News release

News Release Archive

Office of External Affairs

Mission magazine

Vital Signs

University page

Liver tumors prevented in mice with overactive gene

A protein that is absent or reduced in some human liver tumors prompted scientists to ask the question: What if the gene that makes the protein is expressed at a higher than normal level in mice? Will the animals be protected against liver tumors?

The answer is a resounding yes, according to a seminal study by molecular biologists at The University of Texas Health Science Center at San Antonio (UTHSC). The results appeared in a fall issue of Proceedings of the National Academy of Sciences-USA.

The scientists even saw protection in "middle-aged" mice — that is, mice 14 to 16 months old. Older mice are believed to make less of the protein than younger mice.

The protein, known as O6 methylguanine-DNA methyltransferase, is one of many that continuously correct damage in the genetic material of cells. These workhorses are called "DNA repair proteins" because they maintain our DNA, the double-helical molecule that contains the genetic blueprint of life.

"This is one of the few papers in scientific literature to show the preventive effects of enhancing a DNA repair protein," said senior author Christi Walter, Ph.D., professor of cellular and structural biology at UTHSC. "Most people knock out genes to see the opposite result."

Activity of O6 methylguanine-DNA methyltransferase protein has been shown to be reduced or absent in some spontaneous human liver tumors, Dr. Walter said. Spontaneous tumors are not hereditary and are not induced by any known cancer-causing agent. "Our animal model appears to be a good one for learning about the mechanism that leads to some liver cancers and the influence of age," she said. "Hopefully, this will lead to better treatments."

Contact: Will Sansom