(RxWiki News) It’s hard to treat something you don’t understand. A recent study has expanded our understanding of how liver cancer starts. This information might lead to new drugs to treat this bad actor.
The hepatitis C virus (HCV) reprograms the inner workings of liver cells. The virus takes over the cell’s head programmer – microRNA – and uses it to grow and thrive.
In a new study, scientists have nailed down one particular microRNA called miR-122 that could be a master key to unlocking new ways to treat liver cancer.
"Ask your doctor about hepatitis C screening."
This study is the work of Stanley M. Lemon, MD, professor of medicine and microbiology and immunology and member of UNC Lineberger Comprehensive Cancer Center at the Center for Translational Immunology, and the University of North Carolina Center for Infectious Disease.
He and his colleagues sought to solve a major puzzle – why the hepatitis C virus attacks the liver so viciously. What they found in their laboratory studies is that the virus wreaks havoc with mir-122, which has a number of important roles in the cellular world. But once the hepatitis C virus latches on, the mir-122 actually helps HCV go viral – that is, multiply itself to grow and spread.
So Dr. Lemon believes it may be a target for new therapeutic drugs. In fact, according to Dr. Lemon, the pharmaceutical industry is working on drugs that target mir-122 activity. He believes this research can advance the road to discovery.
While the incidence of most cancers is declining, this is not the case for liver cancer. The reason for these trends is the HCV, which is a leading cause of cirrhosis of the liver, liver transplantation and liver cancer. An estimated 4 million Americans are living with the hepatitis C virus and have been for years without even knowing it.
Dr. Lemon told dailyRx News he thinks HCV will continue its march. “I anticipate hepatitis C-associated liver cancer to be an increasingly important cause of cancer-specific mortality in the future.”
This research was published December 17 in Proceedings of the National Academy of Sciences. The study was supported by National Institutes of Health and the North Carolina University Cancer Research Fund. No conflicts of interest were reported.
