Dr. He obtained her Bachelor degree at the Tsinghua University in China, and received her doctoral degree at the Stanford Medical School with Dr. Greg Barsh.  Her PhD work was on the functional role of attractin, and its genetic and biochemical studies. The work has resulted in more than ten high quality publications, including first authorship papers in Nature, Nature Genetics, and Science. After her PhD work, she went to do her postdoctoral fellowship with Dr. Greg Hannon at the Cold Spring Harbor Laboratories. Her studies on the microRNA polycistron as a potential human oncogene and as a component of the p53 tumour suppressor network also resulted in the publication of several ground-breaking papers in Nature, again with Dr. He as the first author on all these papers. Earlier this year, Dr. He was appointed Assistant Professor and Principal Investigator in the Department of Molecular and Cellular Biology, University of California at Berkeley.  Her research program at UC Berkeley is to explore the roles of microRNAs in the oncogenic and tumor suppressor pathways, and the work is supported by grants from the National Cancer Institute.
Dr. He is holding two US patents, the first one is on methods for cancer diagnosis and treatment, and the other one on TP53 function biomarker and miRNA-based therapeutics. In the last several years, Dr. He was invited to speak at many prestigious meetings, notably the East-West Alliance Meeting at Cambridge, UK, the American Association of Cancer Research (AACR) in San Diego, and the Keystone symposium on microRNAs and cancer in Keystone.

miRNAs in Cancer Biology: Small RNAs with a Big Impact
MicroRNAs are a family of small, non-coding RNAs that negatively  regulate gene expression in a sequence specific manner. Recent studies suggest  that microRNA may play an important role in the oncogenic and tumor suppressor  pathways. We have previously identified a microRNA polycistron, mir17-92, as a  potential oncogene for human B-cell lymphomas.  To identify miRNA  components in the tumor suppressor pathways, we compared miRNA expression  profiles of wild-type and p53-deficient cells. This analysis revealed a family  of miRNAs, mir-34, whose expression reflected p53 status.  Precursors of  all three miR-34 family miRNAs are direct transcriptional targets of p53,  whose induction by DNA damage and oncogenic stress depends on p53 both in  vitro and in vivo.  Ectopic expression of miR-34 induces cell  cycle arrest in both primary and tumor-derived cell lines, consistent with the  observed ability of miR-34 to down-regulate a program of genes promoting cell  cycle progression.  The p53 network suppresses tumor formation through  coordinated activation of multiple transcriptional targets, and miR-34 may act  in concert with other effectors to inhibit inappropriate cell  proliferation.