COMBINATION MRI-PET: A UC Davis lab has built a body imaging scanner that combines two technologies: positron emission tomography and magnetic resonance imaging. "We can correlate the structure of a tumor by MRI with the functional information from PET, and understand what's happening inside a tumor," said Professor Simon Cherry, chair of biomedical engineering, whose lab developed the scanner for studies with laboratory mice, for example, in cancer research.

The MRI-PET scanner is a first of its kind. Such systems built the conventional way interfere with each other, because MRI relies on very strong magnetic fields, and those fields seriously affect the detectors and electronics in PET scanning. So, for the PET half of the combination scanner, Cherry's lab used the new silicon avalanche photodiode detector.

Proceedings of the National Academy of Sciences recently published a paper on the work. Cherry's UC Davis-affiliated co-authors: graduate student Ciprian Catana, now at the Martinos Center for Biomedical Imaging, Harvard University; Yibao Wu, postdoctoral researcher; and Jinyi Qi, assistant professor of biomedical engineering. The February issue of Proceedings of the IEEE included a related paper co-authored by Cherry and Angelique Louie, associate professor, biomedical engineering.

-- Andy Fell

'WAITING IN THE WINGS': When a popular breast cancer drug goes after the HER2 gene, a gene called MET "is waiting in the wings and can take over for HER2," says the UC Davis Cancer Center's Colleen Sweeney, explaining a likely reason why the drug sold as Herceptin does not work in 30 percent to 50 percent of patients.

Sweeney was senior author on a paper suggesting that HER2 testing does not tell the whole story. The paper appeared in the March 1 issue of Cancer Research.

The proteins encoded by HER2 and MET are known as receptor tyrosine kinases, or RTKs, leading Sweeney to predict that breast cancer research will increasingly rely on proteomic as well as genetic testing that goes beyond HER2 and focuses on finding therapies that target MET and other RTKs expressed in HER2-positive breast cancers.

-- Karen Finney, UC Davis Health System