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Study suggests cell-cycle triggers might be cancer drug targets

BOSTON--In an experiment that appears to refute current theory, Dana-Farber Cancer Institute scientists have found that removing three key proteins believed essential to cell division and growth had little impact on normal tissue development of a mouse embryo. These same proteins, when overly active, have been linked to cancer cell proliferation.

With one significant exception, the absence of proteins called cyclin D1, D2, and D3 seemed to have no deleterious effect on development of the tissues and organs of laboratory mouse embryos. "D-type cyclins" are molecules that sense growth signals from the cell's environment and, when appropriate, switch on cell division and growth. But when the system is faulty, the cyclins over-respond to the growth signals and can cause cancerous growth. The discovery that these proteins aren't indispensable lends encouragement to an idea that blocking overactive cyclins could halt the growth of cancer.

In the Aug. 20 issue of Cell, lead author Katarzyna Kozar, MD, and senior author Peter Sicinski, MD, PhD, report on developing the first mouse embryos to date in which all three D-type cyclins were absent or "knocked out." It had been thought that at least one cyclin was required for an embryo to be viable and its tissues to form normally. Yet the "triple-knockout" mouse embryos followed a normal course of cell division and proliferation until as late as 13.5 days, when most tissues and organs are already formed. A typical mouse pregnancy last 18 days.

(In a companion paper in Cell, researchers from Spain report similar findings involving protein kinases called CDK4 and CDK6, which are molecular partners of the D-cyclins. Embryonic mice with both CDK molecules knocked out had normal tissue development as well.)

The unexpectedly viable embryos contradict theory and previous laboratory experiments. The only abnormality in the triple knockout mice was a deficiency of blood-forming cells, causing them to be pa
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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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