Gene Studies Offer Insights Into Cancer

One details disease's spread, the other offers potential for better chemotherapy

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By
HealthDay Reporter

WEDNESDAY, April 11, 2007 (HealthDay News) -- Two new studies have identified genes that play a role in the spread of breast cancer to the lungs, and genes that hamper the effect of chemotherapy.

These discoveries could lead to more effective treatments in stopping cancer's spread and to less toxic chemotherapy, the researchers report in the April 12 issue of Nature.

"Contrary to some of the disappointment and skepticism about progress in cancer research, because we still have a high rate of incidence and a high rate of death, these new basic science developments that are springing from the human genome and new technologies are going to pick up the pace with respect to our understanding of the biology of cancer and the identification of targets for the development of new therapeutic approaches," said Michael White, a professor of cell biology at the University of Texas Southwestern Medical Center at Dallas.

In his study, White's team discovered 87 genes that affect how people react to chemotherapy drugs.

"We have identified some key elements of the regulatory basis supporting chemo-resistance in human cancer," White said. "The more we can understand about that, the easier it will be to make current chemotherapy more effective."

When White's group blocked some of these genes in lung cancer cells, they found those cells were up to 10,000 times more sensitive to the chemotherapy drug paclitaxel, brand name Taxol.

The researchers hope that by blocking these genes, lower doses of chemotherapy could be used with increased effectiveness and reduced toxicity.

"We want to identify things that we can target that will kill or negatively impact the spread of cancer cells without having toxic side effects on normal cells," White said. "If we can develop chemical compounds that will inactivate these genes, it will have profound implications for blocking the growth of tumors and have very little side effect on normal tissue."

In the second study, Joan Massague from Memorial Sloan-Kettering Cancer Center in New York City and her colleagues report finding a series of genes in breast cancer that enable the cancer to spread to the lungs.

While it was known that a number of genes help spread cancer, these researchers found how four genes cooperate to make new blood vessels in the cancer tumor, release cancer cells into the bloodstream and help these cells get into the lungs.

The finding helps explain how breast cancer metastases, or spreads, to other organs in the body. These genes could become targets for treatment to help stop breast cancer from spreading, an often deadly development, the researchers said.

Two of these potential gene targets are the cyclooxygenase cox-2 gene and the epidermal growth factor receptor gene (EGFR).

To show that these genes were actually involved in cancer metastasis, Massague's group treated breast cancer cells with the cancer drug cetuximab and the pain medication Celebrex, a cox-2 inhibitor, and found that the rate of growth of the tumor was reduced and metastasis halted.

One expert thinks that both studies could provide the basis for developing new and more effective cancer treatments.

"These are encouraging studies," said Michael Melner, a scientific program director at the American Cancer Society. "There is potential for treatments in the future that might dramatically reduce the amount of these chemotherapeutic drugs that need to be applied in order for them to be effective."

These studies could also lead to treatments that attack the way cancer cells work, Melner said. "By identifying these genes in different types of cancers, you are identifying the sensitive points in the cancer and that might give you further indication of new drugs that could be applied to those particular mechanisms," he said.

More information

For more information on gene therapy, visit the American Cancer Society.

SOURCES: Michael White, Ph.D., professor of cell biology, University of Texas Southwestern Medical Center at Dallas; Michael Melner, Ph.D., scientific program director, American Cancer Society, Atlanta; April 12, 2007, Nature

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