Male sex hormones may explain why men who suffer from the hepatitis B liver disease are more likely to develop liver cancer than women, researchers in Taiwan have found.
In a paper published in the journal Science Translational Medicine on Wednesday, the researchers said hepatitis B viruses attach themselves to receptors of the male sex hormone androgen before going on to damage liver tissue and cause cancer.
“The findings indicate that using drugs to destroy… androgen receptors could be a new way to battle liver cancer at an early stage,” they wrote.
Liver cancer is the fifth most common cancer and the third leading cause of global cancer death.
Hepatitis B virus infection, which is endemic in many Asian countries including China, is a leading cause of liver cancer and accounts for half of liver cancer cases worldwide.
Men are up to seven times more likely than women to develop liver cancer. Among hepatitis B virus carriers, men are up to three times more likely to develop liver cancer than women.
Led by Ming-Heng Wu at the Institute of Basic Medical Sciences in National Cheng Kung University in Tainan, Taiwan, researchers found that hepatitis B viruses have a special DNA sequence which draws it to androgen receptors.
“The androgen receptors in liver cells bind to this sequence and trigger a cascade of damage to liver tissue,” they explained.
In their experiment, the researchers created mice that were infected with the hepatitis B virus and could easily develop liver tumours upon exposure to cancer-causing agents.
Some of these were genetically modified to be lacking in androgen receptors in their livers.
By week 22 in the experiment, more than 90 percent of those mice with androgen receptors had developed liver tumours compared to 27 percent of the mice without androgen receptors.
Tinkering with the receptors did not change overall androgen levels or leave any obvious toxic effects in the mice.
“Targeting the androgen receptor rather an androgen could be a promising therapy for liver cancer,” the researchers said.
SOURCE: Science Translational Medicine, May 19, 2010.