is within the Milan criteria (1 nodule ≥5 cm, 2–3 nodules ≥3 cm), liver transplantation is the treatment of choice. To prevent tumor progression while waiting, nonsurgical treatments including percutaneous ethanol injection, radiofrequency ablation, and transarterial chemoembolization are employed, but drop-out from the waiting list remains a problem. Living donor transplantation is an alternative that can eliminate drop-out and enable liver transplantation for patients with HCC whose disease does not fall within the Milan criteria. There is a need for more effective adjuvant therapies after resection and liver transplantation; newer antiangiogenic agents offer hope for improved outcomes in the future.
Hepatocellular carcinoma (HCC) is the fifth most common cancer worldwide, and is the most rapidly increasing type of cancer in the US. In the vast majority of cases, HCC arises as a consequence of underlying liver disease, usually viral hepatitis, the nature of which varies according to geographical region. Consequently, the mechanisms of hepatocarcinogenesis and the tumor characteristics vary from one part of the world to another. In Africa and Southern Asia, the role of hepatitis B virus (HBV) infection—which is acquired at birth or early in life—is highly predominant, and may be compounded by aflatoxin exposure, causing HCC to develop at a young age. By contrast, in Japan and Western countries, the hepatitis C virus (HCV) is the predominant cause of HCC. The rapid rise of HCC in the West is related to an epidemic of HCV infection due to contamination of the blood supply and, more recently, spread via intravenous drug use. Recent estimates suggest that 4 million people in the US are infected with HCV. Coinfection with HIV is increasingly seen in patients with HCC, and while this may complicate management, there is thus far no clear evidence that coinfection increases the risk of developing HCC.
Cirrhosis from any cause (e.g. alcohol, nonalcoholic steatohepatitis) predisposes to the development of HCC. The incidence is particularly high in the setting of hereditary tyrosinemia, where HCC develops in childhood, and in primary hemochromatosis. The use of sex steroids, both estrogenic and androgenic, is associated with the development of HCC in the absence of cirrhosis.
Summary and Introduction
Summary
Hepatocellular carcinoma (HCC) generally develops as a consequence of underlying liver disease, most commonly viral hepatitis. The development of HCC follows an orderly progression from cirrhosis to dysplastic nodules to early cancer development, which can be reliably cured if discovered before the development of vascular invasion (typically occurring at a tumor diameter of approximately 2 cm). The identifiable population at risk makes screening a realistic possibility, and liver imaging is recommended every 6 months for patients with cirrhosis. For patients with preserved liver function and no portal hypertension who develop HCC that is confined to one region of the liver, resection is the preferred treatment. If resection is not possible because of poor liver function, and the HCC is within the Milan criteria (1 nodule ≥5 cm, 2–3 nodules ≥3 cm), liver transplantation is the treatment of choice. To prevent tumor progression while waiting, nonsurgical treatments including percutaneous ethanol injection, radiofrequency ablation, and transarterial chemoembolization are employed, but drop-out from the waiting list remains a problem. Living donor transplantation is an alternative that can eliminate drop-out and enable liver transplantation for patients with HCC whose disease does not fall within the Milan criteria. There is a need for more effective adjuvant therapies after resection and liver transplantation; newer antiangiogenic agents offer hope for improved outcomes in the future.
Introduction
Hepatocellular carcinoma (HCC) is the fifth most common cancer worldwide, and is the most rapidly increasing type of cancer in the US. In the vast majority of cases, HCC arises as a consequence of underlying liver disease, usually viral hepatitis, the nature of which varies according to geographical region. Consequently, the mechanisms of hepatocarcinogenesis and the tumor characteristics vary from one part of the world to another. In Africa and Southern Asia, the role of hepatitis B virus (HBV) infection—which is acquired at birth or early in life—is highly predominant, and may be compounded by aflatoxin exposure, causing HCC to develop at a young age. By contrast, in Japan and Western countries, the hepatitis C virus (HCV) is the predominant cause of HCC. The rapid rise of HCC in the West is related to an epidemic of HCV infection due to contamination of the blood supply and, more recently, spread via intravenous drug use. Recent estimates suggest that 4 million people in the US are infected with HCV. Coinfection with HIV is increasingly seen in patients with HCC, and while this may complicate management, there is thus far no clear evidence that coinfection increases the risk of developing HCC.
Cirrhosis from any cause (e.g. alcohol, nonalcoholic steatohepatitis) predisposes to the development of HCC. The incidence is particularly high in the setting of hereditary tyrosinemia, where HCC develops in childhood, and in primary hemochromatosis. The use of sex steroids, both estrogenic and androgenic, is associated with the development of HCC in the absence of cirrhosis.
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