A New Target for Breast Cancer Drugs

Researchers from the Dana-Farber Cancer Institute in Boston have identified a specific protein that may be involved in as many as 50 percent of all breast cancers. Writing in the journal Nature, Dr. Piotr Sicinski and colleagues suggested that their finding could lead to a new class of extremely efficient drugs for breast cancer.

Specifically, Sicinski's team found that two cancer-causing genes (oncogenes) called neu and ras can only turn normal cells into cancer cells by sending signals through a protein called cyclin D1. This is important because it appears that about 50 percent of all breast cancers produce an abundance of ("overexpress") cyclin D1.

Oncogenes are naturally occurring genes that can turn a healthy cell into cancer if the gene becomes mutated or overactive.

The researchers theorized that if cyclin D1 could somehow be inactivated or destroyed, the cellular mechanism for breast cancer cell growth could be thwarted. To test this hypothesis, Sicinski's team bred laboratory mice that specifically lacked the cyclin D1 protein. They then crossed these mice with others that contained four known breast cancer oncogenes (neu, ras, Wnt-1, myc).

They found that the cyclin D1-lacking mice were "entirely resistant" to breast cancer tumors induced by the neu and ras oncogenes. However, no protection was seen against Wnt-1 and myc, possibly because these two oncogenes affect molecules and pathways other than cyclin D1.

The researchers noted that their finding is extremely important because it will enable drug companies to develop novel new breast cancer drugs that specifically target the cyclin D1 protein. However, they cautioned that it could take years to develop such cyclin D1-specific therapies.

In an accompanying editorial, Drs. Jiri Bartek and Kiri Lukas of the Danish Cancer Society in Copenhagen concurred about the importance of identifying the role of cyclin D1 in breast cancer development. They called the research "stunning" and said that it might one day lead to customized cancer treatments through the molecular profiling of individual patients.

SOURCES:
Nature, June 28, 2001; 411:1001-1002, 1017-1021
Nature Online: (http://www.nature.com)

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