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[ PhD Program: Cancer Biology Keyword: ]

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NameEmailPhd ProgramResearch InterestsPublications
Ahmed, Shawn email , , , , , publications

Our research group utilizes the nematode C. elegans to investigate germ cell immortality: mechanisms that allow germ cells remain eternally youthful as they are transmitted from one generation to the next. We also study how telomerase functions at chromosome termini, as well as the consequences of telomere dysfunction.

Allbritton, Nancy email , , , , publications

The overall focus of the laboratory is to quantitatively measure the activity of proteins in cellular signaling networks to understand the relationships of these intracellular pathways in regulating cell health and disease. These networks are composed of interacting proteins and small molecules that work together in a concerted manner to regulate the cell in response to its environment. Despite the importance of these key signaling molecules in controlling the behavior of cells, most of these proteins and metabolites can not be quantified in single cells. There is a need throughout biology for new technologies to identify and understand the molecular circuits within single cells. A research goal is to develop new methods that will broaden the range of measurements possible at the single-cell level and then to utilize these methods to address fundamental biologic questions. We are pursuing this task by bringing to bear diverse techniques from chemistry, physics, biology and engineering to develop new analytical tools to track signal transduction within individual cells. Our research is a multidisciplinary program for the development and application of new analytical methods with two main focus areas: 1) techniques to monitor cellular signaling, and 2) microfabricated cellular analysis systems.

Amelio, Antonio L. email , , , , , , , publications

Our laboratory is broadly interested in understanding the molecular mechanisms of transcriptional regulation by cell signaling pathways and the role of pathway cross-talk in cancer biology. In particular, the cAMP signaling cascade directs adaptive cellular responses to a variety of stress stimuli via a combination of acute affects arising from GS-protein coupled receptor (GPCR)-mediated activation of PKA and long-term affects resulting from transcriptional reprogramming directed by CREB and the CREB Regulated Transcription Coactivators (CTRCs). We are applying an interdisciplinary approach to study the consequences of aberrant activation of the cAMP/CREB/CRTC signal circuit on these adaptive responses and how cooperative signaling with other pathways promotes oncogenic processes in oral, head, and neck cancers.

Archer, Trevor email , , , publications

Molecular carcinogenesis: cancer, chromatin, transcription, and epigenetics

Arthur, Janelle C. email , , , , publications

The Arthur lab is interested in mechanisms by which inflammation alters the functional capabilities of the microbiota, with the long-term goal of targeting resident microbes as a preventative and therapeutic strategy to lessen inflammation and reduce the risk of colorectal cancer. We utilize a unique and powerful in vivo system – germ-free and gnotobiotic mice – to causally link specific microbes, microbial genes, and microbial metabolites with health and disease in the gut.  We also employ basic immunology and molecular microbiology techniques as well as next generation sequencing and bioinformatics to evaluate these essential host-microbe interactions.

Baldwin, Albert S. email , , , , , , publications

Our laboratory studies an amazing regulatory factor known as NF-kappaB. This transcription factor controls key developmental and immunological functions and its dysregulation lies at the heart of virtually all major human diseases.

Bautch, Victoria email , , , , , , publications

Blood vessel formation in cancer and development; use mouse culture (stem cell derived vessels) and in vivo models (embryos and tumors); genetic, cell and molecular biological tools; how do vessels assemble and pattern?, dynamic image analysis.

Bear, James E. email , , , , , , , publications

Our lab uses a combination of genetics, high-resolution cellular and animal imaging, animal tumor models and microfluidic approaches to study the problems of cell motility and cytoskeletal organization. We are particularly interested in 1) How cells sense cues in their environment and respond with directed migration, 2) How the actin cytoskeleton is organized at the leading edge of migrating cells and 3) How these processes contribute to tumor metastasis.

Berg, Jonathan email , , , , , publications

My research group is broadly interested in the application of sequencing technologies in medical genetics and genomics, using a combination of wet lab and computational approaches.  As a clinician, I am actively involved in the care of patients with hereditary disorders, and the research questions that my group investigates have direct relevance to patient care.  One project uses genome sequencing in families with likely hereditary cancer susceptibility in order to identify novel genes that may be involved in monogenic forms of cancer predisposition.  Another major avenue of investigation examines the use of genome-scale sequencing in clinical medicine, ranging from diagnostic testing to newborn screening, to screening in healthy adults.

Brennwald, Patrick email , , , , , publications

We are interested in the mechanism by which eukaryotic cells are polarized and the role of vesicle transport plays in the determination and regulation of cell polarity and tumorigenesis.

Bultman, Scott email , , , , publications

Our lab is interested in the role of chromatin-modifying factors and epigenetics in mammalian development and disease. We are particularly interested in two major areas both of which make use of mouse models: (1) the role of BRG1 and SWI/SNF nucleosome-remodeling complexes in various aspects of hematopoiesis including regulation of globin gene expression and inflammation; (2) the role of dietary fiber and gut microflora on histone modifications, CpG methylation, and prevention of colorectal cancer.

Chen, Xian email , , , , publications

Developing and applying novel mass spectrometry (MS)-based proteomics methodologies for high throughput identification, quantification, and characterization of the pathologically relevant changes in protein expression, post-translational modifications (PTMs), and protein-protein interactions.  Focuses in the lab include: 1) technology development for comprehensive and quantitative proteomic analysis, 2) investigation of systems regulation in toll-like receptor-mediated pathogenesis and 3) proteomic-based mechanistic investigation of stress-induced cellular responses/effects in cancer pathogenesis.

Cheney, Richard email , , , , , , publications

Our goal is to understand the fundamental cell biology underlying processes such as neurodevelopment, angiogenesis, and the metastasis of cancer cells.  Most of our experiments focus on molecular motors such as myosin-X and on the finger-like structures known as filopodia.  We generally utilize advanced imaging techniques such as TIRF and single-molecule imaging in conjunction with mammalian cell culture.  We also  use molecular biology and biochemistry and are in the process of developing a mouse model to investigate the functions of myosin-X and filopodia.   We are looking for experimentally driven students who have strong interests in understanding the molecular basis of dynamic cellular processes such as filopodial extension, mechanosensing, and cell migration.

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.

Cook, Jeanette (Jean) email , , , , , , , publications

The Cook lab studies the major transitions in the cell division cycle and how perturbations in cell cycle control affect genome stability. We have particular interest in mechanisms that control protein abundance and localization at transitions into and out of S phase (DNA replication phase) and into an out of quiescence. We use a variety of molecular biology, cell biology, biochemical, and genetic techniques to manipulate and evaluate human cells as they proliferate or exit the cell cycle. We collaborate with colleagues interested in the interface of cell cycle control with developmental biology, signal transduction, DNA damage responses, and oncogenesis.

Copenhaver, Gregory P. email , , , , , publications

The primary research area my lab is the regulation of meiotic recombination at the genomic level in higher eukaryotes.  Genomic instability and disease states, including cancer, can occur if the cell fails to properly regulate recombination.  We have created novel tools that give our lab an unparalleled ability to find mutants in genes that control recombination. We use a combination of genetics, bioinformatics, computational biology, cell biology and genomics in our investigations.  A second research area in the lab is the role of centromere DNA in chromosome biology.  We welcome undergraduates, graduate students, postdoctoral fellows and visiting scientists to join our team.

Cox, Adrienne email , , , , , , publications

Our lab is interested in molecular mechanisms of oncogenesis, specifically as regulated by Ras and Rho family small GTPases. We are particularly interested in understanding how membrane targeting sequences of these proteins mediate both their subcellular localization and their interactions with regulators and effectors. Both Ras and Rho proteins are targeted to membranes by characteristic combinations of basic residues and lipids that may include the fatty acid palmitate as well as farnesyl and geranylgeranyl isoprenoids. The latter are targets for anticancer drugs; we are also investigating their unexpectedly complex mechanism of action. Finally, we are also studying how these small GTPases mediate cellular responses to ionizing radiation – how do cells choose whether to arrest, die or proliferate?

Damania, Blossom email , , , , , publications

The work in our laboratory is focused on understanding the molecular pathogenesis of Kaposi’s sarcoma-associated herpesvirus (KSHV), an oncogenic human virus. KSHV is associated with several types of cancer in the human population. We study the effect of KSHV viral proteins on cell proliferation, transformation, apoptosis, angiogenesis and cell signal transduction pathways. We also study viral transcription factors, viral replication, and the interactions of KSHV with the human innate immune system. Additionally, we are developing drug therapies that curb viral replication and target tumor cells.

Davis, Ian email , , , , publications

With a particular interest in pediatric solid tumors, our lab aims to develop a mechanistic understanding of the role of aberrant or dysregulated transcription factors in oncogenesis.

Der, Channing email , , , , , , , publications

Our research centers on understanding the molecular basis of human carcinogenesis. In particular, a major focus of our studies is the Ras oncogene and Ras-mediated signal transduction.  The goals of our studies include the delineation of the complex components of Ras signaling and the development of anti-Ras inhibitors for cancer treatment.  Another major focus of our studies involves our validation of the involvement of Ras-related small GTPases (e.g., Ral, Rho) in cancer.  We utilize a broad spectrum of technical approaches that include cell culture and mouse models, C. elegans, protein crystallography, microarray gene expression or proteomics analyses, and clinical trial analyses.

Deshmukh, Mohanish email , , , , , , publications

We study how mammalian cells regulate their survival and death (apoptosis).  We have focused our work on identifying unique mechanisms by which these pathways are regulated in neurons, stem cells, and cancer cells.  We utilize various techniques to examine this in primary cells as well as in transgenic and knock out mouse models in vivo.  Our ultimate goal is to discover novel cell survival and death mediators that can be targeted for therapy in neurodegeneration and cancer.

DeSimone, Joseph M. email , , , , publications

The direct fabrication and harvesting of monodisperse, shape-specific nano-biomaterials are presently being designed to reach new understandings and therapies in cancer prevention, diagnosis and treatment.  Students interested in a rotation in the DeSimone group should not contact Dr. DeSimone directly.  Instead please contact Chris Luft at jluft@email.unc.edu.

Dittmer, Dirk email , , , , , publications

Our lab tries to understand viral pathogenesis. To do so, we work with two very different viruses – West Nile Virus (WNV) and Kaposi¹s sarcoma-associated herpesvirus (KSHV/HHV-8).

Dowen, Jill email , , , , , , publications

My lab studies how genes function within the three-dimensional context of the nucleus to control development and prevent disease. We combine genomic approaches (ChIP-Seq, ChIA-PET) and genome editing tools (CRISPR) to study the epigenetic mechanisms by which transcriptional regulatory elements control gene expression in embryonic stem cells.  Our current research efforts are divided into 3 areas: 1) Mapping the folding pattern of the genome 2) Dynamics of three-dimensional genome organization as cells differentiate and 3) Functional analysis of altered chromosome structure in cancer and other diseases.

Duronio, Bob email , , , , , publications

My lab studies how cell proliferation is controlled during animal development, with a focus on the genetic and epigenetic mechanisms that regulate DNA replication and gene expression throughout the cell cycle. Many of the genes and signaling pathways that we study are frequently mutated in human cancers. Our current research efforts are divided into three areas:  1) Plasticity of cell cycle control during development  2) Histone mRNA biosynthesis and nuclear body function  3) Epigenetic control of genome replication and function

Earp, H. Shelton email , , , publications

Our lab is interested in how signals from membrane receptors are transduced to the nucleus altering gene expression, cell shape, proliferation and differentiation. We are particularly interested in tyrosine-specific protein kinases in breast and prostate cancer, as well as lymphoma/leukemia. Particular focus of the lab include the roles of :1) the EGF receptor family and related molecules e.g. HER4/ErbB4 in growth inhibition and differentiation, 2) the intracellular tyrosine kinase Ack which tyrosine phosphorylates the androgen receptor in androgen-independent prostate cancer and 3) a receptor tyrosine kinase that we cloned, Mer, that is expressed ectopically in childhood leukemias conferring a chemoresistant signal.  Mer also function in tumor-associated macrophages in a manner that appears to enhance tumor growth and immune system evasion.

Emanuele, Michael email , , , , , publications

Our lab applies cutting edge genetic and proteomic technologies to unravel dynamic signaling networks involved in cell proliferation, genome stability and cancer. These powerful technologies are used to systematically interrogate the ubiquitin proteasome system (UPS), and allow us to gain a systems level understanding of the cell at unparalleled depth. We are focused on UPS signaling in cell cycle progression and genome stability, since these pathways are universally perturbed in cancer.

Fenton, Suzanne E. email , , , publications

The Reproductive Endocrinology Group in the National Toxicology Program (NTP) Labs, led by Dr. Fenton, focuses on the role of environmental chemicals in breast developmental timing as it relates to puberty, increased susceptibility to form breast tumors, altered lactational ability, and the effects of chemicals on independent breast cancer risk factors such as obesity, breast density and pubertal timing. The projects within the lab often take a systems biology approach to the problem and instead of delving into exact mechanisms of an insult, which is in line with the missions of the NTP. The group also provides expertise in the use of whole mount mammary gland preparations in evaluating early life development of both male and female rat offspring and lifelong effects in female mice.

Franco, Hector L. email , , , , , publications

My lab has a long-standing interest in gene regulation, epigenetics, chromatin and RNA biology, especially as it pertains to cancer. We are interested in studying the formation and function of transcriptional enhancers and the non-coding RNAs that are actively produced at enhancers, known as enhancer RNAs, which are involved in modulating several aspects of gene regulation. In addition, we aim to understand how transcriptional enhancers help orchestrate responses to external stimuli found in the tumor microenvironment. We address these research aims by using an interdisciplinary approach that combines molecular and cellular techniques with powerful genomic and computational approaches.

Furey, Terry email , , , , , publications

The Furey Lab is interested in understanding gene regulation processes in specific cell types, especially with respect to complex phenotypes, and the effect of genetic and environmental variation on gene regulation. We have explored these computationally by concentrating on the analysis of genome-wide open chromatin data generated from high-throughput sequencing experiments; and the development of statistical methods and computational tools to investigate underlying genetic and biological mechanisms of complex phenotypes. Our current projects include determining the molecular effects of exposure to 1,3-butadiene, a known carcinogen, on chromatin, gene regulation, and gene expression in lung, liver, and kidney tissues of genetically diverse mouse strains. We are also exploring chromatin, transcriptional, and microbial changes in inflammatory bowel diseases to identify biomarkers of disease onset, severity, and progression.

Garcia-Martinez, J. Victor email , , , , publications

Over millions of years of coexistence humans and pathogens have develop intricate and very intimate relationships.  These highly specialized interactions are the basic determinants of pathogenesis and disease progression.  Our laboratory is interested in elucidating the molecular basis of disease.  Our multidisciplinary approach to molecular medicine is based on our interest in the translation of basic research observations into clinical implementation.  For this purpose we use a variety of in vitro and in vivo approaches to study AIDS, Cancer, immunological diseases, gene therapy, etc.  Of particular interest is the use of state of the art models such as humanized mice to study human specific pathogens like HIV, EBV, Kaposiâ’s sarcoma, influenza, xenotropic murine leukemia virus-related virus.  In addition, we are interested in the development and implementation of novel approaches to prevent viral transmission using pre-expossure prophylaxis and vaccines.

Gershon, Timothy R email , , , , publications

As a pediatric neurologist and brain tumor researcher, I seek to understand the link between brain growth and childhood brain tumors.  During postnatal cerebellar development, neural progenitors divide rapidly.  This wave of neurogenesis must be strictly controlled to prevent formation of medulloblastoma, a malignant neuroblastic tumor of the cerebellum.  Using transgenic mice that express constitutively active Smoothened, we are able to recapitulate tumorigenesis in mice.  These tumor-prone mice develop medulloblastomas that model the human tumor in pathology and gene expression.  We use this primary brain tumor model to gain novel insight into medulloblastoma pathogenesis and treatment.

Gomez, Shawn email , , , , publications

Our primary research is in the area of computational systems biology, with particular interest in the study of biological signaling networks; trying to understand their structure, evolution and dynamics. In collaboration with wet lab experimentalists, we develop and apply computational models, including probabilistic graphical and multivariate methods along with more traditional engineering approaches such as system identification and control theory, to current challenges in molecular biology and medicine. Examples of recent research projects include: prediction of protein interaction networks, multivariate modeling of signal transduction networks, and development of methods for integrating large-scale genomic data sets.

Gupton, Stephanie email , , , , , , , publications

During cell shape change and motility, a dynamic cytoskeleton produces the force to initiate plasma membrane protrusion, while vesicle trafficking supplies phospholipids and membrane proteins to the expanding plasma membrane. Extracellular cues activate intracellular signaling pathways to elicit specific cell shape changes and motility responses through coordinated cytoskeletal dynamics and vesicle trafficking. In my lab we are investigating the role of two ubiquitin ligases, TRIM9 and TRIM67, in the cell shape changes that occur during neuronal development. We utilize a variety techniques including high resolution live cell microscopy, gene disruption, mouse models, and biochemistry to understand the complex coordination of cytoskeletal dynamics and membrane trafficking driving neuronal shape change and growth cone motility in primary neurons.

Hammond, Scott email , , , , , publications

My lab studies a gene silencing phenomenon called RNA interference, or RNAi.  We are interested in the role of RNAi in regulating endogenous genes, particularly those involved in cancer progression pathways.

Hathaway, Nathaniel A. email , , , , , publications

The Hathaway lab is focused on understanding the biological events responsible for dynamically regulating the selective expression of the mammalian genome. In multicellular organisms, genes must be regulated with high precision during stem cell differentiation to achieve normal development. Pathologically, the loss of proper gene regulation caused by defects in chromatin regulatory enzymes has been found to be a driving force in cancer initiation and progression. My lab uses a combination of chemical biology and cell biology approaches to unravel the molecular mechanisms that govern gene expression. We utilize new tools wielding an unprecedented level of temporal control to visualize changes in chromatin structure and function in mammalian cells and animal models. In addition, we seek to identify small molecule inhibitors that are selective for chromatin regulatory enzymes with the potential for future human therapeutics.

Hayes, David N email , , , publications

Molecular carcinogenesis, research translation, biomarkers, computational toxicology

Huang, Leaf email , , publications

Dr. Huang is a pioneer in nanoparticle vectors for delivery of drugs, genes and vaccines. He has designed a core/membrane type nanoparticle which evades the macrophages in the liver and the spleen and deliver a large fraction of the injected dose to the target cells. The nanomedicine can encapsulate siRNA, peptide or chemotherapy drugs, either alone or in combination, resulting in effective inhibition of tumor growth. The Huang lab is also interested in designing peptide or mRNA vaccines for cancer immunotherapy. He uses nanoparticles as a tool to study the cross talks between cells in the tumor microenvironment.

Hursting, Stephen D email , , , , publications

Dr. Hursting’s lab focuses on the molecular and metabolic mechanisms underlying nutrition and  cancer associations, particularly the impact of obesity and energy balance modulation (eg, calorie restriction, exercise) on cancer development or responses to chemotherapy. Primarily using genetically engineered mouse models of pancreatic, colon and breast cancer, Dr. Hursting has identified the IGF-1/Akt/mTOR and NF-kB signaling pathways as key targets for breaking the obesity- cancer link.  He has also established in several preclinical models of pancreatic and breast cancer that obesity impacts the response to various forms of chemotherapy.  In addition, the Hursting lab is involved in several translational research collaborations linking mouse model studies with clinical trials, and his group has expertise in measuring metabolic hormones, growth factors, inflammatory cytokines and chemokines in serum and tissue from rodents and humans.

Ibrahim, Joseph G email , , , publications

My research involves developing statistical methods in computational biology, including  methods Chip-seq data as well as the development of statistical methods for gene expression and sequence data.

Johnson, Gary L. email , , , , publications

Spatio-temporal regulation of signal relay systems in cells using live cell fluorescence imaging and targeted gene disruption of signaling proteins to define their role in development, physiology and pathophysiology.

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.

Kim, WIlliam Y email , , , , , publications

Our research explores the role of hypoxia-inducible factor (HIF) in tumorigenesis. HIF is a transcription factor that plays a key role in oxygen sensing, the adaptation to hypoxia and the tumor microenvironment. It is expressed in the majority of solid tumors and correlates with poor clinical outcome. Therefore, HIF is a likely promoter of solid tumor growth and angiogenesis.  Our lab uses mouse models to ask if and how HIF cooperates with other oncogenic events in cancer.  We are currently investigating HIF’s role in the upregulation of circulating tumor cells and circulating endothelial cells.

Krupenko, Natalia email , , , , , publications

My laboratory is interested in the role of folate and related metabolic pathways in methyl group metabolism, and their involvement in pathogenesis and etiology of diseases. We have recently discovered a novel function of a folate-binding methyltransferase GNMT in the regulation of cellular proliferation, and now study the genetic variations in GNMT and their effects on new function. Our lab is also interested in the cross talk between folate metabolism and sphingolipid pathways as a mediator of folate stress with the goal of exploiting this connection to improve human health.

Krupenko, Sergey email , , , , publications

Dr. Krupenko’s research is focused on the role of folate metabolism in cellular homeostasis and cancer disease. He is especially interested in the function of a major folate enzyme and a putative tumor suppressor ALDH1L1 as metabolic regulator and a guardian of non-malignant phenotype. At present he studies function of this enzyme and related proteins using mouse knockout models. Recently his research team has also demonstrated that dietary folate regulates cancer metastasis. He now pursues studies of specific signaling pathways involved in metastatic response to dietary folate status.

Laederach, Alain email , , , , , publications

The Laederach Lab is interested in better understanding the relationship between RNA structure and folding and human disease. We use a combination of computational and experimental approaches to study the process of RNA folding and in the cells. In particular, we develop novel approaches to analyze and interpret chemical and enzymatic mapping data on a genomic scale. We aim to fundamentally understand the role of RNA structure in controlling post-transcriptional regulatory mechanisms, and to interpret structure as a secondary layer of information (http://www.nature.com/nature/journal/v505/n7485/full/505621a.html).  We are particularly interested in how human genetic variation affects RNA regulatory structure. We investigate the relationship between disease-associated Single Nucleotide Polymorphisms occurring in Human UTRs and their effect on RNA structure to determine if they form a RiboSNitch.

Lawrence, David S email , , , , , , publications

Living cells have been referred to as the test tubes of the 21st century. New bioactive reagents developed in our lab are designed to function in cells and living organisms. We have prepared enzyme inhibitors, sensors of biochemical pathways, chemically-altered proteins, and activators of gene expression. In addition, many of these agents possess the unique attribute of remaining under our control even after they enter the biological system. In particular, our compounds are designed to be inert until activated by light, thereby allowing us to control their activity at any point in time.

Liu, Pengda email , , , , publications

If you are interested in developing new biochemical/molecular techniques/tools to advance our understanding of biology, and if you are interested in signal transduction pathway analyses and identification of cancer biomarkers, our research group may help you to achieve your goals, as we have the same dreams. We are especially interested in deciphering the molecular mechanisms underlying aberrant signaling events that contribute to tumorigenesis, mediated through protein modifications and protein-protein interactions. Understanding these events may lead to identification of novel drug targets and provide new treatment strategies to combat human cancer.


Lockett, Matthew Ryen email , , , publications

Research in the Lockett group focuses on the development of analytical model systems to: i) chemically modify the surface of thin films, and study chemical and biochemical reactions occurring on those surfaces; ii) study drug metabolism in an environment that closely mimics the human liver; iii) measure tumor invasion in an environment that closely mimics human tissue. /  / While these problems require techniques found in analytical chemistry, biochemistry, molecular biology, bioengineering, and surface science we are particularly interested in the technologies that allow us to quantitatively measure reactions and analytes.

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.

Magness, Scott email , , , , publications

The primary focus of my research is to understand the genetic mechanisms underlying stem cell maintenance and differentiation with the goal of translating this information into therapeutic strategies. Using a Sox9EGFP mouse model and FACSorting we are able to specifically enrich for single multipotent intestinal epithelial stem cells that are able to generate mini-guts in a culture system. Our studies are now focused on manipulating, in vitro, the genetics of stem cell behavior through viral gene therapeutics and pharmacologic agents. Additionally, we are developing stem cell transplantation and tissue engineering strategies as therapies for inborn genetic disorders as well as damage and disease of the intestine. Using novel animal models and tissue microarrays from human colon cancers, we are investigating the role of Sox-factors in colorectal cancer.

Magnuson, Terry email , , , , , publications

The Magnuson Lab works in three areas – (i) Novel approaches to allelic series of genomic modifications in mammals, (ii)Mammalian polycomb-group complexes and development, (iii) Mammalian Swi/Snf chromatin remodeling complexes

Major, Michael Ben email , , , , , , publications

The overall goal of my lab is to understand how alterations in signal transduction pathways contribute to human cancer.  To that end, a systems level approach is employed wherein functional genomics, mass spectrometry-based proteomics, gene expression and mutation data are integrated.  The resulting cancer-annotated physical/functional map of a signal transduction pathway provides us with a powerful tool for mechanistic discovery in cancer biology.  We are currently working in lymphoma and lung cancer models, with a focus on the Wnt/b-catenin and Keap1/Nrf2 pathways.

Makowski, Liza email , , , , , , publications

The Makowski lab focuses on substrate metabolism or “immunometabolism” in immune cells such as macrophages and metabolic reprogramming in complex diseases such as obesity, insulin resistance, atherosclerosis, and cancer. We use mouse models, cell culture, and metabolomics to study the interaction between inflammation and nutrient sensitive pathways. Projects in lab are funded by NIH, AHA, and the Mary Kay Foundation.  Core Techniques include:  Glucose, fatty acid, cholesterol trafficking and metabolism using radiotracer biochemical studies. Cellular bioenergetics. Digital Immunohistochemical Analysis

Marzluff, William email , , , , , , , , , publications

We are interested in the mechanisms by which histone protein synthesis is coupled to DNA replication, both in mammalian cell cycle and during early embryogenesis in Drosophila, Xenopus and sea urchins.

Matera, Greg email , , , , , , , publications

Research in our laboratory is focused on RNA. We aim to understand how ribonucleoprotein particles (snRNPs, mRNPs, etc.) are transcribed, packaged and transported to their final destinations in the cell.  We are also interested in the genetic and epigenetic forces that direct formation of microscopically visible subcellular structures (e.g. nuclear bodies). We use a combination of approaches, including Drosophila genetics, molecular cell biology, biochemistry, digital imaging microscopy and genome-wide analyses. Projects in the lab are focused on two areas:  models of a neurogenetic disease called Spinal Muscular Atrophy (SMA) and the functional analysis of post-translational modifications of chromatin and RNA-binding proteins important in cancer and other diseases.

Matson, Steven email , , , , publications

Research in our laboratory is focused on the enzymatic mechanisms and biological roles of DNA helicases which convert duplex DNA to ssDNA for use as a template in DNA replication and repair or as a substrate in recombination.  Defects in genes encoding DNA helicases have been linked to genomic instability leading to a variety of progeriod disorders and human cancers. Our long-range goal is to understand the mechanism of action of helicases and to define their roles in DNA metabolism. The lab also has an interest in the process of DNA transfer by bacterial conjugation – the unidirectional and horizontal transmission of genetic information from one cell to another. Conjugative DNA transfer plays a role in increasing genetic diversity in addition to propagating the spread of antibiotic resistance and microbial virulence factors. Our long-range goal is to define the function and regulation of the relaxosome, and each protein in this nucleoprotein complex, in conjugative DNA transfer.

McKay, Daniel email , , , , , , publications

Research in the lab focuses on how a single genome gives rise to a variety of cell types and body parts during development. We use Drosophila as a model organism to investigate (1) how transcription factors access DNA to regulate complex patterns of gene expression, and (2) how post-translational modification of histones contributes to maintenance of gene expression programs over time. We combine genomic approaches (e.g. chromatin immunoprecipitation followed by high-throughput sequencing) with Drosophila genetics and transgenesis to address both of these questions. Defects in cell fate specification and maintenance of cell identity often occur in human diseases, including cancer.

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.

Moody, Cary email , , , , publications

The work in my laboratory focuses on the molecular biology of human papillomaviruses (HPV), small DNA viruses that exhibit epithelial tropism. Certain types of HPV are considered the causative agents of cervical cancer and are also associated with cancers of the anus, oropharynx and esophagus.  My lab is interested in defining mechanisms that regulate the productive phase of the HPV life cycle, which is restricted to differentiating epithelia and includes viral genome amplification, late gene expression and virion production. Using various methods of epithelial differentiation, we are studying how HPV proteins modulate cell signaling pathways, including the DNA damage response and apoptosis, to facilitate viral replication, which in turn contributes to viral pathogenesis and possibly transformation. I will be accepting rotation students beginning in the winter of 2010.

Moorman, Nat email , , , , publications

How does a virus gain control over the host cell? My laboratory is interested in answering this question at the molecular level. By combining molecular biology and virology with new technologies (e.g. mass spectrometry, next generation sequencing), we investigate the mechanisms utilized by viruses to hijack infected cells. By understanding the specific function(s) of viral proteins during infection, we identify strategies used by viruses for deregulation of host cell processes. We use this information to characterize novel features of cell signaling pathways during infection, and to identify potential targets for anti-viral therapeutics.

Parise, Leslie email , , , , , , , , publications

The overall goal of our laboratory is to understand the molecular interface between cell signaling and adhesion receptors in blood diseases and cancer in order to develop novel therapeutic targets and approaches. One area of study is platelets because they become activated by cellular signals and adhere to each other and the blood vessel wall via specific adhesion receptors. These events can block blood flow, causing heart attacks and stroke, the leading causes of death in the US. Another area of research is sickle cell disease, since red blood cells in these patients are abnormally adhesive and also cause blood vessel blockages. A third area is cancer since cancer cells use similar cellular signals and adhesion receptors in tumorigenesis and metastasis. Our work involves a wide array  of technologies that include molecular, structural and cellular approaches as well as clinical/translational studies with human patients.

Pecot, Chad Victor email , , , , publications

The development of metastases is the cause of death in nearly all cancer patients, yet the mechanisms driving metastatic biology remain poorly understood. Also, few cancer therapeutics are being developed to specifically control this problem. My laboratory is interested in discovering novel mechanisms that drive metastatic biology, and in utilizing RNA interference (RNAi) strategies (such as nanoparticle delivery of miRNAs/siRNAs) to control this process. We will apply integrative analysis of large bioinformatic datasets, in vitro studies for mechanistic validation, and in vivo metastasis models to assess therapeutic efficacy of our RNAi approaches.

Peifer, Mark email , , , , , , , publications

Cell adhesion, signal transduction, and cytoskeletal regulation during embryogenesis and in cancer.  We focus on the regulation of cadherin-based cell-cell adhesion, and on Wnt signaling and its regulation by the tumor suppressor APC.

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.

Pielak, Gary J. email , , , , , publications

My graduate students and I use the formalism of equilibrium thermodynamics and the tools of molecular biology and biophysics to understand how nature designs proteins.

Purvis, Jeremy email , , , , , publications

We study the behavior of individual cells with a specific focus on “irreversible” cell fate decisions such as apoptosis, senescence, and differentiation. Why do genetically identical cells choose different fates? How much are these decisions controlled by the cell itself and how much is influenced by its environment? We address these questions using a variety of experimental and computational approaches including time-lapse microscopy, single-molecule imaging, computational modeling, and machine learning. Our ultimate goal is to not only understand how cells make decisions under physiological conditions—but to discover how to manipulate these decisions to treat disease.

Pylayeva-Gupta, Yuliya email , , , , publications

The goal of my research is to define molecular mechanisms of immune cell co-option by cancer cells, with the hope of identifying novel targets for immune cell reprogramming. Central to our approach is analysis immune cell subtypes in KRas-driven models of pancreatic cancer. We use cell and animals models to study signals important for pro-tumorigenic activity of immune cells, as well as define role of physiologically relevant oncogenic mutations in driving these signals and enabling immune escape.

Ramsden, Dale email , , , , , publications

The end joining pathway is a major means for repairing chromosome breaks in vertebrates.  My lab is using cellular and cell-free models to learn how end joining works, and what happens when it doesn’t.

Randell, Scott email , , , , , , , publications

Identification of airway epithelial stem cells; innate immunity in the airway; the pathophysiology of post-lung transplant ischemia reperfusion injury and bronchiolitis obliterans syndrome.

Reid, Lola email , , , publications

Two dynamically interacting sets of mechanisms govern tissue-specific gene expression and cell growth. 1) mechanisms in lineage biology regulate stem cells and their descendents, processes that define the repertoire of genes available to be regulated and 2) signal transduction mechanisms, induced by the synergistic effects of extracellular matrix components and soluble signals (hormones, growth factors), regulate the expression of the available genes. Studies in the lab focus on both classes of mechanisms in normal versus neoplastic tissue.

Rogers, Steve email , , , , , , publications

The research in our lab is centered on understanding the mechanisms and principles of movement at the cellular level. Cytoskeletal filaments – composed of actin and microtubules – serve as a structural scaffolding that gives cells the ability to divide, crawl, and change their shape.  Our lab uses a combination of cell biological, biochemical, functional genomic, and  high resolution imaging techniques to study cytoskeletal dynamics and how they contribute to cellular motion.

Samulski, Jude email , , , , , publications

We are engaged in studying the molecular biology of the human parvovirus adeno-associated virus (AAV) with the intent to using this virus for developing a novel, safe, and efficient delivery system for human gene therapy.

Sancar, Aziz email , , , , , publications

We have three main areas of research focus: (1) Nucleotide excision repair: The only known mechanism for the removal of bulky DNA adducts in humans. (2) DNA damage checkpoints:  Biochemical pathways that transiently block cell cycle progression while DNA contains damage.  (3) Circadian rhythm:  The oscillations in biochemical, physiological and behavioral processes that occur with the periodicity of about 24 hours.

Sekelsky, Jeff email , , , , publications

Genome instability is a major cause of cancer. We use the model organism Drosophila melanogaster to study maintenance of genome stability, including DNA double-strand break repair, meiotic and mitotic recombination, and characterization of fragile sites in the genome.  Our primary approaches are genetic (forward and reverse, transmission and molecular), but we are also using biochemistry to study protein complexes of interest, genomics to identify fragile sites and understand the regulation of meiotic recombination, fluorescence and electron microscopy for analysis of mutant phenotypes, and cell culture for experiments using RNA interference.

Serody, Jonathan email , , , publications

Our laboratory is involved in studies to determine the mechanisms and proteins involved in the migration of alloreactive and regulatory T cells to organs involved in graft-versus-host disease after stem cell transplantation using mouse models.

Sharpless, Norman (Ned) email , , , , , , publications

The lab relies on murine genetic approaches to study the roles of the INK4/ARF tumor suppressor locus in human cancer and aging.  At present, the lab has two main focuses:  Stem Cell Aging:
Cancer and degenerative diseases are much more common in old people than young.  Although this has been well-recognized in clinical medicine for decades, scientists do not agree as to why this occurs.  Recently, work from several labs including our own has shown that humans age, in part, because important regenerative cells lose their capacity to divide with the passage of time.  That is, the tissues and organs from old people are less able to replace and regenerate lost or damaged cells than the corresponding tissues and organs from young people.  Our lab has studied mechanisms that underlie this age-dependent failure of cell division; in fact, we have shown the surprising result that cellular programs that function to prevent cancer untowardly also calls aging.  Specifically, cellular senescence is now believed to be of major importance in the process of aging.  Senescence refers to a permanent growth arrest induced in formerly dividing cells by the activation of genes that prevent cancer.  The good news in this system is that the normal functioning of these tumor suppressor genes prevents cancer; the bad news is that these same genetic events appear to cause aging by activating cellular senescence.  Melanoma and Murine Models of Cancer:  Because of the important role of p16INK4a in preventing melanoma, the lab has long been interested in this particularly deadly form of skin cancer.  Specifically, we are interested in using genetically engineered models of cancer to study melanoma genetics.  We have shown a role for the p16INK4a-RB and ARF-p53 tumor suppressor pathways in repressing this important human cancer in response to RAS-RAF activation.  We have generated highly faithful models of human melanoma, and have used these to study novel therapeutics.  We have also discovered a novel human melanoma sub-type based on expression profiling, and have identified a new therapeutic target (CD200) for treatment of melanoma.

Slep, Kevin email , , , , , , , publications

Our lab examines cytoskeletal dynamics, the molecules that regulate it and the biological processes it is involved in using live cell imaging, in vitro reconstitution and x-ray crystallography.  Of particular interest are the microtubule +TIP proteins that dynamically localize to microtubule plus ends, communicate with the actin network, regulate microtubule dynamics, capture kinetochores and engage the cell cortex under polarity-based cues.

Sondek, John email , , , , , , publications

Our laboratory studies signal transduction systems controlled by heterotrimeric G proteins as well as Ras-related GTPases using a variety of biophysical, biochemical and cellular techniques. Member of the Molecular & Cellular Biophysics Training Program.

Strahl, Brian D. email , , , , , publications

Our laboratory is examining the role of histone post-translational modifications in chromatin structure and function.  Using a combination of molecular biology, genetics and biochemistry, we are determining how a number of modifications to the histone tails (e.g. acetylation, phosphorylation, methylation and ubiquitylation) contribute to the control of gene transcription, DNA repair and replication.

Su, Lishan email , , , , , , , publications

Major areas of research: 1) HIV-1 Virology, Immuno-Pathology and Immuno-Therapy, 2) HBV Virology, Immuno-Pathology and Immuno-Therapy, 3) Novel Immune Therapeutics Including Adjuvants and Vaccines, and 4) Humanized Mouse Models of Human Liver and Immune System.  My laboratory studies both virology and immunology of HIV-1 and HBV persistent infection.  We focus on defining viral factors that counteract host innate anti-viral immunity.  We have also developed humanized mouse models to study human immuno-pathology of chronic HIV-1 and HBV infection in vivo.  We investigate how human immune cells are dysregulated and contribute to diseases during HIV-1 and HBV persistent infection.  We are currently focused on the HIV-1/pDC/IFN-I axis that plays a critical role in HIV-1 persistence and AIDS, and on the HBV/Macrophage interaction in liver diseases.  In addition, we are developing novel immune modulatory therapeutics including antibodies, adjuvants and vaccines.

Thomas, Nancy email , publications

Molecular carcinogenesis, environmental toxicology, research translation, biomarkers

Ting, Jenny email , , , , , , , , , , publications

Topics include gene discovery, genomics/proteomics, gene transcription, signal transduction, molecular immunology.  Disease relevant issues include infectious diseases, autoimmune and demyelinating disorders, cancer chemotherapy, gene linkage.

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.

Wan, Yisong email , , , , publications

We are a molecular genetics laboratory studying immune functions by using mouse models. The focus of our research is to investigate the molecular mechanisms of immune responses under normal and pathological conditions. Our goal is to find therapies for various human immune disorders, such as autoimmunity (type 1 diabetes and multiple sclerosis), tumor and cancer, and inflammatory diseases (inflammatory bowel disease, asthma and arthritis).

Wang, Andrew Z. email , , , , publications

My laboratory has two research directions. One is to utilize nanotechnology to develop novel diagnostics and therapeutics to improve cancer treatment. The other is to use techniques developed in tissue engineering to develop in vitro 3D models of cancer metastasis.

Wang, Greg Gang email , , , , , publications

With an emphasis on chromatin biology and cancer epigenetics, our group focuses on mechanistic understandings of how chemical modifications of chromatin define distinct patterns of human genome, control gene expression, and regulate cell proliferation versus differentiation during development, and how their deregulations lead to oncogenesis. Multiple on-going projects employ modern biological technologies to: 1) biochemically isolate and characterize novel factors that bind to histone methylation on chromatin, 2) examine the role of epigenetic factors (chromatin-modifying enzymes and chromatin-associated factors) during development and tumorigenesis using mouse knockout models, 3) analyze epigenomic and transcriptome alternation in cancer versus normal cells utilizing next-generation sequencing technologies, 4) identify novel oncogenic or tumor suppressor genes associated with leukemia and lymphoma using shRNA library-based screening. We are also working together with UNC Center of Drug Discovery to develop small-molecule inhibitors for chromatin-associated factors as novel targeted cancer therapies.

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.

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

Wu, Di email , , , , publications

Our group develops novel statistical bioinformatics tools and applies them in biomedical research to help understanding the precision medicine for cancer (e.g., breast cancer and lung cancer) subtypes, the disease associated integrative pathways across multiple genomic regulatory levels, and the genetics based drug repurposing mechanisms. Our recent focus includes pathway analysis, microbiome data analysis, data integration and electronica medical records (EMR). Our application fields include cancer, stem cell, autoimmune disease and oral biology. In the past, we have developed gene set testing methods with high citations, in the empirical Bayesian framework, to take care of small complex design and genewise correlation structure. These have been widely used in the microarray and RNAseq based gene expression analysis. Contamination detection for data analysis for Target DNA sequencing is work in progress. Recently, we also work on single cell sequencing data for pathway analysis with the local collaborators.

Xiao, Xiao email , , , , publications

Xiao lab is interested in molecular medicine, specifically, gene delivery and therapy for various genetic and acquired diseases. The lab genetically engineers a non-pathogenic and defective DNA virus, named adeno-associate virus (AAV). The engineered AAV has all of its own genes gutted and replaced by our own genes of interests. As a result, the 22-nanometer AAV particles now serve as tiny FedEx/UPS trucks to deliver therapeutic genes to a variety of cells, tissues and even the whole body. Besides its superb efficiency, AAV also offers an excellent safety profile. For example, Xiao lab has developed AAV vectors to treat diseases like muscular dystrophies, heart failure, diabetes, arthritis, hepatitis and cancer, etc. A first of its kind gene therapy for Duchenne muscular dystrophy (DMD), a lethal childhood genetic disease, is in a phase I clinical trial.  In addition to gene delivery for therapeutic purposes, AAV can also be used as a powerful tool to study basic biology such as molecular genetics, signal transduction, apoptosis, mechanisms of pathogenesis and even the engineering of animal models. For example, AAV vectors can be used to deliver protein-encoding genes, antisense RNA, small interference RNA (siRNA) or microRNA to tissues like the muscle, heart, liver, pancreas, kidney, lung, brain and spinal cord, etc., to over-express, up-regulate or knockdown a gene or multiple genes for the purposes of dissecting particular molecular pathways, biological functions and immunology consequences and even creating disease models.

Xiong, Yue email , , , , , publications

Using genetic, cell biology, biochemical and proteomic approaches to determine the function and mechanism of – (1) CDK inhibitors in development and tumor suppression, (2) the p53 degradation and transport, and (3) RING family of ubiquitin ligases.

Yeh, Elaine email , , , publications

The site of microtubule attachment to the chromosome is the kinetochore, a complex of over 60 proteins assembled at a specific site on the chromosome, the centromere. Almost every kinetochore protein identified in yeast is conserved through humans and the organization of the kinetochore in yeast may serve as the fundamental unit of attachment. More recently we have become interested in the role of two different classes of ATP binding proteins, cohesions (Smc3, Scc1) and chromatin remodeling factors (Cac1, Hir1, Rdh54) in the structural organization of the kinetochore and their contribution to the fidelity of chromosome segregation.

Yeh, Jen Jen email , , , , publications

We are a translational research lab. The overall goal of our research is to find therapeutic targets and biomarkers for patients with pancreatic and colorectal cancer and to translate this to the clinic. In order to accomplish this, we analyze patient tumors using microarray analysis, identify and validate targets using forward and reverse genetic approaches in both cell lines and mouse models. At the same time, we evaluate novel therapeutics for promising targets in mouse models in order to better predict clinical response in humans. We also collaborate with the DeSimone and Huang labs to apply nanotechnology to drug delivery and therapeutics. Keywords: genomics, biomarkers, translational research, microarray, signaling, pancreatic cancer, colon cancer, mouse models, GEMM, drug discovery, nanoparticles.

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.

Zhang, Yanping email , , , , , publications

We employ modern technologies – genomics, proteomics, mouse models, multi-color digital imaging, etc. to study cancer mechanisms. We have made major contributions to our understanding of the tumor suppressor ARF and p53 and the oncoprotein Mdm2.