Faculty Database:
[ Phd Program: Pathobiology & Translational Science ]

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NameEmailPhd ProgramResearch InterestsPublications
Bahnson, Edward Moreira email , , , , , , publications

We are interested in studying diabetic vasculopathies. Patients with type 2 diabetes mellitus or metabolic syndrome have aggressive forms of vascular disease, possessing a greater likelihood of end-organ ischemia, as well as increased morbidity and mortality following vascular interventions. Our long term research aims to change the way we treat arterial disease in diabetes by:

  • Understanding why arterial disease is more aggressive in diabetic patients, with a focus in redox signaling in the vasculature.
  • Developing targeted systems using nanotechnology to locally deliver therapeutics to the diseased arteries.
Bellinger, Dwight A. email , publications

Research interests include atherosclerosis, thrombosis and von Willebrand’s disease. The role of von Willebrand factor in arterial thrombosis is being studied in atherosclerotic vessels to gain a better understanding of thrombosis and its possible prevention in people with coronary artery disease. Comparative pathology and the use of animal models in research are also the focus of some research efforts.

Church, Frank C. email , , , , , , publications

Our research is concerned with proteases and their inhibitors in various disease processes (thrombosis and cancer); our science tools are structure-activity, cell biology and signaling, pathobiology, immunohistochemistry, and in vivo models.

Coleman, William B. email , , , , , publications

The research in our laboratory involves several major projects related to the molecular pathogenesis of human cancer and investigations related to the biology of liver stem-like progenitor cells, including (i) characterization of human liver tumor suppressor genes, (ii) analysis of genetic determinants of breast cancer, (iii) investigation of mechanisms governing aberrant DNA methylation in breast cancer, (iv) liver progenitor cell responses after toxic liver injury, and (v) transplantation of liver stem-like progenitor cells for correction of genetic liver disease.

Doerschuk, Claire M email , , , , publications

We study host defense mechanisms in the lungs, particularly the inflammatory and innate immune processes important in the pathogenesis and course of bacterial pneumonia, acute lung injury/acute respiratory distress syndrome, and cigarette smoke-associated lung disease. Basic and translational studies address mechanisms of host defense, including recruitment and function of leukocytes, vascular permeability leading to edema, bacterial clearance and resolution.  Cell signaling pathways initiated by binding of leukocyte-endothelial cell adhesion molecules and molecular mechanisms underlying the functions of neutrophils are two particular areas.

Falk, Ronald J. email , , , publications

As the Director of the UNC Kidney Center, the scope of Dr. Falk’s research interests spans many disciplines, including molecular biology, immunology, genetics, pathology, cell biology, protein chemistry, epidemiology, pharmacokinetics and biostatistics. Dr. Falk is recognized world wide as a leader in research on kidney diseases related to autoimmune responses. He works closely with the basic research scientists within the UNC Kidney Center, including Dr. Gloria Preston, thus this research program provides an environment for Translational Research within the UNC Kidney Center.

Gulati, Ajay email , , , , publications

The work of our laboratory is focused on understanding interactions between the commensal microbiota of the gut and the host epithelium, particularly in the context of chronic inflammatory conditions such as inflammatory bowel diseases (IBD).  Specifically, we are interested in determining the mechanisms by which various susceptibility genes for IBD affect the structure and function of the intestinal microbiota.  In particular, we are exploring the mechanisms by which IBD risk alleles alter the function of intestinal epithelial cells including Paneth, goblet, and stem cells. We expect these studies will lead to the development of safer, patient-specific therapies for individuals with IBD.

Homeister, Jonathon W. email , , , , publications

Our research focuses on understanding the molecular and cellular mechanisms of leukocyte (white blood cell) trafficking and homing in vascular inflammation and immune responses. We are interested in the glycobiology of the Selectin leukocyte adhesion molecules and their ligands, and understanding the roles for these glycoproteins in the pathogenesis of inflammatory/immune cardiovascular diseases such as atherosclerosis and vasculitis. We are also interested in the mechanisms whereby the selectins and their ligands link the inflammatory response and coagulation cascade and thereby modulate thrombosis and hemostasis.

Jennette, Charles J. email , , publications

My research interests and diagnostic responsibilities center around nephropathology and immunopathology. My laboratory carries out basic, translational and clinicopathologic research on kidney diseases. I am most interested in pathogenic mechanisms and pathologic manifestations of glomerular diseases and vasculitis. A major current research focus is on elucidating the pathogenesis of vascular inflammation caused by anti-neutrophil cytoplasmic autoantibodies (ANCA).

Kakoki, Masao email , publications

My research aims at prevention and treatment of cardiovascular diseases and focuses on the identification of genes that confer susceptibility or resistance to the diseases with the use of genetically engineered mice. In collaboration with Dr.Oliver Smithies, I very recently developed a new method for altering gene expression by modifying 3’ untranslated regions in mice which enables fine-tuned modification of gene expression. I am now analyzing the phenotypes of several mouse models generated with this method.

Kaufman, David G. email , , , , , publications

Topic 1  We seek genomic targets for carcinogenesis among segments of DNA replicated in early S phase when cells are most susceptible to carcinogens.  We are mapping genomic sites replicated during early S phase, identifying origins of replication activated in this interval, and characterizing temporal sequencing of replication from these origins.  Topic 2  We are reconstructing differentiated and functional human endometrial tissue from epithelial and stromal cells interacting in culture.  We use these co-cultures to study development of endometrial cancer.

Kesimer, Mehmet email , , , , publications

The upper airways serve to clean inspired air from physical, chemical and pathological detritus that might damage the delicate peripheral airways where oxygen exchange is achieved. It is the heart of a powerful two tiered  innate immune system based upon a  layer of mucus that captures the incoming material that is moved over a bed of cilia. The system is called the muco-ciliary escalator.
Failure of this complex protective system is associated with a wide variety of diseases such as cancer and chronic inflammatory diseases. Biomolecules in mucus are split into two distinct groups, the first group being of globular type proteins between 6 kDa to 200 kDa and the second being of mucins which are large, space-filling glycoconjugates of 200 kDa to 100 MDa, with most of this mass being of carbohydrate in origin. Besides these biomolecules, mucus also contains secreted vesicles (exosomes) with innate immune properties. In chronic inflammatory lung diseases like cystic fibrosis (CF), chronic bronchitis (COPD) and asthma, mucus quantity and quality is altered and it is not efficiently removed from the lungs, causing airway obstruction, impaired gas exchange, bacterial colonization & infection and damage to lung tissue. The long term goal of our laboratory is to understand how this innate immune barrier is dynamically organized around the protective macromolecules under normal and pathological conditions. Currently, research in the Kesimer laboratory is focused on three main fundamentally important areas: 1- How mucins and globular proteins are organized within the airway mucosal barrier and how they are altered in disease pathogenesis, 2- How mucins are processed to mature after granular release for optimal function and how this progression is altered in chronic lung diseases, CF in particular, and 3- The role of extracellular vesicles in the airway mucosal barrier. Our laboratory is established with a wide range of state of the art biochemical, biophysical and proteomics methods including UPLC-Orbitrap mass spectrometry, atomic force microscopy, dynamic and static light scattering, and a variety of surface biophysics tools including QCM-D.

Liu, Jiandong email , , , , , publications

Congenital heart diseases are one of the most common birth defects in humans, and these arise from developmental defects during embryogenesis.  Many of these diseases have a genetic component, but they might also be affected by environmental factors such as mechanical forces. The Liu Lab combines genetics, molecular and cell biology to study cardiac development and function, focusing on the molecular mechanisms that link mechanical forces and genetic factors to the morphogenesis of the heart.  Our studies using zebrafish as a model system serve as the basic foundation to address the key questions in cardiac development and function, and could provide novel therapeutic interventions for cardiac diseases.

Mack, Christopher P. email , , , , , publications

My research goals are to identify the mechanisms by which environmental factors regulate smooth muscle cell phenotype and to define the transcriptional pathways that regulate SMC-specific gene expression.

Mackman, Nigel email , , , , publications

The major focus of Mackman lab is the procoagulant protein tissue factor. This is the primary cellular initiator of blood coagulation. We study its role in hemostasis, thrombosis, inflammation, ischemia-reperfusion injury and tumor growth.  LPS induction of the tissue factor gene in human monocytic cells and endothelial cells is mediated by various transcription factors, such as AP-1, NF-ĸB and Egr-1. More recently, we found that the phosphatidylinositol-3-kinase protein kinase B intracellular signaling pathway suppresses LPS activation of monocytes and endothelial cells.  We found that inhibition of either tissue factor or the downstream coagulation protease thrombin reduced infarct size in a rabbit model of cardiac ischemia-reperfusion injury. We showed that the tissue factor-thrombin pathway increased inflammation during myocardial ischemia-reperfusion injury by inducing chemokine expression and enhancing the recruitment of neutrophils. We have generated a number of mouse models expressing different levels of both mouse and human tissue factor. These mice have been used to provide new insights into the role of tissue factor in hemostasis and thrombosis. In 2007, we developed a new assay to measure levels of microparticle tissue factor in plasma. We found that elevated levels of microparticle tissue factor are associated with venous thromboembolism in cancer patients.

Maeda, Nobuyo N. email , , , , , , , publications

Our research is focused on the genetics and molecular pathology of complex multi-factorial conditions in humans – obesity, diabetes, hypercholesterolemia, insulin resistance, and hypertension.  These conditions underlie cardiovascular diseases, including atherosclerosis, the major cause of death and disabilities in North America. Our approach consists of experiments with mice carrying modifications in various genes important for the maintenance of vascular function, antioxidant defense, and metabolism.  We dissect how gene-gene and gene-environment interaction influences the pathogenesis of these common human conditions and their complications.

Miller, C. Ryan email , , , , , , , , , , publications

My laboratory studies diffuse gliomas, devastating primary tumors of the central nervous system for which few effective drugs are currently available.  We utilize genetically engineered mice, cell culture, and human tumor model systems to explore the molecular pathogenesis of gliomas.  We utilize animal model systems to develop drugs and diagnostic markers for their individualized therapy.  Rotating students gain experience with multiple techniques, including cell culture, molecular biology, genomics, genetic lineage tracing, fluorescence microscopy, and digital image analysis.

Nichols, Timothy C. email , publications

My research interests include the role of von Willebrand factor in thrombosis and atherosclerosis. Our current lab work focuses on the molecular biology of porcine von Willebrand factor.

Perou, Charles M. email , , , , , , , publications

The focus of my lab is to characterize the biological diversity of human tumors using genomics, genetics, and cell biology, and then to use this information to develop improved treatments that are specific for each tumor subtype and for each patient. A significant contribution of ours towards the goal of personalized medicine has been in the genomic characterization of human breast tumors, which identified the Intrinsic Subtypes of Breast Cancer. We study many human solid tumor disease types using multiple experimental approaches including RNA-sequencing (RNA-seq), DNA exome sequencing, Whole Genome Sequencing, cell/tissue culturing, and Proteomics, with a particular focus on the Basal-like/Triple Negative Breast Cancer subtype. In addition, we are mimicking these human tumor alterations in Genetically Engineered Mouse Models, and using primary tumor Patient-Derived Xenografts, to investigate the efficacy of new drugs and new drug combinations. All of these genomic and genetic studies generate large volumes of data; thus, a significant portion of my lab is devoted to using genomic data and a systems biology approach to create computational predictors of complex cancer phenotypes.

Qian, Li email , , , , , publications

Our laboratory is interested in developing innovative approaches to regenerate or repair an injured heart. Our goal is to understand the molecular basis of cardiomyocyte specification and maturation and apply this knowledge to improve efficiency and clinical applicability of cellular reprogramming in heart disease. To achieve these goals, we utilize in vivo modeling of cardiac disease in the mouse, including myocardial infarction (MI), cardiac hypertrophy, chronic heart failure and congenital heart disease (CHD). In addition, we take advantage of traditional mouse genetics, cell and molecular biology, biochemistry and newly developed reprogramming technologies (iPSC and iCM) to investigate the fundamental events underlying the progression of various cardiovascular diseases as well as to discover the basic mechanisms of cell reprogramming.

Taylor, Joan M. email , , , , , publications

The goal of our research is to identify signaling mechanisms that contribute to normal and pathophysiological cell growth in the cardiovascular system.  We study cardiac and vascular development as well as heart failure and atherosclerosis.

Tidwell, Richard R email , , , publications

Dr. Tidwell’s research is focused on the design and synthesis of new drugs for the treatment of AIDS-associated opportunistic infections.  The rationale for design of new drugs is directed at determining the mechanisms of action, antimicrobial activity, and pharmacokinetics of dicationic molecules.  Studies have been initiated to isolate and identify new drug targets from Pneumocystis carinii and Cryptosporidium parvum utilizing molecular modeling and biochemical methods to aid in the determination of new structures.  The role of proteases and imidazoline receptors in the pathogenesis of disease continues to be a major area of research as well as a new prodrug approach for the cationic molecules to allow for much improved bioavailability.

Troester, Melissa email , , , , publications

Dr. Troester’s research focuses on stromal-epithelial interactions, genomics of normal breast tissue, breast cancer microenvironment, and molecular pathology of breast cancer progression. She is a Co-Investigator on the Carolina Breast Cancer Study (CBCS), a resource including breast tumors from thousands of African American women, and she is PI of the Normal Breast Study (NBS), a unique biospecimen resource of normal tissue from women undergoing breast surgery at UNC Hospitals. Dr. Troester has extensive experience in integrating multiple high dimensional data types. She is chair of the Normal Breast Committee for the Cancer Genome Atlas Project where she is leading coordination of histology, copy number, mutation, methylation, mRNA and microRNA expression data. She has more than a decade of experience working with genomic data and molecular biology of breast cancer progression and has published many papers in the area of breast cancer subtypes, breast microenvironment, and stromal-epithelial interactions. She has trained four postdocs, 12 predoctoral students and several undergraduates.

Vaziri, Cyrus email , , , , , , publications

Our broad long-term goal is to understand how mammalian cells maintain ordered control of DNA replication during normal passage through an unperturbed cell cycle, and in response to genotoxins (DNA-damaging agents).  DNA synthesis is a fundamental process for normal growth and development and accurate replication of DNA is crucial for maintenance of genomic stability.  Many cancers display defects in regulation of DNA synthesis and it is important to understand the molecular basis for aberrant DNA replication in tumors.  Moreover, since many chemotherapies specifically target cells in S-phase, a more detailed understanding of DNA replication could allow the rational design of novel cancer therapeutics.  Our lab focuses on three main aspects of DNA replication control:  (1) The S-phase checkpoint, (2) Trans-Lesion Synthesis (TLS) and (3) Re-replication.

Weissman, Bernard E. email , , , , , publications

How the loss of different components of the SWI/SNF complex contributes to neoplastic transformation remains an open and important question. My laboratory concentrates on addressing this question by the combined use of biological, biochemical and mouse models for SWI/SNF complex function.

Whang, Young E. email , , , , publications

My laboratory is interested in characterizing the role of cytoplasmic signal transduction pathways in regulation of androgen receptor activity and progression of prostate cancer.  Our studies have focused on HER-2 receptor tyrosine kinase and we have demonstrated that HER-2 activation stimulates androgen receptor activity and HER-2 inhibition inhibits androgen receptor transcriptional function at the level of recruitment to the androgen responsive enhancers.  These findings have led to the design and initiation of the protocol involving lapatinib, a clinical HER-2 inhibitor, in treatment of patients with prostate cancer.  More recently, we have demonstrated that activated Cdc42-associated kinase Ack1 promotes progression of prostate cancer via tyrosine phosphorylation of androgen receptor at Tyr-267 and Tyr-363 residues.  We are interested in further characterizing the role of tyrosine phosphorylation of androgen receptor in prostate cancer and development of Ack1 targeted therapy for clinical use.

Williams, David C. Jr. email , , , , publications

The overall objective of our research is to understand the connection between structure of protein-DNA complexes, protein dynamics and function.  We currently focus on the methyl-cytosine binding domain (MBD) family of DNA binding proteins.  The MBD proteins selectively recognize methylated CpG dinucleotides and regulate gene expression critical for both normal development and carcinogenesis.  We use a combination of NMR spectroscopy and biophysical analyses to study protein-DNA and protein-protein complexes involving the MBD proteins.  Building on these studies, we are developing inhibitors of complex formation as potential molecular therapeutics for b-hemoglobinopathies and cancer.

Williams, Scott E. email , , , , , , , , publications

Divisions and decisions in development and disease. The mammalian skin epithelium is an ideal model system to study fundamental questions in stem cell and cancer biology. It is accessible; it can be cultured, genetically manipulated and transplanted; and its resident stem cells possess unparalleled regenerative capacity. Our skin, unlike many other organs, undergoes continuous growth and turnover. In development and homeostasis, progenitors in the skin must balance self-renewal and differentiation programs. We have found that asymmetric cell divisions are a critical mechanism by which skin progenitors maintain this equilibrium. We are interested in studying how this asymmetry is controlled at a molecular level, and how division orientation impacts cell fate choices in normal and neoplastic growth. To facilitate these and other studies in diverse epithelia, we have developed a powerful functional tool, lentiviral in vivo RNAi, which allows us to rapidly perform functional studies on any gene in the intact mouse in weeks instead of years. Our broad goal will be to use this technique, in combinations of candidate and screening approaches, to dissect pathways that influence stem cell differentiation. I will be joining the Pathology Department in April, 2013 and am seeking passionate, open-minded, and interactive students for the summer and beyond.

Willis, Monte S. email , , , , publications

We are looking for talented and motivated individuals to join our research team. Dr. Willis’s lab investigates the molecular basis of genetic and lifestyle mediated cardiomyopathic disease (heart failure) using bioinformatics, molecular, and animal model approaches. We are seeking graduate students looking for an exciting and supportive research environment offering a diversity of experiences integrating cardiac phenotyping, mouse models of disease, molecular biology, and ubiquitin proteasome biology. Both national and international training experiences supported by the Leducq Foundation (http://fondationleducq.org/network/proteotoxicity-an-unappreciated-mechanism-of-heart-disease-and-its-potential-for-novel-therapeutics/) are possible,  depending on citizenship and interest in travel.

Wilson, Elizabeth M email , , , , , publications

Our research focus is on mechanisms of action of the androgen receptor (AR), a ligand-dependent transcriptional regulatory protein that mediates the effects of testosterone and dihydrotestosterone. Studies seek to identify and characterize AR coregulatory proteins and their regulation by phosphorylation and the cell cycle. Areas of interest include male sex development, the androgen insensitivity syndrome, and AR action in the ovary, endometrium and prostate cancer. Melanoma antigen gene protein-11 (MAGE-11) was identified as an AR coregulatory protein that belongs to the MAGE gene family of cancer-germline antigens. The MAGE-11 gene is located on the human X chromosome and is exclusively expressed in human and nonhuman primates, providing a gain-of- function to AR. Mechanisms whereby MAGE-11 regulates AR transcriptional activity through its interaction with the AR NH2-terminal FXXLF motif and cell cycle regulatory proteins are being investigated. Our objective is to understand how AR regulates gene transcription and cell proliferation in the human male and female reproductive tracts.  Keywords:  androgen receptor, MAGE-11, male reproduction, female reproduction, prostate cancer, transcription regulation, FXXLF motifs

Wolberg, Alisa email , , , , publications

We investigate cellular, molecular, and biochemical mechanisms of blood coagulation.  Using in vitro, ex vivo, and in vivo models, we focus on mechanisms contributing to cardiovascular disease (heart attack, stroke, deep vein thrombosis), including the effects of plasma proteins, cells, and blood flow (shear) on blood clot biochemical and mechanical stability.  We have shown that abnormalities in blood protein and/or cellular function contribute to bleeding and clotting pathologies including hemophilia and thrombosis, and shown how hemostatic and antithrombotic therapeutics modulate clot quality.  Current efforts are focused on pathophysiologic mechanisms that result in bleeding or prothrombotic disease (e.g., cancer).  Our overall goal is to translate this knowledge into novel approaches for treating bleeding and clotting disorders.

Zhang, Qing email , , , , , publications

The oxygen-sensing pathway contributes largely to the development of tumors. One of the central players in this pathway is prolyl hydroxylase (EglN1, 2 and 3). Our lab currently studies hypoxia signaling, prolyl hydroxylase and cancer, specifically breast and renal cell carcinoma. One project focuses on using proteomic and genomic approaches to screen for novel prolyl hydroxylase substrates that play important roles in cancer. The other project involves integrating CHIP-seq strategy with gene expression profiling in order to identify EglN2 prolyl hydroxylase and hypoxia inducible factor (HIF) targets in the malignant diseases. The ultimate goal is to understand mechanistically how oxygen-sensing pathways contribute to cancer progression, which will facilitate our design of efficient treatment strategies to specifically target cancer.