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THE LAB TEAM EXPERIENCE<\/strong><\/p>\n

The lab experience should be a positive one. As a member of my\u00a0lab each student should achieve mastery\u00a0of new biological lab techniques, an intellectual understanding of research questions and literature, and a feeling of\u00a0collaboration and camaraderie through active learning.\u00a0The lab team experience\u00a0promotes success of both the students and the projects. Graduate and undergraduate students in my lab are expected to participate in\u00a0research\u00a0projects as part of a team. No student\u00a0is singularly responsible for her\/his own\u00a0personal project. Students help each other get experiments finished, troubleshoot problems, and analyze results for posters and publications.\u00a0New students get to learn from the more senior students; senior students in turn test their understanding of concepts and protocols\u00a0by teaching\u00a0the new.\u00a0\u00a0Publications include all members of the team further promoting\u00a0collaboration as well as a sense of accomplishment by everyone. Students are expected to\u00a0participate in weekly lab research progress meetings, journal clubs, and joint meetings with other University lab collaborators.<\/p>\n

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\"UNCClabwithsmile\"<\/a>\"sky\"<\/a><\/p>\n

RESEARCH INTERESTS AND CURRENT LAB PROJECTS<\/strong><\/p>\n

DNA repair and genome stability in mitotic cells using mouse models\u00a0<\/strong><\/em><\/p>\n

Although the role of homologous recombination (HR) to repair DNA damage is well appreciated in meiosis of prokaryotes, yeast, and metazoans. However the role of interchromosomal HR (between TWO different chromosomes) to occur in vivo<\/em> in many different types of\u00a0cells of mammals is only minimally understood. It is important\u00a0to understand when interchromosomal HR can occur because it has the potential maintain\u00a0genome stability, and also drive genetic diversity and evolution, or even genome rearrangements leading to cancer.<\/p>\n

Our laboratory established unique mouse models using green fluorescent protein reporters (GFP) to determine the potential of DNA damage to promote HR\u00a0in vivo<\/em>. These models were the first to demonstrate that interchromosomal HR occurs in vivo<\/em> in multiple organ systems, and provide an ideal platform to further elucidate which cells at specific developmental stages of development or differentiation may be most likely to undergo this type of DSB repair. Our\u00a0research\u00a0will lead to an understanding of the fundamental mechanisms of DSB rejoining at the chromosomal level, and also provide insight on genome stability and genetic evolution.<\/p>\n

DNA damage-induced chromosomal rearrangements in leukemia<\/em><\/strong><\/p>\n

The long-term objective of this research\u00a0is to understand the mechanisms used by hematopoietic (blood) cells to repair of one type of DNA damage — the double-strand break (DSB)– and the initial molecular events that lead to genomic rearrangements such as translocations, which are a hallmark of leukemias. DNA damaging agents are common therapy in the treatment of human cancers, but they also produce chromosomal rearrangements and oncogenic transformation and tumor formation. Recent data from my lab indicates that chromosomal rearrangements analogous to those observed in hematopoietic malignancies are readily formed during DSB repair in both human and mouse hematopoietic stem cell-enriched populations. My lab uses multiple genetic approaches in cultured cell lines and genetically engineered mice to identify the initial events that promote the formation of DNA damage-induced chromosomal rearrangements, and the cooperative mutations or predisposing factors that can promote (or suppress) transformation of cells that acquire them.<\/p>\n

There is a growing list of compounds in our daily life that promote or stabilize chromosomal DSBs and may lead to these chromosomal rearrangements<\/em>. These include dietary supplements and environmental toxins including estrogens used as hormone supplements, bioflavonoids such as genistein and quercetin found in foods, soy products energy drinks and dietary supplements, quinones or benzenes found in paints and flame retardants used in homes and\u00a0furniture.\u00a0Our research will provide an understanding of which of these can produce genome changes that may lead to leukemia and also determine if exposure in utero through maternal exposure may promote infant leukemia. tWe hope this research\u00a0may lead to new approaches to prevention or therapy.<\/p>\n

Biomarkers of Ovarian Cancer\u00a0<\/strong><\/em><\/p>\n

Epithelial ovarian cancer (EOC) is responsible for an estimated 21,800 new cases and 14,000 deaths each year. Overall, patients have a five-year survival rate of 30%-40%. The primary option of treatment is often invasive surgery and adjuvant chemotherapy with cisplatin and taxane (Paclitaxel) that lead to multiple systemic side effects and toxicity, limiting the doses physicians can use. Up to 80% of patients will eventually relapse and become platinum-taxane resistant.<\/p>\n

The overall goals of this\u00a0research are to (1) use genetic, genomic, and proteomic approaches to understand how altered proteins promote ovarian cancer\u00a0and may act as biomarkers of susceptibility and disease, and (2) use knowledge about tumor specific characteristics or biomarkers to develop new targeted therapies.\u00a0Our research used both bioinformatic approaches and proteomic approaches to\u00a0identify\u00a0significant loss of HOXC6 in epithelial ovarian cancer in both the tumor itself and in the serum of patients with this cancer type.<\/p>\n

Archived Research : Targeted Nanoparticle-Aptamer Therapy of Ovarian Cancer<\/em><\/strong><\/p>\n

Epithelial ovarian cancer (EOC) is responsible for an estimated 21,800 new cases and 14,000 deaths each year. Overall, patients have a five-year survival rate of 30%-40%. The primary option of treatment is often invasive surgery and adjuvant chemotherapy with cisplatin and taxane (Paclitaxel) that lead to multiple systemic side effects and toxicity, limiting the doses physicians can use. Up to 80% of patients will eventually relapse and become platinum-taxane resistant.<\/p>\n

We identified single-stranded DNA aptamers a Cell-SELEX screen that we hypothesize will selectively associate with and internalize into ovarian cancer\u00a0cells but not other cells both in cultured cell lines and in a xenograft mouse model. Conjugation of the aptamers to polymer nanoparticles loaded with paclitaxel will be assessed for potential to promote in vivo<\/em> targeting of platinum-based chemotherapeutics directly to tumor cells. In addition to potential translational outcomes, our studies will increase our understanding of the basic biologic characteristics of individual epithelial ovarian tumor cell membranes, aptamer association and internalization, and cellular response to aptamers and nanoparticles. This research\u00a0will provide a significant new effective therapeutic approach to epithelial ovarian cancer treatment.<\/p>\n

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BRIDGES SCHOLARS<\/strong><\/a><\/p>\n

I am director of the Bridges Scholars Program<\/strong><\/em> that supports undergraduate students who transfer from Gaston College or Rowan Cabarrus CC. Students participate in professional development and networking programs and events. Students get paired with a research lab and mentor and have a paid summer internship to perform independent research.<\/p>\n

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Professional Experience<\/strong><\/p>\n