The median overall survival was 15.0 and 15.6 months in the two sorafenib-experienced groups. In comparison, people who switched from sorafenib to a recently approved similar drug, regorafenib (Stivarga), had a median survival of about 11 months. The median survival for the sorafenib-naive group could not be determined because a majority of patients were still alive, but this was projected to be 28.6 months.
Nivolumab (Opdivo), a PD-1 checkpoint inhibitor that helps the immune system fight cancer, was associated with a decrease in tumour size or disease stabilisation in patients with hepatocellular carcinoma (HCC) in the CheckMate 040 study, according to a report at the 2017 AASLD Liver Meeting last month in Washington, DC.
Over years or decades, chronic hepatitis B or C virus (HBV or HCV) infection, heavy alcohol use, fatty liver or other causes of liver damage can lead to of cirrhosis and HCC, a type of primary liver cancer. People with hepatitis C who have progressed to cirrhosis remain at risk for liver cancer even after being cured with effective antiviral therapy. HCC is often diagnosed late, when it is difficult to treat, and it is a leading cause of cancer-related death worldwide.
The kinase inhibitor sorafenib (Nexavar) is the only approved first-line therapy for HCC that cannot be surgically removed, but it typically extends survival by only a few months. The U.S. Food and Drug Administration recently approved nivolumab for second-line therapy after sorafenib. Nivolumab is currently approved in Europe for advanced lung, kidney, bladder and head and neck cancers and Hodgkin lymphoma, but not yet for liver cancer.
Bruno Sangro of Clinica Universidad de Navarra in Pamplona, Spain, presented findings from Bristol-Myers Squibb’s CheckMate 040 trial, which evaluated different doses of nivolumab in people with advanced HCC, including those with chronic hepatitis B or C.
Nivolumab is a monoclonal antibody that blocks the PD-1 (programmed death) receptor on T-cells. PD-1 regulates immune response by suppressing excessive immune activation. Some tumours can use PD-1 to turn off immune responses, and drugs that block PD-1 or its ligand PD-L1 can restore T-cell activity against cancer cells.