Garth Powis, D. Phil.
Research Assistant Professor(s)
Garth Powis' Research Focus
Solid tumors exist in a stressed environment for cell growth. In order to survive, cancer cells initiate specific adaptive and constitutive changes allowing them to adapt to the hostile hypoxic environment, escape cell death and increase formation of new blood vessels and metastasis. All of these responses lead to highly aggressive tumors that are resistant to therapy. In order to identify novel targets for therapeutic intervention that is applicable to a wide variety of tumor types, our lab studies the mechanisms that enable cancer cells to survive stress.
Garth Powis' Bio
Powis is a native of the U.K., where he trained at Oxford University. He worked at the Mayo Clinic, becoming deputy chair of Pharmacology; at University of Arizona Cancer Center as director of Basic Research; and most recently at MD Anderson Cancer Center, where he served as chair of Experimental Therapeutics and director of the Center for Targeted Therapy.
Powis is a molecular and translational pharmacologist with more than 350 publications and 15 patents. His research focuses on the mechanisms that enable cancer cells to survive stress. Powis’ work has resulted in three novel cancer drugs currently in clinical trials. The expertise he brings to SBP encompasses all stages of cancer drug discovery and development, from early target identification to clinical studies with cancer patients.
1970: Merton College, Oxford, United Kingdom, D. Phil., Biochemistry and Pharmacology
1967: Birmingham University, England, United Kingdom, B.Sc., Hons. (1st Class), Biochemistry and Pharmacology
AMPKα modulation in cancer progression: multilayer integrative analysis of the whole transcriptome in Asian gastric cancer.
Kim YH, Liang H, Liu X, Lee JS, Cho JY, Cheong JH, Kim H, Li M, Downey TJ, Dyer MD, Sun Y, Sun J, Beasley EM, Chung HC, Noh SH, Weinstein JN, Liu CG, Powis G
Cancer Res 2012 May 15 ;72(10):2512-21
Sheveleva EV, Landowski TH, Samulitis BK, Bartholomeusz G, Powis G, Dorr RT
Mol Cancer Res 2012 Mar ;10(3):392-400
Effect of KRAS oncogene substitutions on protein behavior: implications for signaling and clinical outcome.
Ihle NT, Byers LA, Kim ES, Saintigny P, Lee JJ, Blumenschein GR, Tsao A, Liu S, Larsen JE, Wang J, Diao L, Coombes KR, Chen L, Zhang S, Abdelmelek MF, Tang X, Papadimitrakopoulou V, Minna JD, Lippman SM, Hong WK, Herbst RS, Wistuba II, Heymach JV, Powis G
J Natl Cancer Inst 2012 Feb 8 ;104(3):228-39
A Robust and Cost-Effective Luminescent-Based High-Throughput Assay for Fructose-1,6-Bisphosphate Aldolase A.
Cho EJ, Devkota AK, Stancu G, Edupunganti R, Debevec G, Giulianotti M, Houghten R, Powis G, Dalby KN
SLAS Discov 2020 May 28 ;:2472555220926146
Fluorescent probes towards selective cathepsin B detection and visualization in cancer cells and patient samples.
Poreba M, Groborz K, Vizovisek M, Maruggi M, Turk D, Turk B, Powis G, Drag M, Salvesen GS
Chem Sci 2019 Sep 28 ;10(36):8461-8477
Absence of HIF1A Leads to Glycogen Accumulation and an Inflammatory Response That Enables Pancreatic Tumor Growth.
Maruggi M, Layng FI, Lemos R Jr, Garcia G, James BP, Sevilla M, Soldevilla F, Baaten BJ, de Jong PR, Koh MY, Powis G
Cancer Res 2019 Nov 15 ;79(22):5839-5848
An Inhibitor of the Pleckstrin Homology Domain of CNK1 Selectively Blocks the Growth of Mutant KRAS Cells and Tumors.
Indarte M, Puentes R, Maruggi M, Ihle NT, Grandjean G, Scott M, Ahmed Z, Meuillet EJ, Zang S, Lemos R Jr, Du-Cuny L, Layng FIAL, Correa RG, Bankston LA, Liddington RC, Kirkpatrick L, Powis G
Cancer Res 2019 Jun 15 ;79(12):3100-3111
A Fluorescence-Based High-Throughput Assay for the Identification of Anticancer Reagents Targeting Fructose-1,6-Bisphosphate Aldolase.
Cho EJ, Devkota AK, Stancu G, Edupunganti R, Powis G, Dalby KN
SLAS Discov 2018 Jan ;23(1):1-10
Katsiampoura A, Raghav K, Jiang ZQ, Menter DG, Varkaris A, Morelli MP, Manuel S, Wu J, Sorokin AV, Rizi BS, Bristow C, Tian F, Airhart S, Cheng M, Broom BM, Morris J, Overman MJ, Powis G, Kopetz S
Mol Cancer Ther 2017 Jul ;16(7):1435-1442