Scientists Spot Key to Breast Cancer Spread

FRIDAY Sept. 11, 2009 -- Too much of two proteins can send noninvasive breast cancer into a deadly spread through the body, researchers say.

In a study at the University of Texas M.D. Anderson Cancer Center in Houston, scientists found that the overproduction of the protein 14-3-3 zeta, when combined with the known breast cancer protein ErbB2, or HER2, can change premalignant epithelial cells into mobile mesenchymal-like cells. The resulting process, known as epithelial-to-mesenchymal transition, triggers cancer spread from one site in the body to another.

"We have discovered a key molecular mechanism for the deadly transition of non-invasive breast cancer into invasive disease," senior author Dr. Dihua Yu, professor in the center's department of molecular and cellular oncology, said in a news release issued by the university.

Cancer involving the two proteins may also be more deadly, based on the findings published in the Sept. 9 issue of Cancer Cell.

In one experiment, the researchers injected a breast cancer cell line with the two overexpressed proteins into mice, resulting in these mice having three times the metastasis, or cancer spread, as mice given a different cancer cell line.

The researchers also found that of 107 human cases of invasive breast cancer they studied, a little more than 20 percent involved cancers that overexpressed both proteins, and these patients did not live as long as those whose tumors produced one or neither of the proteins.

However, the researchers identified a biomarker in 14-3-3 zeta that may help doctors identify these high-risk patients so that more aggressive treatment can be given before the breast cancer has a chance to convert to an invasive kind.

The findings may have far-reaching implications. Yu and her team had previously found that lung, liver, uterine, stomach and several other cancers also overproduce the 14-3-3 zeta protein.

More information

The U.S. National Cancer Institute has more about breast cancer.

Posted: September 2009


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