( ients with the inhibitor. We are going...)New cellular flaw found in some virulent breast cancers

Cyclin D1 is one of a family of proteins that help regulate a cell's passage through its cycle of rest and growth. Overabundance of cyclin D1 has been observed in many cancers. For a number of years, Sicinski's laboratory has carried out a series of experiments to determine whether the protein has an important normal function, or whether it could be blocked by designer drugs to treat breast cancer without harming the patient.

Previously, mice engineered to lack cyclin D1 were found to be highly resistant to certain breast cancers, and other experiments showed that mice in which the cyclin D1 gene had been inactivated developed into more or less normal adults.

However, said Sicinski, it is difficult to design a drug to neutralize the action of a protein like cyclin D1. In the most recent experiments, the research team's objective was to determine precisely which of cyclin D1's several different functions was responsible for causing breast cancer.

By creating laboratory mice with different combinations of genes present or missing, the researchers were able to isolate the various cyclin D1 activities. They demonstrated that cyclin D1's ability to activate CDK4 kinase activity is what causes the aggressive cancers, and that this same activity is required for the cancer to continue to grow.

Additional experiments reported in another Cancer Cell paper found that bioengineered mice in which cyclin D1 could not activate CDK4 kinase were developmentally normal and highly resistant to ErbB-2-caused breast cancers, demonstrating that blocking CDK4 was not harmful to the mice. That research was carried out by scientists at Tufts-New
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Source:Dana-Farber Cancer Institute