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Biomedical Research Apprenticeship Program (BioMed RAP)
Program DescriptionOverviewThe Biomedical Research Apprenticeship Program (BioMed RAP) is a 10-week summer research program for students from groups traditionally under represented in graduate education who are interested in careers in biomedical research. The program traditionally runs from late May until early August. The program is designed to provide participants with an in-depth research experience to prepare them for Ph.D. and M.D./Ph.D. programs in the biomedical sciences. Participants work on independent research projects with faculty skilled in mentoring young scientists. The program exposes students to cutting-edge science and technology and features journal clubs, seminars, individualized career counseling, workshops on applying to Ph.D. and M.D. programs, and social activities. The program concludes with a dinner symposium featuring research presentations by program participants. EligibilityWashington University is committed to training a biomedical research work force which mirrors the diversity of our nation. To this end, the Biomedical Research Apprenticeship Program focuses on providing research opportunities to individuals from groups traditionally underrepresented in the biomedical sciences. BiomedRAP encourages applications from individuals from under represented populations to include but not be limited to ethnic minorities and first generation college students. Unfortunately, students who have already earned a baccalaureate degree AND students who will earn a baccalaureate degree in Spring before the program dates are NOT eligible to apply for this program. Stipend and HousingParticipants will receive a stipend of $3,000 for 10 weeks of residence in the program. Housing will be provided at no charge in university dormitories. Participant travel to and from St. Louis will be covered, and travel and housing funds will be available to offset the cost of travel for the participant's guests at the symposium held at the end of the summer. Research OpportunitiesSelected Participating Labs from 2004 BioMed RAPDr. Herbert Virgin Lab: We study issues at the interface between virology and immunology, working from the hypothesis that viruses manipulate the immune response using immunoevasive gene products as the immune response attempts to eradicate the virus. The resulting delicate balance determines the fate of both virus and host. Analysis of these issues is key to understanding chronic diseases caused by viruses. The diseases that we study include lymphoma induced by γ-herpesviruses, vascular disease including atherosclerosis induced by herpesviruses, and enteric disease induced by noroviruses. Lastly, we are searching for novel human pathogens using molecular and classical methods. Two concepts drive our approach: (1) the simultaneous analysis of immune and viral mechanisms allows novel insights; and (2) genetic tests in vivo are necessary to establish mechanisms. The experimental models used in the lab are infection of mice with the herpesviruses murine cytomegalovirus (MCMV), herpes simplex virus (HSV), and murine gammaherpesvirus 68 (γHV68). In addition, we have found a novel Norwalk-like virus (norovirus, named MNV-1) in mice that is under intensive study. HSV, MCMV, and γHV68 establish latency despite active immunity, contributing to their capacity to cause chronic diseases. MCMV causes vasculitis and atherosclerosis. γHV68 induces lymphoma, vasculitis, and atherosclerosis. MNV-1 causes pneumonia and gastoenteritis. Infection of mice with these viruses provids manipulable models for studying the role of viral and host genes in important disease processes. Current projects include: (1) the cellular and molecular basis of herpesvirus latency; (2) the role of interferon-γ (IFNγ), TNF, perforin, granzymes, B cells, antibody, and T cells in herpesvirus latency; (3) vaccination against latency; (4) molecular mechanisms of IFNγ anti-viral action; (5) herpesvirus tumor induction; (6) herpesvirus-induced vascular disease and atherosclerosis; (7) herpesvirus immune evasion proteins that block antigen presentation and IFN signaling; (8) herpesvirus regulators of apoptosis including the γHV68 v-bcl-2; and (9) norovirus immunology, structure, and pathogenesis; and (10) pathogen discovery. Dr. Mark Watson Lab: Our laboratory is interested in characterizing sets of human genes whose expression pattern may be used to design new diagnostic tests and treatment strategies for solid tumors. We are using high-density oligonucleotide arrays (GeneChips) to perform gene expression profiling on biopsy specimens from patients with breast, pancreatic, prostate, lung, and other carcinomas. Patterns of gene expression are correlated with traditional histopathology data and clinical outcomes to identify diagnostic signatures. In a related project, we are using Laser Capture Microdissection and transcript amplification to examine gene expression profiles in subsets of tumor cells (e.g. carcinoma in situ versus invasive cancer) within a single, histologically complex tumor specimen. The goal of this work is to elucidate the transcriptional regulatory networks involved in the malignant progression of epithelial tumors such as breast and prostate cancer. A second research interest involves further characterization of a family of genes located on chromosome 11q13 and associated with human breast cancer. Mammaglobin and mammaglobin B, two novel genes isolated in our laboratory, as well as lipophilin A, lipophilin B, and CC10 all encode small, secreted epithelial proteins that may form combinatorial heteromers. Mammaglobin gene expression is restricted to the human mammary epithelium. More significantly, mammaglobin is expressed at elevated levels in almost 80 percent of human breast tumors. Understanding the function of mammaglobin and these other homologous proteins as well as the mechanisms controlling their tissue-specific expression will provide new insights into breast development and tumorigenesis. Furthermore, if over-expression of mammaglobin is contributory to breast cancer progression, results from these studies may identify therapeutic targets for modulating aberrant mammaglobin gene expression or protein function. Dr. Douglas Berg Lab: The major focus of my research changed recently to Helicobacter pylori, after years of study of the molecular genetics of Escherichia coli, and especially of the Tn5 transposon. H. pylori is interesting and important because it establishes long term chronic infections in the human stomach, a site where few other microbes grow. Such colonization is a principal cause of gastritis and peptic ulcers and a major risk factor for gastric cancer, although most infections are asymptomatic. We wish to learn how H. pylori establishes and maintains multiyear chronic infections and causes disease. To facilitate molecular genetic analysis, we constructed an ordered cosmid clone library and map of the H. pylori genome. Others had shown that some but not all H. pylori strains produce a novel vacuolating cytotoxin. By hybridization analysis using our cosmids, we discovered a 21 kb DNA segment that is generally present in toxigenic strains and absent from nontoxigenic strains. We are characterizing this segment in detail, in the expectation that functions it encodes may affect host interactions during H. pylori infection - e.g., mucosal immune response, or extents of tissue damage or cell proliferation. In complementary studies, we developed sensitive, efficient PCR-based DNA fingerprinting methods for H. pylori, and found that these methods could easily distinguish most independent clinical isolates from one another. We are using them to detect individuals colonized by multiple strains, to detect and characterize cases of interstrain gene transfer, and to better understand how an H. pylori strain evolves and adapts during long term carriage. In related research, we are studying a potent vacuolating cytotoxin produced by certain strains of Vibrio cholera. We are interested in how this novel toxin causes vacuolation, its possible contribution to colonization or disease, and its evolutionary relationship to the cytotoxin of virulent strains of H. pylori. Principle Investigators (PI)
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Last Reviewed: December 10, 2008 |
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