Sam McBrayer received his bachelor’s degree in biochemistry from Baylor University and went on to obtain his Ph.D. in cancer biology from Northwestern University’s Feinberg School of Medicine. At Northwestern, he worked to explain the molecular underpinnings of enhanced glucose transport activity in multiple myeloma in the laboratory of Dr. Steven Rosen. Dr. McBrayer then joined the laboratory of Dr. William G. Kaelin, Jr. at the Dana-Farber Cancer Institute and Harvard Medical School as an American Cancer Society Postdoctoral Fellow. During his time in the Kaelin Laboratory, he studied metabolic reprogramming in glioma and developed new strategies for brain tumor therapy.
In 2019, Dr. McBrayer joined the faculty of Children’s Medical Center Research Institute at UT Southwestern as an assistant professor in pediatrics. Since then, he has received awards from the National Cancer Institute and the Cancer Prevention and Research Institute of Texas.
The McBrayer lab is working to identify the metabolic mechanisms that push cells to become cancerous and find new ways to inhibit them. To identify these mechanisms, they study the biology of brain tumors driven by mutations in genes that regulate metabolism. Studying these mutations may reveal fundamental connections between metabolism and other aspects of cell biology that are likely to control cancer formation in many different tissues. These insights hold great promise for the development of new therapies for patients with brain tumors and, by extension, for those with other types of cancer.
- Baylor University (2006), Biochemistry
- Graduate School
- Northwestern Univ (2012), Cancer Biology
- Brain Tumor Biology
- Cancer Biology
- Mouse Genetics
- Peptidic degron for IMiD-induced degradation of heterologous proteins.
- Koduri V, McBrayer SK, Liberzon E, Wang AC, Briggs KJ, Cho H, Kaelin WG, Proc. Natl. Acad. Sci. U.S.A. 2019 02 116 7 2539-2544
- Transaminase Inhibition by 2-Hydroxyglutarate Impairs Glutamate Biosynthesis and Redox Homeostasis in Glioma.
- McBrayer SK, Mayers JR, DiNatale GJ, Shi DD, Khanal J, Chakraborty AA, Sarosiek KA, Briggs KJ, Robbins AK, Sewastianik T, Shareef SJ, Olenchock BA, Parker SJ, Tateishi K, Spinelli JB, Islam M, Haigis MC, Looper RE, Ligon KL, Bernstein BE, Carrasco RD, Cahill DP, Asara JM, Metallo CM, Yennawar NH, Vander Heiden MG, Kaelin WG, Cell 2018 09 175 1 101-116.e25
- Autochthonous tumors driven by Rb1 loss have an ongoing requirement for the RBP2 histone demethylase.
- McBrayer SK, Olenchock BA, DiNatale GJ, Shi DD, Khanal J, Jennings RB, Novak JS, Oser MG, Robbins AK, Modiste R, Bonal D, Moslehi J, Bronson RT, Neuberg D, Nguyen QD, Signoretti S, Losman JA, Kaelin WG, Proc. Natl. Acad. Sci. U.S.A. 2018 04 115 16 E3741-E3748
- Multiple myeloma exhibits novel dependence on GLUT4, GLUT8, and GLUT11: implications for glucose transporter-directed therapy.
- McBrayer SK, Cheng JC, Singhal S, Krett NL, Rosen ST, Shanmugam M, Blood 2012 May 119 20 4686-97
- Integrative gene expression profiling reveals G6PD-mediated resistance to RNA-directed nucleoside analogues in B-cell neoplasms.
- McBrayer SK, Yarrington M, Qian J, Feng G, Shanmugam M, Gandhi V, Krett NL, Rosen ST, PLoS ONE 2012 7 7 e41455