Study suggests cell-cycle triggers might be cancer dr...( le and anemic and was ultimately fatal...)

le and anemic, and was ultimately fatal. But the Dana-Farber researchers can't yet say if this would create problems for an anti-cyclin cancer therapy in patients. "It's not known whether D cyclins are required for blood cell generation in adults," said Sicinski. "We are addressing this in ongoing experiments."

The blood system issue aside, the results remove a major theoretical objection to developing drugs that would inhibit, or block, overactivity of cyclin D proteins, according to the study's authors. Excess cyclin D production has been seen in tumors of the breast, head and neck and stomach, and in some blood cancers.

The main function of the D cyclins is a linking one. They respond to signals outside the cell and turn the cell-cycle machinery on when needed, enabling the cell to adjust to changes in environment. How this process is carried out in the mouse embryos with no D-type cyclins is a puzzle, says Sicinski who is also an associate professor at Harvard Medical School. "There must be alternative mechanisms that allow the cell to respond to the environment when the D-type cyclins are missing," he speculates.

But the blood-forming cells may lack such an alternative pathway, said Sicinski, and it is highly likely that cancer cells don't, making them vulnerable to future drugs aimed at D-cyclins, or their partners, the CDK kinases.

In the Cell report, the researchers say they attempted to induce cancer in cells taken from embryos lacking the cyclins, and they remained stubbornly normal. By contrast, cells that contained the cyclins were easily made cancerous by the insertion of cancer-causing oncogenes.

That was what the scientists had hoped they would see, based on experiments reported by Sicinski in 1995 showing that mice lacking cyclin D1 had very little breast tissue and, when crossed with cancer-prone mice, had offspring that were largely protected against breast cancer.

It was those and other findings
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Contact: Bill Schaller
william_schaller@dfci.harvard.edu
617-632-5357
Dana-Farber Cancer Institute
19-Aug-2004

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