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Lee, Eun D. Ph.D.

  • Program Cancer Biology
  • Department
    Assistant Professor, Department of Microbiology and Immunology, School of Medicine
  • Phone 804-828-2423
Department affiliations
Assistant Professor, Department of Microbiology and Immunology, School of Medicine
PhD, University of Cincinnati, 2002
Disease focus of research

Ovarian, Gynecologic

Research keywords

Biomarkers,Cancer therapy,Immunotherapy,Inflammation,Targeted therapies,Tumor microenvironment

Research description
Our preliminary research addresses the fundamental yet a profound question in cancer immunotherapy: How can we flag solid tumors so the patient's immune cells preferentially recognize and eliminate only the cancer cells without harming the good cells? This proposal explores this critical question to improve immunotherapy specificity and efficacy. Patient's immune cells are the best defense against cancer development. However, when immune cells are activated by current therapeutic methods, they attack not only the cancer cells, but also the healthy cells, causing the patient to face additional health issues. The difficulty of targeting solid tumors is compounded by the following reasons: 1) tumor antigen shortage, 2) a strong immunosuppressive environment, and 3) an inability of the immune cells to infiltrate into solid tumors. This proposal exploits to improve these challenges by introducing an antigen-processing enzyme, Endoplasmic Reticulum Aminopeptidase 2 (ERAP2) that can increase the tumor antigen to specifically flag the solid tumor, decreasing the immunosuppressive environment and augmenting the lymphocyte infiltration. ERAP2 enzyme trims amino acid residues from the NH2 terminus prior to presentation on cell surface by HLA class I molecules. ERAP2 is expressed in many tissues, and are strongly induced by type I and type II interferons and tumor necrosis factor-alpha. The loss of ERAP2 expression is observed in renal carcinoma, colon adenocarcinoma, melanoma, and ovarian cancers. This suggests lack of ERAP2 may benefit cancer growth or maintenance by avoiding immune surveillance. Conversely, the presence of ERAP2N isoform alters tumor microenvironment unfavorable for cancer cells eliciting increased apoptosis via NK cells, reduce angiogenesis and increased cell migration of immune cell infiltrates.
Published research (during tenure as a Massey Cancer Center member)
Contact information