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Normal cells in tumors may aid cancer growth

A study led by researchers at The Ohio State University Comprehensive Cancer Center Arthur G. James Cancer Hospital and Richard J. Solove Research Institute has found that the normal cells in tumors, known collectively as the tumor stroma, may lose more regions of DNA than do the cancer cells in the course of tumor development.

When DNA is lost, the genes located in those regions are also lost. "Cancer geneticists have looked upon the stroma as just innocent soil that passively receives the seed in which cancer grows," says Charis Eng, the Dorothy E. Klotz Chair of Cancer Research and director of the clinical cancer genetics program.

"But our study indicates that genetic damage occurs in stromal tumors cells, and that that damage may play an important role in tumor development."

The findings might help explain why tumors often behave differently, and respond differently to treatment, in people with seemingly identical cancers. The genetic changes in stromal cells also may provide new targets for future anti-cancer drugs and present a new strategy for treating and preventing cancer, says Eng, a recipient of the Doris Duke Distinguished Clinical Scientist Award.

The study is published in the Oct. 15 issue of the journal Cancer Research.

How the DNA damage occurs in stromal cells isn't yet known, but it might result from exposure to carcinogens, Eng says. It's also too soon to say how genetic damage to stromal cells might influence tumor growth.

However, stromal cells can produce growth factors and other substances that can influence the behavior of cancer cells. The loss of chromosome regions may result in the loss of genes that control these substances. Stromal cells may also produce factors that limit the growth of nearby cells. Loss of genes for such factors would remove those inhibitors and allow cancer cells to grow.

"But those are only hypotheses," Eng says. "I think that th
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Contact: Darrell E. Ward
Ward-15@medctr.osu.edu
614-293-3737
Ohio State University
15-Oct-2004


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