Guri Giaever PhD
Dr. Guri Nina Giaever completed a bachelor of science in electrical engineering at Brown University in Providence, Rhode Island and a doctor of philosophy in biophysics at Harvard University in Cambridge, Massachusetts. She was also a National Institutes of Health postdoctoral fellow, senior genome scientist at the Stanford Genome Technology Center in Palo Alto, California. In that role, Dr. Giaever started the HIPHOP chemogenomics laboratory.
Prior to joining UBC, Dr. Giaever was an associate professor and Tier II CRC chair in chemical biology at the Donnelly Centre at the University of Toronto. Her teaching areas of interest include drug discovery, genetics, medicinal chemistry, and functional genomics.
The primary research objectives of Dr. Giaever's lab include screening known and novel drugs to understand their precise mechanisms of action. The unique, genome-wide assays have the ability to uncover drug targets and mechanisms of drug action in a cellular context. Specifically, genome-wide assays are employed that allow the identification of all genes required for growth in the presence of drug to identify specific genes perturbed by a drug with a focus on the model organism yeast S. cerevisiae. Her experimental approach reports a genome-wide view of cellular response to compounds, providing a rich resource for the discovery of the relationship between genes, drugs and biological processes. In an orthogonal approach, Dr. Giaever's lab recently established a genome-wide screen for alleles involved in drug resistance, employing NGS (next-generation sequencing) technologies. The lab continues to improve and expand its automated technologies, including the development of robust bioinformatic and cheminformatics methodologies. Dr. Giaever is also translating findings to patient samples.
Giaever G, Nislow C. The yeast deletion collection: a decade of functional genomics. Genetics. 2014 Jun;197(2):451-65. doi: 10.1534/genetics.114.161620. Epub 2014 Jun 17. PMID: 24939991; PMCID: PMC4063906.
Lee AY, St Onge RP, Proctor MJ, Wallace IM, Nile AH, Spagnuolo PA, Jitkova Y, Gronda M, Wu Y, Kim MK, Cheung-Ong K, Torres NP, Spear ED, Han MK, Schlecht U, Suresh S, Duby G, Heisler LE, Surendra A, Fung E, Urbanus ML, Gebbia M, Lissina E, Miranda M, Chiang JH, Aparicio AM, Zeghouf M, Davis RW, Cherfils J, Boutry M, Kaiser CA, Cummins CL, Trimble WS, Brown GW, Schimmer AD, Bankaitis VA, Nislow C, Bader GD, Giaever G. Mapping the cellular response to small molecules using chemogenomic fitness signatures. Science. 2014 Apr 11;344(6180):208-11. doi: 10.1126/science.1250217. Erratum in: Science. 2014 May 23;344(6186):1255771. PMID: 24723613; PMCID: PMC4254748.
Nile, A., Tripathi, A., Yuan, P. et al. PITPs as targets for selectively interfering with phosphoinositide signaling in cells. Nat Chem Biol 10, 76–84 (2014). https://doi.org/10.1038/nchembio.1389
Sukhai MA, Prabha S, Hurren R, Rutledge AC, Lee AY, Sriskanthadevan S, Sun H, Wang X, Skrtic M, Seneviratne A, Cusimano M, Jhas B, Gronda M, MacLean N, Cho EE, Spagnuolo PA, Sharmeen S, Gebbia M, Urbanus M, Eppert K, Dissanayake D, Jonet A, Dassonville-Klimpt A, Li X, Datti A, Ohashi PS, Wrana J, Rogers I, Sonnet P, Ellis WY, Corey SJ, Eaves C, Minden MD, Wang JC, Dick JE, Nislow C, Giaever G, Schimmer AD. Lysosomal disruption preferentially targets acute myeloid leukemia cells and progenitors. J Clin Invest. 2013 Jan;123(1):315-28. doi: 10.1172/JCI64180. Epub 2012 Dec 3. PMID: 23202731; PMCID: PMC3533286.
Skrtić M, Sriskanthadevan S, Jhas B, Gebbia M, Wang X, Wang Z, Hurren R, Jitkova Y, Gronda M, Maclean N, Lai CK, Eberhard Y, Bartoszko J, Spagnuolo P, Rutledge AC, Datti A, Ketela T, Moffat J, Robinson BH, Cameron JH, Wrana J, Eaves CJ, Minden MD, Wang JC, Dick JE, Humphries K, Nislow C, Giaever G, Schimmer AD. Inhibition of mitochondrial translation as a therapeutic strategy for human acute myeloid leukemia. Cancer Cell. 2011 Nov 15;20(5):674-88. doi: 10.1016/j.ccr.2011.10.015. PMID: 22094260; PMCID: PMC3221282.