Undergraduate Research Opportunities in Biomedical Sciences

De Jesus Lab

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The focus of the De Jesus laboratory is to understand the early events of how antigens (micro and nanoparticle delivery vehicles) and microbes (fungi such as Candida albicans and Candida tropicalis) are sampled by the intestinal mucosa. We are particularly interested in the how immune system cells within intestinal Peyer’s patches (PPs) capture, process and yield a specific immune response to these antigens and microbes. We have recently identified a specific dendritic cell (DCs) subset called Langerin+ DCs within Peyer’s patches that can capture a variety of micro and nanoparticles, fungi, algae and peanut antigens. Our aim is to understand why these DCs can sample such a variety of antigens and microbes and how do these contribute to intestinal immunity.

Derbyshire Lab

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Conjugation in mycobacteria. Mycobacterium tuberculosis accounts for more deaths worldwide than any other infectious agent. The development of new treatments for mycobacteria requires an understanding of the biology of these bacteria and the ability to manipulate their genomes to determine the genetic basis of pathogenesis and drug resistance. We are studying the process of DNA transfer by conjugation in the non-pathogenic species Mycobacterium smegmatis. In particular, we wish to identify the genes and DNA sequences required for DNA transfer and its regulation, as our current studies have shown that DNA transfer occurs by a novel mechanism. This research project will involve characterization of DNA transfer between strains of M. smegmatis and will involve a variety of molecular techniques including, transformation, electroporation, conjugation, cloning, DNA sequence analysis and transposon mutagenesis of mycobacteria and general bacterial genetics in E. coli.

Herschkowitz Lab

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The research in my laboratory involves integrative approaches, utilizing multidisciplinary techniques including methods in molecular biology, cell biology, mouse models, histology, microscopy, flow cytometry, genomics, bioinformatics and systems biology to elucidate the molecular mechanisms involved in breast cancer progression and therapeutic resistance. Evidence from our laboratory and others has shown that there exist cells within tumors that have an intrinsic resistance to radiation and chemotherapeutics compared to the bulk of the tumor. These cells, often referred to as cancer stem cells (CSCs) or tumor initiating cells may also be responsible for metastatic dissemination and tumor dormancy and recurrence. Breast CSCs can have an epithelial to mesenchymal transition (EMT) phenotype and inducing EMT in human mammary epithelial cells can confer on them the properties of stem cells. In addition, we identified an aggressive molecular subtype of breast cancer that is enriched for CSCs. In recent years it has been appreciated that along with protein coding genes, much of our genome encodes tens of thousands of functional RNAs that do not make proteins. This includes small RNAs called microRNAs which have been very well studied as well as a large class of long noncoding RNAs (lncRNAs) the functions of which still very much need to be explored. We hypothesize that lncRNAs play a critical role in an EMT gene expression program governed in part by RNA-mediated epigenetic regulation leading to resistance to conventional therapies in breast cancer. Our goal, using several model systems, is to first identify and then investigate the mechanisms of action of lncRNAs that regulate the EMT/CSC phenotype of claudin-low breast tumors using siRNA or antisense knockdown, CRISPR genome engineering, and lentiviral overexpression in cell culture and in animal models.

Kuznetsov Laboratory

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Due to the recent technological advances in genomic data acquisition, bioinformatics has become a crucial element of genomics. The main task of bioinformatics is to develop computational tools capable of dealing with diverse types of genomic data, filtering out noise, and finding reliable patterns associated with biological properties of interest. Our laboratory is developing bioinformatics methods, stand-alone and web-based software for the analysis of various types of genomic data and applying these methods to genome research. We do this by utilizing a variety of methods from statistics, information theory, classification/pattern recognition, and data mining.

Lee Lab

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The laboratory engages in basic research designed to better understand and modulate immunological memory or general host defense. The two main projects we study are 1) the CD4 T lymphocyte which directs both cellular and humoral (antibody-mediated) immune responses. Stimulation of CD4 T cells and promoting their differentiation is a key element that underlies vaccination. 2) Bat immunity. Bats are currently the subject of intense interest due to their decimation by the disease White Nose Syndrome. Projects employ animal models and tissue culture, cellular immunology, flow cytometry, and immunochemical techniques to study immune cell development, activation, regulation, and function.

Li Laboratory

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We study the molecular structure, function, and mechanism of proteins or complexes related to bacterial or viral infection and host response, using crystallography, biochemistry, and molecular biology. Current projects include bacterial and viral superantigens, signaling proteins involved in apoptosis and stem cell regulation, and rational drug design against key viral enzymes.

McDonough Laboratory

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The focus of Dr. McDonough's laboratory is gene regulation in the context of bacterial pathogenesis, or the means by which bacteria cause disease. The team is primarily interested in two well-known pathogens: Mycobacterium tuberculosis, the bacterium that causes TB, and Yersinia pestis, the etiologic agent of bubonic and pneumonic plague. The lab uses a variety of techniques in their studies with both pathogens, ranging from molecular genetics and biochemistry to bioinformatics, proteomics and fluorescence microscopy.

Moslehi Laboratory

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Dr. Moslehi is a genetic epidemiologist with expertise in designing family-based and population-based genetic epidemiologic investigations and in statistical analysis of genetic and epidemiologic data. The overall objectives of most of Dr. Moslehi's studies are to identify genetic factors involved in the etiology of human disorders and to quantify the effects of genetic and environmental factors on disease risk. Various malignant and pre-malignant conditions have been the focus of most of her research activities; however, Dr. Moslehi's research projects have also involved other complex disorders besides cancer. Dr. Moslehi has been studying cancer risks associated with DNA repair gene mutations for a number of years. In the past few years, she has also initiated several studies into the role of DNA repair and transcription genes in human reproduction and fetal development.

Parasitology Laboratory

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The parasite Trypanosoma brucei is a blood-borne pathogen that causes both human and zoonotic disease. T. brucei and related trypanosomatids are early eukaryotes and successful pathogens. Currently no preventative therapies are available and treatment is difficult, despite our knowledge of several unique biological processes with the potential to be exploited as drug targets. One such unusual process is RNA editing. RNA editing is found in many organisms including plants, yeast, humans and other mammals, although the mechanisms of editing are distinct. Within the trypanosomatids RNA editing is achieved by the insertion of non-encoded uridines or the deletion of encoded uridines. In the most extreme cases over 50% of the mature mRNA is the result of post-transcriptional editing. Editing takes place exclusively in the mitochondria, where it is required in order to generate mature mRNAs competent for translation into the correct proteins, and is carried out by a large ribonucleoprotein complex. Our work focuses on the biochemistry of editing by this multiprotein complex. We have identified a protein, RNA-Editing Associated Protein-1 (REAP-1), which specifically recognizes RNAs requiring editing. Evidence suggests that REAP-1 acts as a recruitment factor to deliver RNAs to the editing complex. REAP-1 is one of only two proteins that have been identified as components not of the core catalytic complex but of a larger (35-40S) complex believed to function in vivo. Through a combination of genetic and biochemical approaches, current work in the lab involves understanding how REAP-1 specifically recognizes and binds to its RNA targets, identifying other proteins with which REAP-1 interacts and determining how REAP-1 influences editing complex assembly and regulation of RNA editing.

Pata Laboratory

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DNA replication is a fundamentally important process in all cells. Mistakes during replication cause mutations as well as large scale genome rearrangements, which can ultimately cause antibiotic resistance in bacteria as well as aging, cancer and resistance to chemotherapy in humans. Over the past decade, the number of known polymerases responsible for genome duplication has expanded dramatically, yet our understanding of how all these enzymes contribute to genome stability is far from complete.

Reliene Laboratory

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The focus of the lab is on translational cancer research on gene-environment and gene-nutrient interactions. We investigate whether mutations in DNA repair genes enhance susceptible to cancer associated with environmental causes and whether the risk of cancer can be reduced with intake of dietary antioxidants. For example, we are currently exploring the concept that antioxidant-rich pomegranate extract protects against breast cancer. Other projects include studies on genotoxic and cancer risks of engineered nanoparticles used in consumer products. We use genomic technologies in combination with cell and molecular biology and whole animal approaches to dissect the complexity of cancer.

Tenniswood Lab

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Inflammatory breast cancer (IBC) is the most aggressive and lethal form of breast cancer. Despite its lethality, very little research is focused on understanding the origins of inflammatory breast cancer or development of targeted treatments. Recent studies by our laboratory using cell lines derived from IBC, have identified a non-toxic drug, CG-1521, that is capable of inducing dramatic tumor cell death in cell culture and in animal models of IBC. Microarray analyses of the changes in the expression of microRNAs and mRNAs indicate that CG-1521 targets numerous pathways including: cell cycle progression and cell-to-cell adhesion. Strikingly, the molecules pertinent to the spindle assembly checkpoint are significantly altered, suggesting that CG-1521 disrupts the formation of the mitotic spindle and induces mitotic catastrophe. The next step in the research, which will involve undergraduate students, is to validate the changes in mRNA and microRNA expression using Real-Time PCR and Western analysis. In addition we will use immuno-histochemistry of proteins implicated in spindle checkpoint arrest and mitotic catastrophe, both in cell culture and in tissue sections from orthotopic tumors grown in nude mice.

The Agrawal Laboratory

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The Agrawal laboratory is engaged in studies of the protein-synthesizing machine, the ribosome, which interacts with messenger RNA (mRNA), transfer RNAs, and a number of protein factors, to facilitate translation of the genetic information encoded by the mRNA into the amino-acid sequence of a protein. In particular, his research explores (i) the structure and function of organellar ribosomes, and (ii) the structural dynamics of ligands that interact with the ribosome during protein synthesis.

The Arbovirus Laboratory

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The research program of the Arbovirus Laboratories focuses on basic and applied field and laboratory studies examining the interaction of mosquito and tick-borne arboviruses, arthropod vectors, and vertebrate hosts, and how this interaction impacts transmission intensity and perpetuation of the pathogen.

The Conklin Laboratory

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Research interests: Functional genomics of cellular proliferation regulation, mammalian cell genetics.

The Curcio Laboratory

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There is no cure for diseases caused by retroviruses such as HIV-1, the infectious agent that has given rise to the human AIDS pandemic. Antiretroviral therapies can slow the progression of HIV/AIDS, but their usefulness is limited by their toxicity to human cells. The goal of our research is to identify highly specific targets for antiretroviral therapies by identifying replication mechanisms that are conserved among retroviruses and related endogenous retrotransposons but unnecessary for host cell replication or survival.

Wade Laboratory

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Our laboratory studies how bacteria regulate their gene expression. We are particularly interested in transcriptional regulation in the non-pathogenic model organism Escherichia coli, and in pathogenic strains of Salmonella and Yersinia. We also study regulation of mRNA stability and of translation by non-coding RNAs.

Welsh Lab

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Our lab studies nutrition, nuclear receptors, genomics and cancer in relation to several types of cancers, including breast, prostate, skin and colon. Our specific focus is to identify molecular mechanisms by which dietary-derived nuclear receptor ligands reduce the risk of cancer development and progression. Students will contribute to NIH funded research on nuclear receptor signaling and cancer. Projects may include defining the mechanisms by which vitamin D and other nutrients reduce the risk of breast cancer, studying how different cells interact in complex tissues to alter cancer development, analysis of normal and tumor tissue by histochemical methods, or characterization of stem cell differentiation in vitro. Students will work alongside graduate students and/or post-doctoral fellows and may utilize cellular, molecular or whole-animal models as experimental approaches.