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BREAST CANCER: FIGHTING BACK : Search for New, High-Powered Weapons : Growing understanding of the disease and biological approaches under study may eventually lead to preventive solutions as alternative treatments.

October 22, 1995|STEVE EMMONS | TIMES STAFF WRITER

Breast cancer is not an invader. It's a traitor.

Your own cells, misled by faulty genes, multiply and spread out of control, eventually crowding out the normal cells you need to stay alive.

Over the past two decades, methods of treating breast cancer have been refined, but the basic approach remains unchanged: surgery to remove the cancer, then X-ray radiation or chemicals to mop up surviving cancer cells. There is still no way of knowing whether you got them all.

"We really haven't gotten very far from slash, burn and poison," says Susan M. Love, director of the Revlon/UCLA Breast Center. "The treatments are still pretty grim. The newer biological approaches are where the answers are."

Researchers are studying antibodies grown in mice and adapted for humans that interfere with the cancer cells' growth cycle. Scientists hope the antibodies will be able to kill a tumor and hunt down stray cancer cells, perhaps eliminating the need for both surgery and follow-up radiation and chemotherapy.

Tamoxifen, a drug used to treat breast cancer since the 1970s, is now being tested as a possible cancer prevention drug in healthy but cancer-prone women. A Vitamin A derivative is also being tested that might increase Tamoxifen's effectiveness.

"My prediction is these trials are going to work, and I think that's fabulous," says Marc Lippman, director of the Lombari Cancer Center at Georgetown University. "And I think there will be better agents out there too."

From 1973 to 1990, the rate of death from breast cancer in the United States varied hardly at all. During that time, about one in every 3,700 women died from the disease each year.

Lately there have been improvements. Deaths were down nearly 5% between 1989 and 1992, probably due to the refinement of standard treatment techniques, researchers say.

"If you optimally treat women today with so-called 'nasty' chemotherapy, fully a quarter of the patients that would have died don't die," Lippman says. "That's not trivial. That's a significant advance.

"If you get lung cancer, you'll die of it. Diagnosis and death are virtually synonymous. But with breast cancer, fewer than 25% die. A long time ago it used to be half."

New and potentially more effective avenues of attack on cancer are coming from recent discoveries of cancer-causing gene defects within human cells. They can be either inherited from parents, developed in response to something in the environment or appear as spontaneous mutations.

Dennis J. Slamon, director of the Revlon/UCLA Women's Cancer Research Program, says research is concentrating on two broad classes of genes, those that promote cell growth and those that suppress it.

There are a large number of these genes, perhaps as many as 100, and they are scattered on different chromosomes. Each gene may have scores of different cancer-promoting defects. While that makes research difficult, it also makes the spread of cancer difficult.

"Probably for almost all cancers, it takes more than one gene alteration. Think about it: If it didn't, if it were easy for cancer to spread, we'd be in big trouble," Slamon says.

Instead, it takes a chain of genetic events over 10, 20, perhaps 30 years for cancer to develop, says Patricia A. Ganz, director of cancer prevention and control research at UCLA's Jonsson Comprehensive Cancer Center.

"If we can find ways to slow that development, we won't have those cancers to treat," she says.

How Cancer Attacks

A human body produces new cells by the billions every day. An elaborate and only partially understood system of chemical signals among cells tells each when more cells are needed and when that's enough.

When you cut your finger, cell reproduction is accelerated to heal the wound, and when it's healed, the signal to stop is issued. But if the stop signal is not issued--or if it is not recognized by some cells--cell division continues. Those extra cells form a tumor.

Not all tumors are cancerous; some are just nuisances. But breast cancer tumors are life-threatening because their defective genes give them the green light to divide at a much faster rate, and the green light never turns red.

They no longer act in concert with normal cells. They are on their own, obeying and replicating their own outlaw genes. They multiply, expand their boundaries and create their own blood vessels for nourishment. Now the normal cells have competition for the body's life-sustaining resources, a contest the normal cells will eventually lose if the cancer goes unchecked.

Typically, breast cancer cells begin growing somewhere in the breast's lobules, where milk is created, or in the ducts, which carry milk to the nipple. It only takes one cancer cell to break through the lobule or duct wall and begin a tumor in the breast's fat and surrounding tissues.

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