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Cancer of the Liver

Hepatocellular carcinoma (HCC) (liver cancer) is an aggressive disease.1 Worldwide, HCC is the second leading cause of cancer death among men, and the sixth leading cause of cancer death among women.2 In the US for the year 2009, there were approximately 4.9 new cases of liver cancer per 100,000 people. 3

Hepatitis C (HCV) accounts for about one-third of cases of liver cancer in the US population. Among people with HCV, HCC appears to develop almost exclusively in those with cirrhosis. In studies of people with HCV, the risk for HCC increased as much as 3% per year after diagnosis of cirrhosis.4

In one study conducted in 384 people with HCV who had compensated cirrhosis, risk of developing liver cancer increased steadily over time after diagnosis of cirrhosis. 5

Factors that increase risk for liver cancer

In people with HCV infection, cirrhosis is a major risk factor for developing HCC. Studies show an increased risk of HCC for HCV patients with genotype 1b or genotype 3. It is also thought that HCV infection itself may promote development of liver cancer.5,6

Hepatitis B (HBV) infection is a recognized risk factor liver cancer. A major difference between HBV and HCV is that HBV increases liver cancer risk without cirrhosis. Additionally, there is some evidence that obesity, fatty liver disease, diabetes, and alcohol consumption may contribute to increased risk of HCC.1,4

Treatment of HCV with antiviral therapy appears to decrease risk for HCC. People who achieve sustained virologic responses (SVR), or complete clearance of the virus, achieve the greatest risk reduction. Patients with cirrhosis, regardless of HCV status, have an increased HCC risk.7

Chronic inflammation and cellular turnover

Scientists think that HCC develops in HCV patients because of chronic inflammation and rapid cell turnover in the liver. In fact, the same processes on a cellular level—loss of balance in proteins and chemicals within the liver—that lead to cirrhosis may also promote HCC. 1

Are there factors that protect against HCC?

In addition to antiviral HCV treatment, several factors appear to protect against development of HCC. These include statins (lipid-lowering treatments) and dietary factors, such as consumption of white meat, fish and omega-3 fatty acids, increased intake of vitamin E, and coffee consumption.1

In an analysis from 10 studies that included over 1.5 million subjects, people who received statins had a 37% reduction in risk for HCC compared with those who did not use statin therapy.8

Coffee (and caffeine) contains high levels of antioxidants that may protect against the development of cancer. Several studies have found evidence that coffee consumption can reduce risk for HCC. In one analysis of several studies, consumption of at least two cups of coffee per day was linked to a decrease in liver cancer risk of 43%. 9 Coffee consumption has also been associated with decreased risk for cirrhosis.

If you have chronic HCV infection with advanced fibrosis and cirrhosis, routine screening for HCC is recommended.10 Screening is done using imaging techniques, including ultrasound, computed tomography (CT) scan, and magnetic resonance imaging (MRI). Typically, ultrasound is used for screening in combination with a blood test that measures alpha-fetoprotein, which is often elevated in people with HCC.11

Treatment of HCC

Surgical resection (surgical removal of the part of the liver affected by cancer) is considered an optimal approach to treatment of HCC. However, surgery is only appropriate in people who have sufficient portion of the liver unaffected by cancer, so that liver function is preserved. Other treatment options for HCC depend on the extent and severity of the cancer and include12:

  • Liver transplantation
  • Radiofrequency ablation and microwave ablation
  • Percutaneous ethanol or acetic acid ablation
  • Transarterial chemoembolization (TACE)
  • Radioembolization
  • Cryoablation
  • Radiation therapy and stereotactic radiotherapy
  • Systemic chemotherapy and molecularly targeted therapies
Written by: Jonathan Simmons | Last reviewed: March 2015.
  1. Schwartz JM, Carithers RL, Jr. Epidemiology and etiologic associations of hepatocellular carcinoma. Uptodate. Tanabe KK, Di Bisceglie AM, Travis AC, Savarese DMF, eds. Accessed at: 2014..
  2. Jemal A, Bray F, Center MM, Ferlay J, Ward E, Forman D. Global cancer statistics. CA Cancer J Clin 2011;61:69-90..
  3. Altekruse SF, McGlynn KA, Reichman ME. Hepatocellular carcinoma incidence, mortality, and survival trends in the United States from 1975 to 2005. J Clin Oncol 2009;27:1485-91..
  4. Chopra S. Clinical manifestations and natural history of chronic hepatitis C virus infection. Uptodate. Di Bisceglie AM, Bloom A, eds. Accessed at: 2014..
  5. Fattovich G, Giustina G, Degos F, et al. Morbidity and mortality in compensated cirrhosis type C: a retrospective follow-up study of 384 patients. Gastroenterology 1997;112:463-72..
  6. Kanwal F, Kramer JR, Ilyas J, Duan Z, El-Serag HB. HCV genotype 3 is associated with an increased risk of cirrhosis and hepatocellular cancer in a national sample of U.S. Veterans with HCV. Hepatology 2014;60:98-105..
  7. Liver (Hepatocellular) Cancer Screening (PDQ®). National Cancer Institute. Available at: Access on 080314..
  8. Singh S, Singh PP, Singh AG, Murad MH, Sanchez W. Statins are associated with a reduced risk of hepatocellular cancer: a systematic review and meta-analysis. Gastroenterology 2013;144:323-32..
  9. Larsson SC, Wolk A. Coffee consumption and risk of liver cancer: a meta-analysis. Gastroenterology 2007;132:1740-5..
  10. Recommendations for testing, managing, and treating hepatitis C. American Association for the Study of Liver Diseases and Infectious Disease Society of America. March, 2014. Available at: Accessed on 04/05/14..
  11. Schwartz JM, Carithers RL, Jr. Clinical features and diagnosis of primary hepatocellular carcinoma. Uptodate. Chopra S, Travis AC, Savarese DMF, eds. Accessed at: 2014.
  12. Abdalla EK, Stuart KE. Overview of treatment approaches for hepatocellular carcinoma. Uptodate. Tanabe KK, Goldberg RM, Savarese DMF, eds. Accessed at: 2014.