Andrew Kung, MD, PhD

Department	Hematology/Oncology
Hospital Title	Assistant in Medicine
Academic Title	Associate Professor of Pediatrics
Phone	617-632-5731
Fax	617-582-8096
Email	Andrew Kung
Location	Dana-Farber Cancer Institute 450 Brookline Avenue Boston, MA 02215

Research Overview

The overarching goals of Andrew Kung's research program are to move basic laboratory discoveries into clinical testing to advance the diagnosis and treatment of patients with cancer. The translational oncology research in the Kung laboratory is powered by the horizontal integration of diverse experimental approaches including molecular biology, genomics, proteomics, bioinformatics, cell biology, drug development, mouse models, and molecular imaging. The Kung laboratory has previously established proof-of-concept (PoC) for targeting several signal transduction pathways that are aberrantly activated in cancer, including Hypoxia-Inducible Factor 1 (HIF-1), CXCR4, Insulin-Like Growth Factor 1 Receptor (IGF1R), and the Inhibitor of Apoptosis Proteins (IAP). His laboratory continues to have active research programs focused on:

• Transcriptional regulation by HIF-1, and therapeutic targeting of HIF-1 in cancer.
• Therapeutic strategies to modulate targets considered "undruggable" by conventional discovery methods such as oncogenic transcription factors (e.g., EWS/FLI).
• The role of epigenetics in cancer development and potential therapeutic targeting of histone modifying enzymes.
• Combinatorial strategies utilizing therapeutic modulators of apoptosis.

To accelerate preclinical and early clinical PoC studies, the Kung laboratory has developed extensive expertise in the use of non-invasive imaging to assess drug response. In his capacity as Director of Preclinical Imaging, Dr. Kung was responsible for the design and construction of the Lurie Family Imaging Center (LFIC), a 14,000 square foot state-of-the-art preclinical imaging and experimental therapeutics center. The LFIC is a barrier facility containing space for >16,000 experimental animals, along with 7T MRI, PET/CT, ultrasound, and optical imaging instruments as well as radiochemistry, radiotherapy, physics, and pharmacology support. Studies at the LFIC are focused on the identification and validation of novel cancer therapies and imaging probes for PoC studies in preclinical and clinical trials.

About Andrew Kung

Andrew Kung received his MD from Stanford University School of Medicine. He completed an internship and residency at Boston Children's Hospital and a fellowship at Boston Children's Hospital and Dana-Farber Cancer Institute.

Dr. Kung received the Howard Temin Award from the National Cancer Institute in 2001. He has been a Fellow in the Howard Hughes Medical Institute, and is an elected member of the American Society for Clinical Investigation and the Society for Pediatric Research.

Key Publications

• Chen Z, Cheng K, Walton Z, Wang Y, Ebi H, Shimamura T, Liu Y, Tupper T, Ouyang J, Li J, Gao P, Woo MS, Xu C, Yanagita M, Altabef A, Wang S, Lee C, Nakada Y, Peña CG, Sun Y, Franchetti Y, Yao C, Saur A, Cameron MD, Nishino M, Hayes DN, Wilkerson MD, Roberts PJ, Lee CB, Bardeesy N, Butaney M, Chirieac LR, Costa DB, Jackman D, Sharpless NE, Castrillon DH, Demetri GD, Jänne PA, Pandolfi PP, Cantley LC, Kung AL, Engelman JA, Wong KK. A murine lung cancer co-clinical trial identifies genetic modifiers of therapeutic response. Nature 2012, 483: 613-617.

• Bernt KM, Zhu N, Sinha AU, Vempati S, Faber J, Krivtsov AV, Feng Z, Punt N, Daigle A, Bullinger L, Pollock RM, Richon VM, Kung AL, Armstrong SA. MLL-rearranged leukemia is dependent on aberrant H3K79 methylation by DOT1L. Cancer Cell 2011, 20: 66-78.

• Xia X, Lemieux M, Li W, Carroll JS, Brown M, Liu XS, Kung AL. Integrative analysis of HIF binding and transactivation reveals its role in maintaining histone methylation homeostasis. Proc Natl Acad Sci USA 2009, 106: 4260-4265.

• Ziegler DS, Wright RD, Kesari S, Lemieux M, Tran MA, Jain M, Zawel L, Kung AL. Resistance of human glioblastoma multiforme cells to growth factor inhibitors is overcome by blockade of inhibitor of apoptosis proteins. J Clin Invest 2008, 188: 3109-3122.

• Mitsiades CS, Mitsiades NS, McMullan CJ, Poulaki V, Shringarpure R, Akiyama M, Hideshima T, Chauhan D, Joseph M, Libermann TA, Hofmann F, Garcia-Echeverria C, Pearson MA, Anderson KC, Kung AL. Inhibition of the Insulin-Like Gorwth Factor Receptor-1 Tyrosine Kinase Activity as a Therapeutic Strategy for Multiple Myeloma, Other Hematologic Malignancies and Solid Tumors. Cancer Cell 2004, 5: 221-230