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Developing better cancer vaccines;

Dr. Z. Kurago investigates the functions of the mucosal defenses of the upper aerodigestive tract in health and disease, including infectious disorders and malignant neoplasia. In collaboration with Drs. D. Malamud and W. Abrams (NYU), and D. Weismann (U. Penn), studies were designed to better understand the differences in HIV transmission at mucosal portals by mapping the periluminal distribution of the HIV-binding molecule gp340 (DMBT1) and HIV targets CD4+ and CD16+ cells in normal oral, cervical, and rectal/sigmoid mucosae. While soluble gp340, present in saliva, can neutralize HIV binding to cells, cell-associated gp340 facilitates transmission. This study defined important distinctions between portals of HIV entry that help explain differences in transmission rates. (PLOS One. 2015, 10(7):e0132942). The Kurago Laboratory also collaborates with M.E. Elsalanty’s laboratory (GRU), which developed a rat model of osteonecrosis of the jaws related to bisphosphonate treatment. Bisphosphonate treatment is widely used in patients with multiple myeloma, breast cancer, and prostate cancer to reduce bone resorption and suppress bone metastases. This model has proven useful for mechanistic studies of causes and prevention strategies. (PLOS ONE. 2015, 10.1371/journal.pone.0132520). The Kurago Laboratory also collaborated with C. Cutler’s group (GRU) on a study related to periodontal disease and its systemic implications. This study described the mechanisms of survival of a periodontal pathogen P. gingivalis in human dendritic cells. (PLOS Pathogen. 2015, 10.1371/journal.ppat.1004647). Associate Professor Zoya Kurago, DDS, PhD Page 14Cancer immunology, Inflammation, & Tolerance Associate Professor Kebin Liu, PhD Research in the Liu Laboratory is currently devoted to studying the dynamic interactions between tumor cells and immune cells in the tumor microenvironment. One of their major areas of focus is to elucidate the molecular mechanisms underlying epigenetic regulation of tumor suppressor genes in human colon carcinoma cells. It has recently been shown that FasL of cytotoxic T lymphocytes (CTLs) is essential for host cancer immune surveillance. Fas, the physiological receptor for FasL, is often silenced in advanced human colon carcinoma cells, suggesting that colon carcinoma cells may use silencing Fas as a mechanism to evade host cancer immune surveillance. Using combined approaches of genome-wide ChIP-Seq with an epigenetic inhibitor, the Liu Laboratory determined that H3K9me3 of the FAS promoter is a dominant mechanism underlying FAS silencing, resulting in colon carcinoma immune evasion and progression (J. Immunol. 2015, 195:1868-82). In addition, they determined that GPR109A acts as a tumor suppressor in colon cancer and that the host immune system uses IFNγ to counteract DNA methylationmediated GPR109A silencing as a mechanism to suppress colon cancer development (Cancer Immunol Res. 2015, 3:795-805). The long-term goal of the Liu Laboratory is to develop molecular target-based cancer therapy to increase cancer cell sensitivity to immunotherapeutic agents, to enhance the efficacy of cancer immunotherapy