© University of Rochester 1996-2012
Many scientists like to discuss how each form of cancer is a distinct disease with its own causes and its own treatments. But researcher Hartmut (Hucky) Land, the Robert and Dorothy Markin Professor and chair of the Department of Biomedical Genetics, takes the opposite approach. He’s hunting for the most basic rules that all cancers share to make good cells go bad.
His unique, far-reaching effort to understand the disease at its roots poses a challenge whose enormity is matched by its potential payoff: findings that could lead to new treatments for many forms of cancer.
The project has taken a significant step forward with a $2.7 million grant from the National Cancer Institute to unravel the gene networks at the heart of colon cancer. The funding will support work for the next five years in the laboratory of Land, who is scientific director of the James P. Wilmot Cancer Center.
The grant comes on the heels of one of the most important findings Land has made in his three decades as a scientist. Earlier this year, in the journal Nature, Land’s team demonstrated a promising way to pinpoint the genes that are essential in turning normal cells cancerous.
“No matter what type of cancer a person has, a similar program is happening in every cell that becomes cancerous,” Land says. “We’re trying to figure out that program and dismantle or destroy it.”
The new funding is focusing on the genes behind colon cancer, which claims approximately 50,000 lives in the United States each year. But researchers predict that the same genes play important roles in a number of other types of cancer, as well. Helping Land unravel the puzzle are Craig Jordan, professor of medicine and director of translational research at the Wilmot Cancer Center, and Anthony Almudevar and Peter Salzman, assistant professors in the Department of Biostatistics and Computational Biology.
A cell that makes the journey from normal to cancerous undergoes thousands of modifications. Scientists face the tremendous task of distinguishing between changes that cause the transformation and changes that occur as a result. The task, Land says, is like sorting out the molecular “drivers” that push a cell to become cancerous versus the molecular “passengers” that are simply along for the ride.
In a work published earlier this year, his team found a straightforward way to make the distinction. The team discovered that most of the important genes in the whole genome are much more likely to respond to several mutations in a synergistic way, increasing in activity more than would be expected if the changes caused by any of these mutations were simply added together.
The research provides a sought-after prize for scientists trying to decide which genes and proteins to target in the fight against cancer.
“We believe this is a way to identify what we call cancer addiction genes. These are the genes that cancer simply must affect to cause the disease,” Land says.
“Now that we have a way to identify the genes that cancer is addicted to, we’re moving to the next step and working out the relationship among them,” he adds. “These additional targets dramatically expand our opportunity for intervention to help patients.”
Tom Rickey is a senior science writer for Medical Center Public Relations.
© University of Rochester 1996-2012