Office: JSCBB B316
Lab Office: JSCBB B355
Lab Phone: 303-492-7794
Ph.D.: Massachusetts Institute of Technology, 2009
Postdoctoral Fellow: Stanford University, 2010-2014
Areas of Expertise
Awards and Honors
- NIH Director’s New Innovator Award (10/2018 – 9/2023)
- American Cancer Society - Research Scholar Grant (7/2018 – 6/2022)
- Pew-Stewart Scholar Award (8/2017 – 7/2021)
- Beckman Young Investigator Award (8/2016 – 7/2020)
- Searle Scholar Award (7/2016 – 6/2019)
- Kimmel Scholar Award (7/2016 – 6/2018)
- Boettcher Foundation Early Career Investigator Award (7/2016 – 6/2019)
- K22 Career Development Award, National Cancer Institute, NIH (9/2014 - 8/2017)
- Robert and Mary Ann Forsland Postdoctoral Fellowship, American Cancer Society (4/2013-8/2014)
- Postdoctoral Fellowship, Damon Runyon Cancer Research Foundation (3/2010-3/2013)
- Steinmetz Fellowship, Santa Fe Institute (7/2004-8/2004)
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 firstname.lastname@example.org.
Publications from the Spencer Lab
10. Yang C*, Tian C*, Hoffman T, Jacobsen N, Spencer SL. Signaling plasticity mediates rapid escape from BRAF inhibition in single melanoma cells. Submitted. bioRxiv 2020.03.15.992982; doi: https://doi.org/10.1101/2020.03.15.992982
9. Tian C*, Yang C*, Spencer SL. EllipTrack: A Global-Local Cell-Tracking Pipeline for 2D Fluorescence Time-Lapse Microscopy. Resubmitted. bioRxiv 2020.04.13.036756; doi: https://doi.org/10.1101/2020.04.13.036756
8. Min M, Rong Y, Spencer SL. Temporal integration of mitogen history in mother cells controls proliferation of daughter cells (2020). Science, doi: 10.1126/science.aay8241
7. Ashraf HM, Moser J, Spencer SL. Senescence Evasion in Chemotherapy: A Sweet Spot for p21 (2019). Cell, 178(2):267-269. [Preview]
6. Min M and Spencer SL. Spontaneously slow-cycling subpopulations of human cells originate from activation of stress-response pathways (2019). PLoS Biology, 17(3):e3000178.
5. Moser J, Miller I, Carter D, Spencer SL. Control of the Restriction Point by Rb and p21 (2018). PNAS, 115(35):E8219-E8227.
4. Miller I*, Min M*, Yang C, Tian C, Gookin S, Carter D, Spencer SL. Ki67 is a graded rather than a binary marker of proliferation vs. quiescence (2018). Cell Reports 24(5):1105-1112.
-Recommended in Faculty of 1000
3. Arora M and Spencer SL. A cell-cycle “safe space” for surviving chemotherapy (2017). Cell Systems 5(3):161-162. [Preview]
2. Gookin S*, Min M*, Phadke H, Chung M, Moser J, Miller I, Carter, D, Spencer SL. A map of protein dynamics during cell-cycle progression and cell-cycle exit (2017). PLoS Biology 15(9):e2003268.
1. Arora M, Moser J, Phadke H, Akbar-Basha A, Spencer SL. Endogenous replication stress in mother cells leads to quiescence of daughter cells (2017). Cell Reports 19(7):1351-1364.
- Covered in a News and Views by JE Purvis. (2017) Nature 549:343-344.
Publications from postdoctoral work
4. Cappell SD, Chung M, Jaimovich A, Spencer SL, Meyer T (2016). Irreversible APCCdh1 inactivation underlies the point of no return for cell-cycle entry. Cell 166:167-80.
3. Yang Z, Broz DK, Noderer W, Ferreira J, Overton KW, Spencer SL, Meyer T, Tapscott S, Attardi L, Wang CL (2015). p53 Suppresses Muscle Differentiation at the Myogenin Step in Response to Genotoxic Stress. Cell Death and Differentiation, 10.1038/cdd.2014.189.
2. Overton KW, Spencer SL, Noderer WL, Meyer T, Wang CL (2014). Basal p21 controls population heterogeneity in cycling and quiescent cell-cycle states. PNAS, 111:E4386-93.
1. 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.
- Recommended in Faculty of 1000
- Perspective by T. Zhang. (2013) Science Signaling, 6:pe37.
- Research Watch by E. McKenna. (2013) Cancer Discovery, DOI: 10.1158/2159-8290.CD-RW2013-220.
- Research Highlight by K. Minton. (2013) Nature Review Molecular Cell Biology, DOI:10.1038/nrm3687.
Publications from PhD work
7. 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.
6. 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.
5. Spencer SL and Sorger PK (2011). Measuring and modeling apoptosis in single cells. Cell 144:926-39.
4. 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.
3. 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.
2. 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.
1. 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.
Publications from work prior to PhD
3. Pepper JW, Findlay CS, Kassen R., Spencer SL, Maley CC (2009). Cancer research meets evolutionary biology. Evolutionary Applications 2, 62-70.
2. Spencer SL, Gerety RA, Pienta KJ, Forrest S (2006). Modeling somatic evolution in tumorigenesis. PLoS Computational Biology 2:e108.
1. Spencer SL, Berryman MJ, García JA, Abbott D (2004). An ordinary differential equation model for the multistep progression to cancer. Journal of Theoretical Biology 231, 515-524.