Sabrina Spencer

Spencer Lab

Research in my lab is focused on understanding how signaling events control cell fate.  Studying these processes in single cells reveals remarkable cell-to-cell variability in response to stimuli, even among genetically identical cells in a uniform environment.  We seek to understand the sources and consequences of this heterogeneity in cellular response to stimuli such as growth factors, cell stress, and targeted cancer therapeutics.  To do this, we develop genetically encoded fluorescent sensors for signaling events of interest and use long-term live-cell microscopy and cell tracking to quantify the dynamics of upstream signals and link them to cell fate (proliferation, quiescence, apoptosis, differentiation).  Our long-term goal is to understand the normal mechanistic functioning of signaling pathways, to understand how these signals go awry in cancer, and eventually to alter the fate of individual cells.  

Projects in the lab range from regulation of the cell cycle, to sensor and tool development, to more translational projects looking at the misregulated proliferation of cancer cells. We are actively recruiting new members, so if you would like to hear more about specific projects in the lab, please contact Sabrina Spencer at sabrina.spencer@colorado.edu.

Overton KW, Spencer SL, Noderer WL, Meyer T, Wang CL (2014). Basal p21 controls population heterogeneity in cycling and quiescent cell-cycle states. Proceedings of the National Academy of Sciences, 111:E4386-93.

Spencer SL, Cappell, SD, Tsai FC, Overton KW, Wang CL, Meyer T (2013). The proliferation-quiescence decision is controlled by a bifurcation in CDK2 activity at mitotic exit. Cell 155:369-83. 

• Research Watch by E. McKenna. (2013) Cancer Discovery, DOI: 10.1158/2159-8290.CD-RW2013-220. 
• Research Highlight by K. Minton. (2013) Nat Rev Mol Cell Biol. 14(11):691. 
• Perspective by T. Zhang. (2013) Science Signaling, 6:pe37.

Flusberg D, Roux J, Spencer SL, Sorger PK (2013). Cells surviving fractional killing by TRAIL exhibit transient but sustainable resistance and inflammatory phenotypes. Molecular Biology of the Cell 24:2186-200.

Gaudet S*, Spencer SL*, Chen W, Sorger PK (2012). Exploring the contextual sensitivity of factors that determine cell-to-cell variability in receptor-mediated apoptosis. PLoS Computational Biology 8:e1002482.

Spencer, SL and Sorger, PK (2011). Measuring and modeling apoptosis in single cells. Cell 144:926-39.

Kim, KA, Spencer SL, Albeck JG, Burke JM, Sorger PK, Gaudet S, Kim do H. (2010). Systematic calibration of a cell signaling network model. BMC Bioinformatics 11:202.

Niepel M*, Spencer SL*, Sorger PK (2009). Non-genetic cell-to-cell variability and the consequences for pharmacology. Current Opinion in Chemical Biology 13:556-61.

Spencer SL*, Gaudet S*, Albeck JG, Burke JM, Sorger PK (2009). Non-genetic origins of cell-to-cell variability in TRAIL-induced apoptosis. Nature 459:428-32. 

• News and Views by P. Bastiaens. (2009) Nature 459:334-5. 
• Preview by P. Loriaux & A. Hoffmann. (2009) Molecular Cell, 34:257-8. 
• Editor's Choice by L. B. Ray. (2009) Science Signaling, 2:ec178. 
• Front page article by David Cameron. Harvard FOCUS, May 15 2009. 
• Recommended as "Exceptional" (8 out of 9 stars) in Faculty of 1000.

Pepper JW, Findlay CS, Kassen R., Spencer SL, Maley CC (2009). Cancer research meets evolutionary biology. Evolutionary Applications 2, 62-70.

Albeck JG*, Burke JM*, Spencer SL, Lauffenburger DA, Sorger PK (2008). Modeling a snap-action, variable-delay switch controlling extrinsic cell death. PLoS Biology 6:e299.

Spencer SL*, Gerety RA*, Pienta KJ, Forrest S (2006). Modeling somatic evolution in tumorigenesis. PLoS Computational Biology 2:e108.