Gregory R J Thatcher, PhD

Professor, Pharmacology & Toxicology

Links

Biography

Thatcher joined the University of Arizona in 2020 from the University of Illinois College of Pharmacy at UIC. In his career, he has graduated 55 students with PhD’s and training in biological and medicinal chemistry and all aspects of drug discovery from conception through clinical trials. Thatcher founded a campus-wide and disease-agnostic drug discovery center at UIC, focused on small molecule drug discovery, which continues to play an active role in academic drug discovery across Chicago. Dr. Thatcher created his first start-up biotech company in 1997, which successfully took an Alzheimer’s drugs into human clinical trials and continues to move his research forwards directly to benefit human health.

Cancer Focus

Building upon 20 years of experience in estrogens and breast cancer, Thatcher’s research has resulted in two small molecules that have recently completed Phase 1 trials in estrogen receptor positive breast cancer. A focus on endocrine-resistance has led to exploitation of epigenetic mechanisms for targeted therapeutics to overcome resistance and current research is exploring combinations with checkpoint inhibitors. This research and other kinase inhibitor projects have shifted focus to pancreatic cancer although other solid tumors are also of interest. Thatcher was founder/leader of the Translational Oncology Program in the University of Illinois Cancer Center before moving to UA.

Research Program Role

Cancer Biology Program

Display Name

Gregory R J Thatcher, PhD

Publications

Phase 1 study of TTC-352 in patients with metastatic breast cancer progressing on endocrine and CDK4/6 inhibitor therapy.

Dudek AZ, Liu LC, Fischer JH, Wiley EL, Sachdev JC, Bleeker J, Hurley RW, Tonetti DA, Thatcher GRJ, Venuti RP, et al. 2020. Phase 1 study of TTC-352 in patients with metastatic breast cancer progressing on endocrine and CDK4/6 inhibitor therapy. Breast Cancer Res Treat. 183:617–627. doi:10.1007/s10549-020-05787-z.

G1T48, an oral selective estrogen receptor degrader, and the CDK4/6 inhibitor lerociclib inhibit tumor growth in animal models of endocrine-resistant breast cancer.

Andreano KJ, Wardell SE, Baker JG, Desautels TK, Baldi R, Chao CA, Heetderks KA, Bae Y, Xiong R, Tonetti DA, et al. 2020. G1T48, an oral selective estrogen receptor degrader, and the CDK4/6 inhibitor lerociclib inhibit tumor growth in animal models of endocrine-resistant breast cancer. Breast Cancer Res Treat. 180:635–646. doi:10.1007/s10549-020-05575-9.

Mixed lineage kinase 3 inhibition induces T cell activation and cytotoxicity.

Kumar S, Singh SK, Viswakarma N, Sondarva G, Nair RS, Sethupathi P, Sinha SC, Emmadi R, Hoskins K, Danciu O, et al. 2020. Mixed lineage kinase 3 inhibition induces T cell activation and cytotoxicity. Proc Natl Acad Sci U S A. 117:7961–7970. doi:10.1073/pnas.1921325117.

Novel Pyrrolopyridone Bromodomain and Extra-Terminal Motif (BET) Inhibitors Effective in Endocrine-Resistant ER+ Breast Cancer with Acquired Resistance to Fulvestrant and Palbociclib.

Li Y, Zhao J, Gutgesell LM, Shen Z, Ratia K, Dye K, Dubrovskyi O, Zhao H, Huang F, Tonetti DA, et al. 2020. Novel Pyrrolopyridone Bromodomain and Extra-Terminal Motif (BET) Inhibitors Effective in Endocrine-Resistant ER+ Breast Cancer with Acquired Resistance to Fulvestrant and Palbociclib. J Med Chem. 63:7186–7210. doi:10.1021/acs.jmedchem.0c00456.

Design and Synthesis of Basic Selective Estrogen Receptor Degraders for Endocrine Therapy Resistant Breast Cancer.

Lu Y, Gutgesell LM, Xiong R, Zhao J, Li Y, Rosales CI, Hollas M, Shen Z, Gordon-Blake J, Dye K, et al. 2019. Design and Synthesis of Basic Selective Estrogen Receptor Degraders for Endocrine Therapy Resistant Breast Cancer. J Med Chem. 62:11301–11323. doi:10.1021/acs.jmedchem.9b01580.