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Alison Moliterno Lab
The Alison Moliterno Lab studies the molecular pathogenesis of myeloproliferative disorders (MPDs), including polycythemia vera, essential thrombocytosis and idiopathic myelofibrosis. Our research is focused on the genetic and epigenetic lesions associated with MPDs, with the goal of improving diagnosis and treatment for these disorders.
Andrew Lane Lab
The Lane laboratory is focused on understanding molecular mechanisms underlying chronic rhinosinusitis and particularly the pathogenesis of nasal polyps. Diverse techniques in molecular biology, immunology, physiology, and engineering are utilized to study epithelial cell innate immunity, olfactory loss, the sinus microbiome, and drug delivery to the nose and sinus cavities. Ongoing work explores how epithelial cells participate in the immune response and contribute to chronic sinonasal inflammation. The lab creates and employs transgenic mouse models of chronic sinusitis to support research in this area. Collaborations are in place with the School of Public Health to explore mechanisms of anti-viral immunity in influenza and rhinovirus, and with the University of Maryland to characterize the bacterial microbiome of the nose and sinuses in health and disease.
Ashwin Balagopal Lab
Research in the Ashwin Balagopal Lab examines innate immunology and hepatic inflammation. Specifically, we explore microbial translocation Kupffer cells in HIV- hepatitis C virus (HCV) coinfection, while also developing in situ liver studies of HIV-HCV pathogenesis. Previous work has focused on antiretroviral therapy, interferon sensitivity and virologic setpoint in HIV/hepatitis C virus coinfected patients.
The Bert Vogelstein Laboratory seeks to develop new approaches to the prevention or treatment of cancers through a better understanding of the genes and pathways underlying their pathogenesis.
Our major focus is on cancers of the colon and rectum. We have shown that each colon neoplasm arises from a clonal expansion of one transformed cell. This expansion gives rise to a small benign colon tumor (called a polyp or adenoma). This clonal expansion and subsequent growth of the tumors appears to be caused by mutations in oncogenes and tumor suppressor genes, and the whole process is accelerated by defects in genes required for maintaining genetic instability. Mutations in four or five such genes are required for a malignant tumor to form, while fewer mutations suffice for benign tumorigenesis. As the mutations accumulate, the tumors become progressively more dangerous.
Current studies are aimed at the further characterization of the mechanisms through which these genes act, the ident...ification of other genes that play a role in this tumor type, and the application of this knowledge to patient management. view more
Brendan Cormack Laboratory
The Brendan Cormack Laboratory studies fungal pathogenesis, particularly the host-pathogen interaction for the yeast pathogen Candida glabrata.
We are trying to identify virulence genes (genes that evolved in response to the host environment) by screening transposon mutants of C. glabrata for mutants that are specifically altered in adherence to epithelial cells, in survival in the presence of macrophages and PMNs. We also screen mutants directly in mice for those unable to colonize or persist in the normal target organs (liver, kidney and spleen).
We also focus research on a family of genes--the EPA genes--that allow the organism to bind to host cells. Our research shows that a subset of them are able to mediate adherence to host epithelial cells. We are trying to understand the contribution of this family to virulence in C. glabrata by figuring out what the ligand specificity is of different family members, how genes are normally regulated during infection, and what mechanism...s normally act to keep the genes transcriptionally silent and how that silence is regulated. view more
The Clinical Laboratory and Biomarkers Cores will coordinate access to laboratory expertise, testing, training, specimen repositories and Good Clinical Laboratory Practices (GCLP). The goals of this core are to assure that all JHU HIV investigators have access to and utilize appropriate, validated and, where applicable, certified laboratory assays. The core will also maintain a biomarker specimen repository for storage cataloguing and utilization of biological specimens.
David Graham Lab
The David Graham Lab studies the consequences of HIV interactions with the immune system, the resulting pathogenesis and how to sabotage these interactions. We apply advanced technologies like mass spectrometry to dissect processes at the molecular level. We are also actively involved in cardiovascular research and studies the ways proteins are organized into functional units in different cell types of the heart.
Major projects in our lab are organized into three major areas: (1) H/SIV pathogenesis and neuropathogenesis, (2) Cardiovascular disease, and (3) High technology development
Molecular and Comparative Pathobiology
David Thomas Lab
The David Thomas Lab oversees clinical research projects that aim to understand the natural history and pathogenesis of hepatitis C virus infection. A special area of clinical and research focus is liver disease in HIV-infected people.
Diane Griffin Lab
Research in the Diane Griffin Lab focuses on the viral, cellular and immunologic determinants of diseases caused by alphaviruses and the measles virus. Our current studies aim to understand the immune-system mechanisms behind viral clearance and disease enhancement. Our team is also working to understand the pathogenesis of the measles virus, with a focus on developing new vaccines and learning how the virus induces immunosuppression.
Douglas Ball Lab
The Douglas Ball Lab conducts clinical trials and pre-clinical laboratory studies of thyroid cancer. Our clinical trials, performed in collaboration with research staff in the upper aero-digestive group in the Sidney Kimmel Comprehensive Cancer Center, have included protocols for advanced radioiodine-refractory differentiated thyroid cancer and medullary thyroid cancer. Our pre-clinical research, conducted with Dr. Nelkin, Dr. Agrawal and other Kimmel Cancer Center researchers, includes pathogenesis and mechanisms of treatment resistance in medullary thyroid cancer, and pathogenesis and immune-directed therapy of anaplastic thyroid cancer.
The Fuchs Laboratory uses cellular electrophysiology, immunolabeling and electron microscopy to study synaptic connections between sensory hair cells and neurons in the cochlea. One effort focuses on an unusual cholinergic receptor that mediates efferent inhibition of hair cells, driving discovery of the molecular mechanisms, and offering a target for protection against acoustic trauma. A second topic concerns the small number of unmyelinated "type II" afferent neurons whose synaptic connectivity and response properties argue for a role as the pathway for noxious (too loud) sound. Our studies are motivated by curiosity about fundamental mechanisms, and to provide a foundation for understanding cochlear pathogenesis.
Research in the Gary S. Hayward Laboratory is related to human herpesvirus. Specifically, researchers are seeking to understand how the different classes of herpes viruses take control of transcription, DNA replication, cell cycle and other nuclear processes of their host cells and how they also block or evade apoptotic and immune responses in both the lytic and latent state.
Gregg Semenza Lab
The Gregg Semenza Lab studies the molecular mechanisms of oxygen homeostasis. We have cloned and characterized hypoxia-inducible factor 1 (HIF-1), a basic helix-loop-helix transcription factor.
Current research investigates the role of HIF-1 in the pathophysiology of cancer, cerebral and myocardial ischemia, and chronic lung disease, which are the most common causes of mortality in the U.S.
Investigators in the IBD and Autoimmune Liver Diseases Laboratory conduct basic and translational research in inflammatory bowel disease (IBD) and autoimmune liver diseases. One area of focus is discovering and developing biomarkers for diagnosing and prognosticating IBD and other autoimmune liver diseases (AILDs). We also are exploring the molecular pathogenesis of—and developing novel therapies for—IBD. In addition, we are working to understand the molecular reason why many IBD patients fail to respond to mainstay drug therapies—and to develop diagnostic assays that can predict non-responders before starting them on those therapies. These biomarker studies have led to our application for four U.S. and international patents.
Our research is focused on understanding the basic mechanisms of programmed cell death in disease pathogenesis. Billions of cells die per day in the human body. Like cell division and differentiation, cell death is also critical for normal development and maintenance of healthy tissues. Apoptosis and other forms of cell death are required for trimming excess, expired and damaged cells. Therefore, many genetically programmed cell suicide pathways have evolved to promote long-term survival of species from yeast to humans. Defective cell death programs cause disease states. Insufficient cell death underlies human cancer and autoimmune disease, while excessive cell death underlies human neurological disorders and aging. Of particular interest to our group are the mechanisms by which Bcl-2 family proteins and other factors regulate programmed cell death, particularly in the nervous system, in cancer and in virus infections. Interestingly, cell death regulators also regulate many other cel...lular processes prior to a death stimulus, including neuronal activity, mitochondrial dynamics and energetics. We study these unknown mechanisms.
We have reported that many insults can trigger cells to activate a cellular death pathway (Nature, 361:739-742, 1993), that several viruses encode proteins to block attempted cell suicide (Proc. Natl. Acad. Sci. 94: 690-694, 1997), that cellular anti-death genes can alter the pathogenesis of virus infections (Nature Med. 5:832-835, 1999) and of genetic diseases (PNAS. 97:13312-7, 2000) reflective of many human disorders. We have shown that anti-apoptotic Bcl-2 family proteins can be converted into killer molecules (Science 278:1966-8, 1997), that Bcl-2 family proteins interact with regulators of caspases and regulators of cell cycle check point activation (Molecular Cell 6:31-40, 2000). In addition, Bcl-2 family proteins have normal physiological roles in regulating mitochondrial fission/fusion and mitochondrial energetics to facilitate neuronal activity in healthy brains. view less
James Hamilton Lab
The main research interests of the James Hamilton Lab are the molecular pathogenesis of hepatocellular carcinoma and the development of molecular markers to help diagnose and manage cancer of the liver. In addition, we are investigating biomarkers for early diagnosis, prognosis and response to various treatment modalities. Results of this study will provide a molecular classification of HCC and allow us to identify targets for chemoprevention and treatment. Specifically, we extract genomic DNA and total RNA from liver tissues and use this genetic material for methylation-specific PCR (MSP), cDNA microarray, microRNA microarray and genomic DNA methylation array experiments.
Jean Kim Lab
The Jean Kim Laboratory performs translational research in the
area of chronic rhinosinusitis, with a niche interest in the pathogenesis of hyperplastic nasal
polyposis. Studies encompass clinical research to basic wet laboratory research in
studying the underlying immune and autoimmune mediated mechanism of polyp growth and
perpetuation of disease. Human cell and tissue culture models are used. Techniques in the
laboratory include cell and tissue culture, real time PCR, immunoblot, ELISA, flow cytometry,
immunohistochemistry, electron microscopy, gene array analysis, and other molecular
approaches including genetic knockdowns. Approaches used in Dr. Kim’s clinical study
designs include prospective and retrospective analysis of patient outcomes and clinical
biomarkers, as wells controlled clinical trials.
Jerry Spivak Lab
Research in the Jerry Spivak Lab focuses on chronic myeloproliferative disorders, particularly their molecular mechanisms and methods for distinguishing them diagnostically and interventionally. By analyzing gene expression in polycythemia vera stem cells, we have learned that patients with polycythemia vera can be differentiated from those with erythrocytosis and can be diagnosed as having either aggressive or slow-growing disease. We are also studying the roles played by specific molecular markers in the pathogenesis and diagnosis of polycythemia vera.
Joel Blankson Lab
Work in the Joel Blankson Lab explores the mechanism of control of HIV-1 replication in a cohort of patients known as elite controllers or elite suppressors. These patients are HIV-1 seropositive but maintain levels of viremia that are below the limit of detection of standard clinical assays. We feel that elite suppressors represent a potential model for a therapeutic HIV vaccine. Our central hypothesis is that many of these patients are infected with fully replication-competent HIV-1 isolates that are held in check by the immune system. To test this hypothesis, we are studying many different host and viral factors in these patients.