Dr. Jean Zhao's lab is interested in...
How kinases in general, and phosphatidylinositol 3-kinases (PI3K) in particular, control malignant transformation. The work of our laboratory integrates molecular biology, tissue engineering and novel mouse models of human cancer to study oncogenic alterations in kinases that are involved in tumor formation and metastasis. In addition to our unique genetically engineered mouse models, we have developed a number of additional experimental systems, including, synthetic human tumors, and kinome-wide libraries of activated kinases to elucidate the mechanisms by which kinases function in cancer.
Oncogenic PIK3CA-driven mammary tumors frequently recur via PI3K pathway-dependent and PI3K pathway-independent mechanisms
Featured on the Dana-Farber Website: Read the Story! In this issue, Liu et al. (p 1116) uncover new mechanisms of mammary tumor resistance to PI3K-targeted therapy. The artwork on the cover is by Haiming Cheng, sister of one of the authors, entitled The Promise and the Challenge of PI3K-Targeted Therapy in Breast Cancer. Also in this issue, Korpal et al. (p 1101) reveal a new role for miR-200 in metastatic colonization of breast cancer, and Lyons et al. (p 1109) uncover molecular pathways responsible for the increased risk and malignancy of postpartum breast cancer.
The phosphoinositide 3-kinase (PI3K) pathway is a key signal transduction system that links oncogenes and multiple receptor classes to many essential cellular functions, and is perhaps the most commonly activated signalling pathway in human cancer. This pathway therefore presents both an opportunity and a challenge for cancer therapy. Even as inhibitors that target PI3K isoforms and other major nodes in the pathway, including AKT and mammalian target of rapamycin (mTOR), reach clinical trials, major issues remain...
Meet the Lab
Find contact information and meet the members of the Zhao Lab