Sang Eun Lee, Ph.D.

The common property of cancer cells is genetic instability.  Frequent alterations of structure and chromosome numbers in cells contribute to the initiation and the progression of many types of cancer. The ultimate cure of this disease should thus come from a better understanding of the mechanisms preserving genome integrity. The overarching goal of my research program is to define cellular mechanisms to suppress genetic instability in the face of DNA damaging agents, in particular, DNA double strand breaks.

• Professional Background

  Education

  • 1996 - PhD - Molecular Biology - Brown University
  • 1990 - MA - Molecular Biology - Seoul National University
  • 1988 - BA - Molecular Biology - Seoul National University
  • Postdoctoral Fellowship - Genetics - Brandeis University

  Appointments

  • 11/2012 - Chief - The University of Texas Health Science Center at San Antonio, Radiation Oncology, San Antonio
  • 1/2012 - Adjunct Professor and Adjunct Professor - Pohang University of Science and Technology, Life Sciences, Pohang
  • 9/2011 - Professor - The University of Texas Health Science Center at San Antonio, Molecular Medicine, San Antonio

• Instruction & Training

  • 11/2016 - Present, Post-Doctoral Student Supervision, The University of Texas Health Science Center at San Antonio
  • 1/2016 - Present, Post-Doctoral Student Supervision, The University of Texas Health Science Center at San Antonio
  • 5/2015 - Present, Post-Doctoral Student Supervision, The University of Texas Health Science Center at San Antonio
  • 11/2013 - Present, Pre-Doctoral Student Supervision, The University of Texas Health Science Center at San Antonio
  • 1/2013 - Present, Membership on Supervising Committee, The University of Texas Health Science Center at San Antonio
  • 12/2010 - Present, Membership on Supervising Committee, The University of Texas Health Science Center at San Antonio
  • 12/2009 - Present, Membership on Supervising Committee, The University of Texas Health Science Center at San Antonio
  • 7/2009 - Present, Membership on Supervising Committee, The University of Texas Health Science Center at San Antonio
  • 6/2009 - Present, Ph.D. Dissertations Directed, The University of Texas Health Science Center at San Antonio

• Research & Grants

  DNA Damage Response

  Cancer Development and Progression Program 

  Research profile

  Grants

  Federal

  Funding Agency NIH Title Hypovitaminosis D promotes MED12-associated genomic instability in uterine fibroids Status Active Period 8/2017 - 7/2022 Role Co-Investigator Grant Detail : Vitamin D3 signaling modulates the level of DNA damage, including that likely arising from R-loop induced replication stress, in MED12 mutation positive uterine fibroids. These findings provide sound support to investigate whether, and also how, low vitamin D3 levels, a known risk factor for uterine fibroid development, compound DNA damage accumulation and genetic instability found in MED12 mutant tumors.

  Private

  Funding Agency William and Ella Owens Medical Research Foundation Title Targeting Microhomology-Mediated End Joining to sensitize recombination-deficient cancer cells. Status Complete Period 1/2016 - 6/2017 Role Principal Investigator Grant Detail  

• Publications

  Abstract

  Obeidat, M, Cline, K, Stathakis S, Papanikolaou N, Rasmussen KH, Gutierrez AN, Ha CS, Lee SE, Shim EY, Kirby NA. Optimizing the Response and Cost of a DNA Double-Strand Break Dosimeter; 2015 Jan. (Med Phys; vol. 43, no. 3872).

  Journal Article

  Seol J.-H, Shim E.Y., Lee SE. Microhomology-mediated end joining: Good, bad and ugly Mutation Research 2018 Jan;. Sinha S., Li F, Villarreal D., Shim J.H., Yoon S., Myung K., Shim E.Y., Lee SE. Microhomology-mediated end joining induces hypermutagenesis at breakpoint junctions PLOS genetics 2017 Apr;13(4):743-758. Sinha S., Villarreal D., Shim E.Y., Lee SE. Risky business: Microhomology-mediated end joining Mutation Research 2016 Jun;788:17-24. Liu Y., Sung S., Kim Y., Li F, Gwon G., Jo A., Kim A.-K., Kim T., Song O.-K., Lee SE, Cho Y. ATP-dependent DNA binding, unwinding, and resection by the Mre11/Rad50 complex EMBO Journal 2016 Apr;35(7):743-758. Sung S., Li F, Park Y.B., Kim J.S., Kim A.-K., Song O.-K., Kim J., Che J., Lee SE, Cho Y. DNA end recognition by the Mre11 nuclease dimer: Insights into resection and repair of damaged DNA EMBO Journal 2014 Oct;33(20):2422-2435. Lee SE, Sarangi P., Altmannova V., Holland C., Hao F., Krejci L., Zhao X., Bartasova Z., Anrather D., Ammerer G. A versatile scaffold contributes to DNA repair through sumoylation and nuclease interactions Cell Report 2014 Oct;9(1):143-152. Lee SE. Sumoylation of the Rad1 nuclease promotes DNA repair and regulates its DNA association Nucleic Acids Research 2014 Jun;42(10):6393-6404.

  Not Specified

  Lee SE, Che S., Smith S, Kim Y.J., Shim EY, Myung K. Hyper-acetylation of Histone H3K56 limits break-induced replication by inhibiting extensive repair synthesis PLOS genetics 2015 Feb;11(2).