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Stacey Mont

Undergraduate Major: Molecular Biology

McNair Mentor:
Dr. Kiminobu Sugaya,
Ph.D. (Burnett School of Biomedical Sciences, College of Medicine)

Graduate Program: Currently a graduate student in the Vanderbilt IMSD Program.

Stacey Mont

Stacey Mont was born in Tampa, Fl. She is the daughter of Cuban immigrants. Her research interests include cancer biology and developmental cell biology. In addition to research with Dr. Sugaya at UCF, starting in 2007, she conducted summer research at two additional institutions. During the summer of 2007, she participated in the Research in Science and Engineering Program (RISE) and the IGERT Summer Undergraduate Research Frontiers (ISURF) program at Rutgers University. During the summer of 2008, she was awarded the American Cancer Society Summer Research Fellowship to perform cancer research at the University of Florida College of Medicine. She is interested in translational research in biomedical sciences and is currently a graduate student in the Vanderbilt IMSD Program. The following are abstracts of research Stacey completed as an undergraduate at UCF:

Title: Method of Promoting Apoptosis of Glioblastoma Tumor Cells

Conducted at the University of Central Florida as part of the Ronald E. McNair Scholars Program, January 2007 – August 2008. (Patent filed as co-inventor on September 23, 2008 )

Mentors: Kiminobu Sugaya, Ph.D. (Burnett School of Biomedical Sciences, College of Medicine); Angel Alvarez, Ph.D. graduate student (Burnett School of Biomedical Sciences, College of Medicine).

Abstract: This research design began with the conception of trying to see how human neural stem cells (hNSCs) can be used as a method of treatment for glioblastoma (GBM) patients. Ideas of this research began in spring 2007 combining published research on GBM in several animal models and imaging data in order to propose a novel treatment method for the apoptosis of GBM tumor cells while allowing endogenous hNSCs to repair brain tissue lost in the resection of the tumor. This research is collaboratively supported by the Florida Hospital, in Orlando, FL.

Title: Tracking Biointerfacial Cellular/Molecular Cues for Cancerous Progression of Stem Cells

Conducted at the UMDNJ-Robert Wood Johnson Medical School, as part of the Research in Science and Engineering (RISE) summer program, as well as the NSF-IGERT Summer Undergraduate Research Frontiers (ISURF) program during the Summer of 2007.

Mentors: Prabhas Moghe Ph.D, P.I (Department of Biomedical Engineering); Hak-Joon Sung Ph.D., Co-P.I (New Jersey Center for Biomaterials); Er Liu, Ph.D. Graduate Student (Department of Biomedical Engineering).

Abstract: The cancer stem cell theory hypothesizes that the origin of cancer and tumorgenesis may be due to a sub-population of adult stem cells. Adult stem cells do not divide as rapidly as cancer cells and thus are not affected by chemotherapy targeted to rapidly proliferating cells. A group of precursor cells remain within every population of adult stem cells. We hypothesize that such precursor cells may progressively convert into sarcoma lineage under certain molecular or biomaterials-related microenvironments. The hypothesis was tested by monitoring the progression into osteosarcoma of human Mesenchymal Stem Cells (hMSCs) and of their osteogenic precursors (OPs). The change in expression of specific protein markers and their morphological variance were examined in three distinct configurations of co-cultures designed to modulate the differentiating capacity of the hMSCs and OPs into osteosarcoma. The culturing techniques used were: Transwell systems (disallowing direct contact but enabling paracrine signaling), randomly cocultured cells allowing direct cell-to-cell contact using hMSCs or OPs with SAOS-2–GFP cells, and conditioning by culturing hMSCs or OPs with conditional SAOS-2 media. Preliminary results indicate that Topoisomerase II and NumA appears to be good selective markers for osteosarcoma progression as well as a morphological effect was observed in hMSCs/OPs when co-cultured with SAOS-2 cells. Future studies will determine if hMSCs/OPs express more Topoisomerase II and NumA in culture as well as quantifying morphometric descriptors of cytoskeletal organization. The results from this current research may yield a greater understanding of how osteosarcoma develops which may guide more molecularly targeted cancer therapies.

Title: Therapeutic Targeting of a Novel Protein-Protein Ineteraction Between the TRIP-Br1 and HPV E6 oncoproteins—Towards Developing Small Molecule Inhibitors for the Specific Treatment of Human Papilomavirus-Associated Diseases

Conducted at the University of Florida College of Medicine as part of the American Cancer Society Summer Research Fellowship in the Summer of 2008.

Mentors: Stephen I-Hong Hsu M.D, Ph.D., P.I (Division of Nephrology, Hypertension and Renal Transplantation, College of Medicine); Zhi Jiang Zang, Ph.D., Post-Doctorate (Division of Nephrology, Hypertension and Renal Transplantation, College of Medicine); Liyun Lai, Ph.D., Post-Doctorate (Division of Nephrology, Hypertension and Renal Transplantation, College of Medicine); Christopher Allen Fuhrman, Ph.D. Gradate Student (Division of Nephrology, Hypertension and Renal Transplantation, College of Medicine).

Abstract: Cervical cancer caused by genital human papillomavirus (HPV) type 16 accounts for the second most prevalent type of cancer in women worldwide. Recent studies estimate that a total of 11,150 women were diagnosed with cervical cancer in the United States within the past year accounting for 3,670 deaths. Despite the current availability of a novel vaccine targeted against HPV that is protective for the development of cervical cancer, there is no specific therapy for established HPV-associated cervical cancer. Yeast two-hybrid screens were recently reported with HPV6 and HPV11 E6 proteins that identified TRIP-Br1 as a novel direct protein-protein interaction partner. Our finding that TRIP-Br1 is a novel cellular target of the E6 oncoprotein from both “low risk” and “high risk” HPV types is also the first to demonstrate that the recruitment by protein-protein interaction of E6 to a transcription complex on DNA through interaction with TRIP-Br1, leads to functional co-activation of the TRIP-Br1/E2F1/DP1 complex on E2F-responsive genes, as a possible mechanism for its transforming properties. These findings suggest that the TRIP-Br1/E6 protein-protein interaction may serve as a potential “transcription-based” therapeutic target and that disruption of this interaction by small molecule inhibitors may be the basis for the development of the first class of drugs specifically targeted for the treatment of HPV-associated diseases such as genital warts and cervical cancer. Coupled with future efforts at fine-resolution mapping by site-directed mutagenesis, the HPV16 E6 deletion constructs generated in this preliminary study will be crucial for the process of identifying the key residues on E6 involved in direct protein-protein interaction with TRIP-Br1. Studies are already underway to map the TRIP-Br1 binding site(s) on E6 using in vitro binding assays and by co-immunoprecipitation of co-expressed HPV E6 and human TRIP-Br1 proteins in cultured human cancer cell lines. In parallel, we will explore the half-solved structure of E6 for possible small molecule inhibitors. This approach will allow us to move towards the development of novel lead compounds for the treatment of solid tumors and lymphoproliferative disorders, as well as HPV-associated diseases across the spectrum from warts to cervical cancer.