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Basic Rules That Make Good Cells Go Bad In All Cancers

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The general approach to cancer research is to treat each cancer as a unique disease. Now Hartmut "Hucky" Land, Ph.D., is taking the opposite approach: what do all cancers have in common and how can scientists create treatments from those similarities? The James P. Wilmot Cancer Center at the University of Rochester Medical Center has received a $2.7 million grant from the National Cancer Institute to study gene networks at the heart of colon cancer. Dr. Land is the Director of the James P. Wilmot Cancer Center.

Dr. Land who is professor and chair of the Department of Biomedical Genetics published an article in the prestigious journal Nature recently, that describes a new discovery that pinpoints genes that are involved in changing normal cells to cancer cells. The article "Synergistic Response to Oncogenic Mutations Defines Gene Class Critical to Cancer Phenotype", Nature 453, 7198 (25 May 2008) identifies a major scientific breakthrough.

"No matter what type of cancer a person has, a similar program is happening in every cell that becomes cancerous. We’re trying to figure out that program and then dismantle or destroy it."

The new study focuses on colon cancer which claims 50,000 lives each year. Others involved are Craig Jordan, Ph.D., professor of Medicine and director of translational research at the James P. Wilmot Cancer Center, and Anthony Almudevar, Ph.D., and Peter Salzman, Ph.D., who are both assistant professors in the Department of Biostatistics and Computational Biology.

Normal cells that turn cancerous go through thousands of changes and it is hard to tell which changes are necessary to the end result of cancer and which changes are merely a result of the process. To distinguish between those changes is a big problem in cancer research. Land says the task is like sorting out the molecular "drivers" that push a cell to become cancerous vs. the molecular "passengers" that are simply along for the ride.

In Nature article, Land describes a simple distinction in that the important genes in the whole genome respond to several mutations in a synergistic way, increasing their activity to a greater extent than would be expected if the changes caused by any of these mutations separately were simply added together. The research helps scientists who are 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."

Twenty-five years ago Land discovered that the development of cancer always involves more than one mutation. Since then, he has focused on how genes must cooperate for cancer to occur.

When a cell is becoming cancerous a complex scene, similar to a battlefield appears under the microscope. Land’s team is sorting out the scene to find order beyond the chaos and identify the key elements in command of cancer’s assault on cells.

"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 relationships among them. These additional targets dramatically expand our opportunity for intervention to help patients."

Cancer will be cured through work like that at The University of Rochester.