Yun Yen, M.D., Ph.D.
The laboratory of Yun Yen, M.D., Ph.D., is involved in: (1) elucidating the molecular mechanism of chemotherapeutic drug resistance by studying the enzyme ribonucleotide reductase (RR); (2) developing novel chemotherapeutic agents useful for circumventing drug resistance in cancer by inhibiting RR; (3) developing surrogate markers for enhancing cancer drug therapeutic effect from human samples collected from RR inhibitor studies; and (4) studying the role of the growth arrest DNA damage-inducible gene 45β (GADD45 β) in human hepatocellular cancer and FGFR3 in myeloma.

David K. Ann, Ph.D.
The research program goals of David K. Ann, Ph.D., are to understand both the molecular mechanisms and signal transduction processes that maintain genomic integrity following DNA damage and to develop novel molecular therapies for human cancers by targeting dysfunctional or deregulated responses to DNA damage. The DNA damage-induced signaling pathway involves a kinase-dependent signaling cascade that regulates cell cycle progression, DNA repair and apoptosis (cell death). It is the coordination of these events that ensures genomic stability. His current interest is to decipher the signaling transduction pathways and molecular mechanisms underlying genomic instability and to enhance the tumor selectivity or DNA-targeted agents. Specifically, he currently works on (1) HMGA2 and genomic instability, (2) SUMOylation and DNA damage response and (3) autophagy and drug resistance.

Warren Chow, M.D.
Dr. Chow’s group focuses on the development of novel therapeutics for treatment of sarcomas, which are rare cancers of connective tissues. He has focused on new therapies for (1) Ewing's sarcoma/primitive neuroectodermal tumors by targeting surface membrane tyrosine kinase receptors with small molecule inhibitors; (2) chondrosarcomas with a novel multitargeted antifolate drug due to the finding of frequent deletions of the methylthioadenosine phosphorylase gene; and (3) liposarcomas by upregulating genes integral for two distinct mechanisms of programmed cell death, apoptosis and autophagy.

Vincent Chung, M.D.
Vincent Chung, M.D., has been working on novel therapeutics for the treatment of pancreatic cancer. Many receptor and non-receptor tyrosine kinases are found to be constitutively activated in cancers. One of the pathways that appear to be associated with aggressive tumor growth is mediated by c-Src, which signals through the signal transducer and activator of transcription-3 (STAT3) molecule. He has been working with a small-molecule tyrosine kinase inhibitor that targets the Src family of kinases and collecting patient samples while on this treatment to evaluate mechanism of action in relation to response. Also, he has been using epigenetic drugs to alter gene expression and combining them with targeted agents to increase apoptosis.

Timothy W. Synold, Pharm.D.
The laboratory of Timothy W. Synold, Pharm.D., is involved in: (1) the molecular and clinical pharmacology of drugs targeting mitotic cell division; (2) inducible drug clearance and tumor cell resistance through the orphan nuclear receptor, SXR; (3) regulation of MDR1 expression in vivo and in vitro; (4) pharmacokinetics and pharmacodynamics of anticancer agents in phase I and II settings; and (5) the clinical pharmacology of anticancer agents in special patient populations (e.g., elderly patients and patients with hepatic or renal insufficiency).