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Cancer develops in a long and complex process that begins with a genetic mutation. The mutation might be one that instructs the cell to begin dividing unrestrainedly, or it might be one that impairs the function of a gene to halt cancerous processes before they can advance too far. As we now know, both kinds of mutation can result in changes that disrupt the activities of whole networks of genes.
Prof. Varda Rotter, Head of the Molecular Cell Biology Department at the Weizmann Institute, has spent many years researching the role of p53, a “master key” gene that suppresses cancer growth. This gene is found to have been inactivated in a large number of cancers. To understand p53’s role in preventing cancer, an analytical model was developed in her lab, a replica of cancer formation in which the gene was turned off at specific, defined stages. But how does one begin to identify entire gene networks affected by p53 loss? Prof. Rotter’s team turned to some of the latest, most powerful bioinformatics tools – DNA chips.
DNA chips are able to detect the expression of up to 50,000 different genetic sequences, and they yield mountains of raw data. Prof. Eytan Domany of the Physics of Complex Systems Department and his team have developed algorithms that are able to compare the properties of a great number of genes. For instance, they can spot genes that share similar patterns of expression. Within this group, custom-designed analytical tools can unearth clusters of genes containing related segments or activated by the same “master key.” Together, Rotter and Domany were able to analyze information from the lab model and identify specific patterns of gene expression.
Rotter and Domany’s combined study has already resulted in the discovery of several gene networks that are controlled by p53, and these findings may lead to the development of new p53-related cancer therapies. They are also working toward characterizing “genetic signatures” – patterns of gene expression that can identify stages of tumor development and possibly point the way to new avenues of treatment or prevention. “Having the ability to study the interactions of whole networks of genes, rather than a gene here and a gene there, has completely changed the scope of our research. Our horizons have expanded several times over,” says Rotter.
Prof. Varda Rotter’s research is supported by the Women's Health Research Center; the Flight Attendant Medical Research Institute; the Levy-Markus Foundation; the Milan Committee for the Weizmann Institute; the Ridgefield Foundation; and the Shepard Broad Foundation. Prof. Rotter is the incumbent of the Norman and Helen Asher Chair of Cancer Research.
Prof. Eytan Domany’s research is supported by the Clore Center for Biological Physics; the M.D. Moross Institute for Cancer Research; the Levine Institute of Applied Science; the Yad Abraham Research Center for Cancer Diagnostics and Therapy; and the Ridgefield Foundation. Prof. Domany is the incumbent of the Henry J. Leir Professorial Chair.