"The Sontag Foundation Distinguished Scientist Award was instrumental to my success as a scientist. The Sontag Foundation recognized my potential very early in my career, at a time when our science was in a fledgling state, and I was an unproven independent scientist. Their investment supported my laboratory to develop novel scientific methodologies that have become a mainstay of our research. I am grateful for their continued engagement as it pushes us to produce cutting-edge science."
- Dr. Steven J. Bensinger
- Associate Professor, Departments of Microbiology, Immunology, and Molecular Genetics and Molecular and Medical Pharmacology, UCLA David Geffen School of Medicine, 2015-present
- Director Shared Resources, Jonsson Comprehensive Cancer Center, Immunity, Inflammation, Infection, & Transplantation (I3T) Research Initiative, UCLA David Geffen School of Medicine, 2015-present
- Co-director Metabolomics Core, University of California, Los Angeles, 2014-present
About DSA-Funded Research
High-grade gliomas are highly aggressive tumors that are associated with a very poor prognosis. Current therapeutic approaches are largely palliative and novel therapies that could extend disease free intervals or survival times are desperately required. Interestingly, intracellular lipid or "fat" metabolism has emerged as an important regulator of cancer growth and behavior. We have discovered that inactivating a key component of lipid metabolism, the SREBP proteins, markedly decreases human glioma growth. In-depth mechanistic studies in the laboratory revealed that SREBP influences multiple aspects of brain tumor cell biology, including sugar and fat metabolism, proliferation and survival. In combination, these studies argue that SREBP could be a compelling therapeutic target in brain cancer. However, many more studies need to be done so that we can better understand the impact of SREBP activity in brain cancer. In this application, we propose three aims designed to expand on our knowledge of how the SREBP-driven metabolic program of brain cancer is controlled, and to determine the functional consequences of SREBP activity on chemo-therapeutic resistance. These studies explore a poorly understood aspect of brain cancer biology, and will help to determine if targeting the SREBP pathway is a viable therapeutic approach for the treatment of brain cancer.
"Steve's strongest attributes are his profound intellect and his laser-like focus on the scientific problem at hand. He has the uncanny ability to choose the right experiment."
Peter Tontonoz, M.D., Ph.D.
University of California, Los Angeles
Howard Hughes Medical Institute
"Dr. Bensinger is an exciting and proven talent in the emerging field of cancer cell metabolism. He has enormous potential to contribute to the field of brain cancer."
Jonathan Braun, M.D., Ph.D.
University of California, Los Angeles
- Williams KJ, Argus JP, Zhu Y, Wilks MQ, Marbois BN, York AG, Kidani Y, Pourzia AL, Akhavan D, Lisiero DN, Komisopoulou E, Henkin AH, Soto H, Chamberlain BT, Vergnes L, Jung ME, Torres JZ, Liau LM, Christofk HR, Prins RM, Mischel PS, Reue K, Graeber TG, Bensinger SJ. An essential requirement for the SCAP/SREBP signaling axis to protect cancer cells from lipotoxicity. Cancer Res. 2013 May 1;73(9):2850-2862. PMCID: PMC3919498
- Akhavan D, Pourzia AL, Nourian AA, Williams KJ, Nathanson D, Babic I, Villa GR, Tanaka K, Nael A, Yang H, Dang J, Vinters HV, Yong WH, Flagg M, Tamanoi F, Sasayama T, James CD, Kornblum HI, Cloughesy TF, Cavenee WK, Bensinger SJ*, Mischel PS*. De-repression of PDGFRß transcription promotes acquired resistance to EGFR tyrosine kinase inhibitors in glioblastoma patients. Cancer Discov. 2013 Apr 23. PMCID: PMC3651754 * Co-corresponding authors
- Ahler E, Sullivan WJ, Cass A, Braas D, York AG, Bensinger SJ, Graeber TG, Christofk HR. Doxycycline alters metabolism and proliferation of human cell lines. PLoS One. 2013 May 31;8(5):e64561. doi: 10.1371/journal.pone.0064561. PMCID: PMC3669316
- Mercer JL, Argus JP, Crabtree DM, Keenan MM, Wilks MQ, Chi JT, Bensinger SJ, Lavau CP, Wechsler DS. Modulation of PICALM Levels Perturbs Cellular Cholesterol Homeostasis. PLoS One. 2015 Jun 15;10(6):e0129776. doi: 10.1371/journal.pone.0129776 PMCID: PMC4467867
- York AG, Argus JP, Williams KJ, Brar G, Vergnes L, Gray EE, Zhen A, Wu NC, Yamada DH, Cunningham CR, Wilks MQ, Casero D, Gray D, Yu A, Brooks DG, Sun R, Kitchen SG, Wu T1, Reue K, Stetson DB and Bensinger SJ. Limiting cholesterol biosynthetic flux engages type I IFN signaling in a STING-dependent manner. Cell. 2015 Dec 17;163(7):1716-29 PMCID: PMC4783382