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David Shackelford, Ph.D. [ Edit Your Profile ]

Work Email Address: dshackelford@mednet.ucla.edu

Work Phone Number: 310-567-3835

Office Address:
10833 Le Conte Avenue
Los Angeles, CA 90095 AR-255

Work
CTSI Member, CTSI
UCLA Member, themes Associate Adjunct Professor, Pulmonary and Critical Care Medicine

Research Interests

Medicine- Pulmonary Diseases


Education:
Degrees:
Ph.D.

Honors and Awards:
Recipient of Ruth L. Kirschstein Postdoctoral Research Award
Recipient of UCLA KL2 Translational Science Award

About

Dr. David Shackelford's career in cancer research began studying acute myelogenous leukemia at Brandeis University, where he received his PhD. He did his postdoc in Dr. Reuben Shaw’s lab at The Salk Institute, where he began studying signal transduction and metabolism during carcinogenesis of solid tumors. His research is translational in focus and integrates the study of human tumors and genetically engineered mouse models of cancer. His goals are to uncover the molecular mechanisms driving lung carcinogenesis, developing new in vitro and in vivo cancer models, and identifying new personalized therapies to treat cancer based on the tumor’s genetic and molecular alterations. Dr. Shackelford's current work on lung tumors focuses on exploiting the tumor’s Achilles’ heel, which is a dependence on oncogenic signaling and high rates of cellular metabolism. In a recent study he has demonstrated a previously unrecognized vulnerability in non-small cell lung tumors to undergo tumor cell death following treatment with the metabolic therapeutic phenformin. Their study opens up the possibility of repurposing therapeutics, originally designed to treat metabolic disease to be used as anti-cancer agents in the clinic.

Publications
Wei Wei, Shi Qihui, Remacle Francoise, Qin Lidong, Shackelford David B, Shin Young Shik, Mischel Paul S, Levine R D, Heath James R, Hypoxia induces a phase transition within a kinase signaling network in cancer cells. Proceedings of the National Academy of Sciences of the United States of America. 2013; 110(15): E1352-60.
Shackelford David B, Abt Evan, Gerken Laurie, Vasquez Debbie S, Seki Atsuko, Leblanc Mathias, Wei Liu, Fishbein Michael C, Czernin Johannes, Mischel Paul S, Shaw Reuben J, LKB1 inactivation dictates therapeutic response of non-small cell lung cancer to the metabolism drug phenformin. Cancer cell. 2013; 23(2): 143-58.
Egan Daniel F, Shackelford David B, Mihaylova Maria M, Gelino Sara, Kohnz Rebecca A, Mair William, Vasquez Debbie S, Joshi Aashish, Gwinn Dana M, Taylor Rebecca, Asara John M, Fitzpatrick James, Dillin Andrew, Viollet Benoit, Kundu Mondira, Hansen Malene, Shaw Reuben J, Phosphorylation of ULK1 (hATG1) by AMP-activated protein kinase connects energy sensing to mitophagy. Science (New York, N.Y.). 2011; 331(6016): 456-61.
Shackelford David B, Shaw Reuben J, The LKB1-AMPK pathway: metabolism and growth control in tumour suppression. Nature reviews. Cancer. 2009; 9(8): 563-75.
Shackelford David B, Vasquez Debbie S, Corbeil Jacqueline, Wu Shulin, Leblanc Mathias, Wu Chin-Lee, Vera David R, Shaw Reuben J, mTOR and HIF-1alpha-mediated tumor metabolism in an LKB1 mouse model of Peutz-Jeghers syndrome. Proceedings of the National Academy of Sciences of the United States of America. 2009; 106(27): 11137-42.
Gwinn Dana M, Shackelford David B, Egan Daniel F, Mihaylova Maria M, Mery Annabelle, Vasquez Debbie S, Turk Benjamin E, Shaw Reuben J, AMPK phosphorylation of raptor mediates a metabolic checkpoint. Molecular cell. 2008; 30(2): 214-26.

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