Double Whammy for Breast Cancer
Two drugs are better than one at suppressing tumors, study finds
THURSDAY, Jan. 24, 2002 (HealthDayNews) -- Using two drugs in a novel treatment approach, a group of Italian researchers have controlled the growth of breast cancer cells in a laboratory far better than when either drug was used alone.
The two medicines -- Herceptin and Iressa -- differ from other cancer drugs because they interrupt a specific process necessary for breast cancer cells to grow.
As study author Dr. Nicola Normanno explains, the drugs block a kind of a biochemical "lock-and-key" process. The lock is the overproduction of a substance known as a growth factor receptor, and the key is the growth factor, which encourages tumors to grow. When the lock fits the key, the cancer cells get what they need to continue dividing, and the tumor thrives.
"But when the lock is blocked, the key -- the growth factor -- has no effect anymore, so the tumor cannot grow," says Normanno.
The goal of the dual drug treatment, says Normanno, is to keep the growth factor and the receptor from joining forces, thus starving cancer cells. The findings appear in the current issue of the Annals of Oncology.
In this specific situation, Herceptin works on the growth factor receptor known as HER2, which is overproduced in the breast cells of about 15 percent of women with breast cancer.
Iressa, which hasn't even been licensed yet, works to block the pathways of still another growth factor receptor known as EGFR, which is involved in about 70 percent of all breast cancers.
However, when an overproduction of HER2 and even a modest level of EGFR appear together -- which happens in 36 percent of all breast cancers -- the drug duo keeps the tumor under control 70 percent of the time, Normanno says. When used alone, each drug is between 30 percent and 55 percent effective.
For breast cancer expert Dr. Clifford Hudis, the study is provocative and likely to have at least some direct impact on patient care.
"This particular kind of [drug] combination is almost certain to be studied clinically. In fact, I think it is overwhelmingly likely to be in process at the moment," says Hudis, chief of the Breast Cancer Medical Service at Memorial Sloan-Kettering Cancer Center in New York City.
The one caveat: "This study was done on a cell line in a laboratory, so we don't know if the results will translate over to breast cancer cells in women," cautions Hudis. However, "this study was well-done, and does offer excellent support for the planned clinical trials."
The study involved cells that both overproduced HER2 and produced some EGFR. Those cells were divided into 48 containers, and treated with either the drug combination or only one of the two drugs every 24 hours. After five days, a series of tests analyzed cell death and growth in all the samples.
In the final analysis, the growth of the cancer was far more likely to be controlled in the cell lines treated with the drug combination than in those treated with either medication on its own.
"We initially had two aims: to find out whether Iressa was able to block the growth of tumor cells that express very high levels of HER2 and moderate levels of the EGFR, and to assess whether drugs against these two receptors could be combined," says Normanno.
In both instances, Normanno says, "we reached our goal," and the same approach may work on other forms of cancer, particularly ovarian cancer.
Right now, the drug combination will only be tried on patients with advanced breast cancer. However, researchers are confident that, if used early, the drug combo may also halt metastasis -- the spread of cancer to other organs. Additionally, tests have shown a low toxicity for both drugs, making them ideal to combine with other chemotherapies.
What To Do
For more information on the latest treatments for breast cancer, visit The National Cancer Institute.
To learn more about how breast cancer tumors grow, visit Novartis.
To learn the truth about more than a dozen common breast cancer myths, visit The National Breast Cancer Foundation.