Focus
October 10, 2008

Michael Greenberg (left), Yingxi LinNEUROBIOLOGY: Toward Curbing Enthusiasm
After birth, the brain wires itself under the direction of excitatory impulses representing images, sensations, and abstract notions. A study appearing online Sept. 24 in Nature from Michael Greenberg (left), Yingxi Lin, and their co-authors reveals that the same process installs an unsung system of inhibitory connections. Scientists believe neurological disorders may emerge from problems in the ratio of these connections as they are established in response to experiences in infancy and childhood. The findings are expected to accelerate research on the often overlooked but powerful GABA signaling neurons and synapses.

President Drew Faust and Dean Jeffrey FlierINNOVATION: Entrepreneur Gives $125m To Harvard for Bioengineering Institute
Engineer, entrepreneur, and philanthropist Hansjörg Wyss, MBA ’65, has donated $125 million to create the Hansjörg Wyss Institute for Biologically Inspired Engineering. According to Harvard President Drew Faust (left), the institute “will form the bedrock for Harvard’s emerging efforts in this critical area.” Among these efforts is the Strategic Planning Initiative of Dean Jeffrey Flier (right) and its proposal for a major collaboration in bioengineering. The founding director of the Wyss Institute is Donald Ingber, the Judah Folkman professor of vascular biology at Children’s Hospital Boston and HMS, and professor of bioengineering at the Harvard School of Engineering and Applied Sciences.

George Daley (left) and Mohammad AzamBIOCHEMISTRY: View Cleared on “Gatekeeper” Mutation as Bar to Cancer Drug
The lab of George Daley (left) has identified a common mechanism behind resistance to kinase inhibitors in the treatment of cancer. This discovery pinpoints a single change, called the “gatekeeper” mutation, which alters a shared feature of many different kinases. The modification renders the kinases resistant to standard inhibitors. The researchers, including Mohammad Azam, also found that this mutation activates the kinase on its own, potentially implicating it in cancer development and progression. Reported in the September Nature Structural & Molecular Biology, the discovery may help guide the design of new therapies to treat drug-resistant cancer.

Nick Dyson (left) and William HahnONCOLOGY: Two Studies Identify Oncogene Tied to Colorectal Tumors
Large-scale genetic screens have the potential to yield big surprises—including previously unsuspected oncogenes. Using a genetic screen in Drosophila, Nick Dyson (left) and colleagues discovered that the activity of the tumorigenic protein beta-catenin can be enhanced by the kinase CDK8. William Hahn and his team independently identified CDK8 as an activator of beta-catenin and determined that it is frequently amplified in human colorectal tumors. The work of both groups appears in the Sept. 25 Nature.

Copyright 2008 by the President and Fellows of Harvard College