Scott Thomas, PhD

Staff Scientist
Department of Medicine
Division of Hematology and Oncology
Helen Diller Family Cancer Center
University of California
1450 3rd Street, HD 250
San Francisco, California 94158, USA

 

Biography

Dr. Thomas studied Cell Division as a Doctoral candidate with Professor Kenneth Kaplan at the University of California Davis and as a Postdoctoral Fellow he received training in translational oncology with Dr. Pamela Munster at the University of California San Francisco. Dr. Thomas is currently a Staff Scientist in the Department of Medicine at UCSFs Helen Diller Family Comprehensive Cancer Center.

Research Interest

His research interests includes: Development of novel therapeutics targeting cellular epigenetics for the treatment of cancer and translating these approaches to the clinic.

Scientific Activities

HONORS

• (1998-1999) Graduate Assistance in Areas of National Need Fellowship
• (1999) Achievement Rewards for College Scientists Scholarship
• (2000) First place graduate research poster, Research Infrastructure in Minority Institutions Biomedical Research Conference
• (2000) Distinguished Achievement Award for Academic Excellence
• (2000) College of Science and Engineering Graduating Honors
• (2002) Henry Jastro and Peter Shields Research Scholarship
• (2006) Floyd and Mary Schwall Medical Research Fellowship
• (2006) George Lee Fellowship

MEMBERSHIPS

• (2001-2007) American Association of Cell Biology, Associate Member
• (2008-Present) American Association of Cancer Research, Member

Publications

SELECTED PUBLICATIONS

1. Holmes EH, Yen TY, Thomas S, et al. Human alpha 1,3/4 fucosyltransferases. Characterization of highly conserved cysteine residues and N-linked glycosylation sites. J Biol Chem. 2000; 275(32): 24237-24245. doi: 10.1074/jbc.M000888200
2. Thomas S, Yen TY, Macher BA. Eukaryotic glycosyltransferases: cysteines and disulfides. Glycobiology. 2002; 12(2): 4G-7G.
3. Rodrigo-Breni MC, Thomas S, Bouck DC, Kaplan KB. Sgt1p and Skp1p modulate the assembly and turnover of CBF3 complexes required for proper kinetochore function. Mol Biol Cell. 2004; 15(7): 3366-3378. doi: 10.1091/mbc.E03-12-088
4. Gillis AN, Thomas S, Hansen SD, Kaplan KB. A novel role for the CBF3 kinetochore-scaffold complex in regulating septin dynamics and cytokinesis. J Cell Biol. 2005; 171(5): 773-784. doi: 10.1083/jcb.200507017
5. Thomas S, Kaplan KB. A Bir1p-Sli15p kinetochore passenger complex regulates septin organization during anaphase. Mol Biol Cell. 2007; 18(10): 3820-3834. doi: 10.1091/mbc.E07-03-0201
6. Thomas S, Kaplan KB. Kinetochore regulation of anaphase and cytokinesis. In: De Wulf P, Earnshaw WC, eds. The Kinetochore: From molecular discoveries to cancer therapy. New York: Springer Science+Business Media, LLC, 2009: 371-394.
7. Thomas S, Munster PN. Histone deacetylase inhibitor induced modulation of anti-estrogen therapy. Cancer Lett. 2009; 280(2): 184-191.
8. Munster PN, Machion D, Thomas S, et al. Phase I trial of vorinostat and doxorubicin in solid tumours: histone deacetylase 2 expression as a predictive marker. Br J Cancer. 2009; 101(7): 1044-1050.
9. Thurn KT, Thomas S, Moore A, Munster PN. Rational therapeutic combinations with histone deacetylase inhibitors for the treatment of cancer. Future Oncol. 2011; 7(2): 263-283. doi: 10.2217/fon.11.2
10. Thomas S, Miller A, Thurn KT, Munster PN. Clinical applications of histone deacetylase inhibitors. In: Tollefsbol T, ed. Handbook of Epigenetics: The New Molecular and Medical Genetics. New York: Academic Press, 2011: 597-615.
11. Munster PN, Thurn KT, Thomas S, et al. A phase II study of the histone deacetylase inhibitor vorinostat combined with tamoxifen for the treatment of patients with hormone therapy-resistant breast cancer. Br J Cancer. 2011; 104(12): 1828-1835. doi: 10.1038/bjc.2011.156
12. Raha P, Thomas S, and Munster PN. Epigenetic modulation: A novel therapeutic target for overcoming hormonal therapy resistance. Epigenomics. 2011; 3(4): 451-470.
13. Thomas S, Thurn KT, Biçaku E, Marchion DC, Munster PN. Addition of a histone deacetylase inhibitor redirects tamoxifen-treated breast cancer cells into apoptosis, which is opposed by the induction of autophagy. Breast Cancer Res Treat. 2011; 130(2): 437-447. doi: 10.1007/s10549-011-1364-y.
14. Thomas S, Thurn KT, Raha P, Chen S, Munster PN. Efficacy of Histone deacetylase and estrogen receptor inhibition in breast cancer cells due to concerted down regulation of Akt. PLOS One. 2013. doi: 10.1371/journal.pone.0068973
15. Thurn KT, Thomas S, Raha P, Qureshi I, Munster PN. Histone Deacetylase Regulation of ATM-Mediated DNA Damage Signaling. Mol Cancer Ther. 2013; 12(10): 2078-2078. doi: 10.1158/1535-7163.MCT-12-1242
16. Raha P, Thomas S, Thurn KT, Park J, Munster PN. Combined histone deacetylase inhibition and tamoxifen induces apoptosis in tamoxifen-resitant breast cancer models, by reversing Bcl-2 overexpression. Breast Cancer Res. 2015; 17: 26. doi: 10.1186/s13058-015-0533-z
17. Park J, Thomas S, Munster PN. Epigenetic modulation and immunotherapy: A review. Epigenomics. 2015; 7(4): 641-652. doi: 10.2217/epi.15.16.