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Yale scientists find microRNA regulates Ras cancer gene

instead they make an excess of their cells.

After identifying let-7 as a cell division regulator, Slack's team used bioinformatics and found the relationship to Ras. Let-7 in humans is identical to the sequence in the worm, and both binding site and pathway for Ras are highly conserved.

Tissue from lung cancer tumors, compared with their normal adjacent tissue, had reduced let-7 and increased Ras -- the brakes on Ras were removed in lung tumors.

"The discovery of a new aspect of the regulation and targeting of a well-known gene involved with cancer progression will have profound implications as we continue to focus on the causes of tumor development," said Richard L. Edelson, M.D., director of Yale Cancer Center.

Other Yale researchers were Steven M. Johnson, Helge Grosshans and Kristy L. Reinert; collaborators at Ambion, Inc. included Jaclyn Shingara, Mike Byrom, Rich Jarvis, Angie Cheng, Emmanuel Labourier and David Brown. Support for the research came from the Human Frontiers Science Program, the National Institutes of Health and the National Science Foundation.


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Contact: Janet Rettig Emanuel
janet.emanuel@yale.edu
203-432-2157
Yale University
17-Mar-2005


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