Liver Cancer Research Might Pave Way for Prevention
Thursday, June 14, 2018
Aram Hezel, M.D.
Based on new data from the Wilmot Cancer Institute, researchers now understand more about the gene mutations and risk factors that work together to jump-start the second most common type of liver cancer, known as intrahepatic cholangiocarcinoma.
The information could help physicians devise new screening strategies and ways to predict how treatments will work in patients, said corresponding author Aram F. Hezel, M.D., chief of Hematology/Oncology at UR Medicine and Wilmot, and the John and Ethel Heselden Professor of Medicine.
“We usually think of cholangiocarcinoma, or bile duct cancer, as one disease, and we used to think of it as having one cellular origin,” Hezel said. “But our latest study shows that it has a number of different starting points, involving different cell types in the liver. Some liver cells are very susceptible to becoming malignant because of mutations, for example, while other types of liver cells turn cancerous after a combination of genetic mutations and injury due to inflammation or infection.”
The study was published online this month in the journal Cancer Research. Although liver cancer is relatively rare, the incidence is rising. Risk factors include being middle-aged or older, obesity and fatty liver disease, infections such as hepatitis, heavy alcohol consumption, and cirrhosis of the liver.
Hezel’s research in mice showed that liver injury from external risk factors primes the pump for cancer development, especially when two well-known cancer-causing gene mutations, Tp53 and Kras, are also present.
The study also showed that oncologists may be able to glean valuable information about prognosis and how well a person will respond to treatment, based on the cells of origin for the cancer. If pre-cancerous cells or lesions can be identified, this could be relevant for screening and other prevention strategies, the study said. Learn more.
Margaret Hill, M.S., Ph.D., a former graduate student in Biomedical Genetics at URMC, and William Alexander, an M.D./Ph.D. candidate who conducts research in Hezel’s lab, are co-first authors on the paper. Another key collaborator was Christa Whitney-Miller, M.D., associate professor and director of Surgical Pathology at URMC.
Funding was provided by the National Cancer Institute and the “For Pete’s Sake” Memorial Golf Tournament, in memory of Pete Osterling, who died from a rare form of cancer in 2010. This year’s tournament takes place on July 8 at Victor Hills Golf Club; the group has raised approximately $30,000 for cancer research at Wilmot. For more information: email@example.com.