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Rb2 expression could play vital role in ovarian cancer Temple University researchers find

Protein expression of the tumor suppressing gene Rb2/p130 could play a vital role in ovarian cancer, according to a study by researchers at the Sbarro Institute for Cancer Research and Molecular Medicine in the Center for Biotechnology at Temple University (http://www.shro.org).

Their study, "Frequent loss of Rb2/p130 in human ovarian carcinoma," will be published in the May 1 issue of Clinical Cancer Research (http://clincancerres.aacrjournals.org).

In the study, led by Antonio Giordano, M.D., Ph.D., director of the Sbarro Institute and co-director of the Center for Biotechnology at Temple, the researchers examined 45 primary ovarian carcinoma samples and found that 40 percent had a decrease or complete loss of Rb2 protein expression. Giordano discovered the Rb2 gene while working at Temple's Fels Cancer Institute in the early 1990s.

"In the samples where the protein was decreased or lost, there was an inverse correlation to the aggressiveness of the cancer," says Giuseppina D'Andrilli, Ph.D., a research fellow in the Sbarro Institute and the study's lead author. "This is consistent with the theory that if the Rb2 protein is still present in the tumor tissue, the aggressiveness of the tumor is less."

The researchers then used a viral delivery system to introduce correct copies of the Rb2 gene into the ovarian tumor cells that had shown decreased or no Rb2 protein expression.

"Introducing the gene Rb2/p130 allowed the cells to produce more proteins, and this increased protein production brought about a dramatic arrest of cells in the G1, or initial, phase of the cell cycle," says D'Andrilli.

The Temple researchers' findings were comparable to earlier studies at the Sbarro Institute in which correct copies of Rb2 were introduced into mice with lung tumors. When the Rb2 gene was over-expressed in the cancer cells, it caused the tumors in the mic
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Contact: Preston M. Moretz
pmoretz@temple.edu
215-204-7476
Temple University
1-May-2004


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