Cancer cells differ from normal cells in, among other things, the way they divide. When a normal cell complies with a signal telling it to divide, it also begins to activate a "braking system" that eventually stops cell division and returns the cell to a resting state. When that braking system is faulty, uncontrolled cell division and the growth of cancer can result. Weizmann Institute scientists studied this system of brakes, and identified a number of the genes involved.
According to the study's findings, which appeared in Nature Genetics online on February 25, aberrations in the activities of these genes are tied to certain types of cancer, as well as to the relative aggressiveness of the cancer. These insights may, in the future, lead to the development of ways to restore the brakes on runaway cell division and halt the progression of cancer.
First, the scientists mapped the network of genes that is activated in normal cells upon receiving the order to divide. The "divide!" signal comes from outside the cell in the form of a chemical called a growth factor, and it initiates a chain of events inside the cell. The genes activated in this sequence produce proteins, some of which cause cell division and others that put the brakes on that division. To find which genes were responsible, the scientists needed to sift through a huge quantity of data on genes and their activities. To cope with this monumental task, a team of Weizmann Institute researchers from diverse fields pooled their knowledge and experience: Prof. Yosef Yarden of the Biological Regulation Department, Prof. Eytan Domany of the Physics of Complex Systems Department, Prof. Uri Alon of the Molecular Cell Biology Department, and Dr. Eran Segal of the Computer Science and Applied Mathematics Department. Working with them were Prof. Gideon Rechavi of the Sheba Medical Center and researchers from the M.D. Anderson Cancer Center in Houston, Texas, headed by Prof. Gordon B. Mills.
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Contact: Jennifer Manning
jennifer@acwis.org
212-895-7952
American Committee for the Weizmann Institute of Science
26-Feb-2007