I am a physician-scientist with research and clinical interests in the prediction of outcomes in kidney disease. The research in my laboratory focuses on the discovery and validation of biomarkers in renal diseases including acute kidney injury, diabetic nephropathy, chronic kidney disease and glomerular diseases like IgA nephropathy. We use targeted analysis of candidate markers by multiplexed bead array, ELISA and mass spectrometry and proteomic discovery analyses by liquid chromatography/mass spectrometry to identify and qualify biomarkers in animal models and humans.
My lab is focused on Alzheimer’s disease. Current research is examining the role of diabetes-related disruptions in glucose metabolism and the impact this has on brain function. Evidence indicates that both Alzheimer’s and diabetes involve processes connected to inflammation, which has been another of my longstanding areas of research.
We study the pathogenesis of the Borrelia spirochetes that cause Lyme disease and relapsing fever.
The overall objective of my research is to elucidate biological mechanisms of cardiovascular injury from exposure to ionizing radiation and to identify potential methods for intervention. We focus on radiation-induced heart disease as a side effect of radiation therapy to the chest and cardiovascular effects of exposure to space radiation. Our research is performed with animal models of whole-body irradiation and image-guided localized irradiation combined with in vivo non-invasive echocardiography, ex vivo cardiac function measurements, and histological and molecular analyses.
Dr. Nagalo’s research interests include translational virotherapy and gene therapy for patients with advanced hepatocellular carcinoma and pancreatic cancers, and addressing health disparities in liver cancer, cancer therapy and cancer-focused research.
The overall aim of our program is to promote life-long health starting from the very beginning of a human’s life. Specifically, our research program is focused on studying the effects of physical activity, alone and in combination with nutrition, on optimal growth and development of children, including underlying biological mechanisms. We seek to understand the mechanistic consequences of inactivity and suboptimal nutrition on obesity and related metabolic disorders, and also how maternal physical activity during fetal development (i.e., training during pregnancy) and physical activity during childhood can prevent and/or reverse these conditions.
My research focuses on how environmental and occupational exposure, nutrition, and genetic diversity influence cancer initiation, promotion, and progress.
The lab studies the structure and function of carbohydrate-binding proteins in prostate cancer and reproduction.
Virology, cancer biology, immunology! Gammaherpesviruses are cancer-causing viruses that infect the majority of humans. We are working to define functions of viral proteins in infection and disease, identify host factors that block viral infection and prevent virus-driven cancers, and understand immune responses to chronic viral infections. Our major goal is to comprehend the complex relationship between gammaherpesviruses and their hosts. PLUS, we get to do cool science and figure out how stuff works!
My laboratory studies lung macrophages and their roles during the infection of Mycobacterium tuberculosis. We aim to understand the ontogeny of lung macrophages and how different metabolic pathways regulate their functions in tuberculosis. In addition, we are particularly interested in the crosstalk between cellular metabolism and epigenetic regulation in lung macrophages.
Cancer vaccine and immunotherapy; Tumor glycans; Tumor progression and metastasis; Cancer and metabolism.
My lab is interested in tumor biology. Our work has focused on extracellular matrix degrading proteases and their roles in facilitating tumor growth and metatstasis.
Our overall research goal is to identify the molecular mechanisms behind the genomic instability at critical oncogenes in lymphoma and the role DNA secondary structures may play in facilitating these genomic alterations. We are also interested in the impact of HIV infection on the molecular oncogenesis of lymphoma. To address these important questions we integrate basic and translational science using in silico, ex vivo, cell-based and tissue-based genomic and proteomic approaches.
The main goal of the research in Kiaei lab is to understand the process of neurodegeneration (e.g. in amyotrophic lateral sclerosis (ALS) or Lou Gehrig’s Disease), mimic the disease in the lab and develop an effective therapy for this currently “cureless” disease.
I am interested in breast cancer classification and factors affecting breast cancer development and progression.
Elucidation of biochemical mechanisms involved with kidney damage during sepsis and transplantation. Focus on mitochondria, cell death, and oxidant generation as well as novel therapies to reduce damage.
I am working on identification of the cellular mechanisms that control cell growth and development. I am particularly interested in the role and regulation of stem cells in neural development and in cancer.
Not accepting students as a major advisor
We are interested in studying primary effusion lymphoma (PEL), an aggressive B cell cancer caused by the Kaposi’s sarcoma-associated herpesvirus or human herpesvirus 8 (KSHV/HHV8). PEL tumor cells rely on the constitutive expression of virally encoded genes that globally reprogram host gene expression to create a conducive environment optimal for tumor cell proliferation and survival.
We utilize genetically modified mouse models to understand the function of poorly characterized genes that have a function in skeletal development, homeostasis or disease. A special interest is in proteins that post-translationally modify collagens and in osteogenesis imperfecta.
Cell-mediated immunity against human papillomavirus (HPV), HPV therapeutic vaccine development, cancer immunotherapy
My research focuses on the area of applied bioinformatics/computational biology and systems biology for biomedical research. I have developed novel advanced algorithms and frameworks to accelerate the utilization and mining for biological interpretation of omics data (genome, transcriptome, proteome and metabolome) for biomedical research translation (cancer, obesity, diabetes, autoimmune disease, metabolic dysfunction, etc.). In addition, I also focus on the impact of human gut microbiome on diseases progression and development.
We want to understand the cellular and molecular mechanisms that cause bone loss with aging, estrogen-deficiency, and glucocorticoid excess.
Our laboratory is interested in autophagy in osteoblast lineage cells in efforts to understand the role of autophagy in bone remodeling and age-related bone loss.
The overall goal of our research program is to better understand the role of the mitochondrion in health and disease. Areas of focus include studying the role of mitochondrial proton leaks in the regulation of metabolic rate, as well as studying the impact of lifestyle (i.e. diet/exercise) and pharmacological interventions on bioenergetics in several settings including developmental programming, obesity and trauma.
We are interested in understanding the mechanisms by which scavenger receptors regulate macrophage function in chronic inflammatory disease.
Dr. Qin's research focuses on cancer oncology and microbiology. He has an active NIH/NCI research award titled Periodontal Bacteria Enhance Oral KSHV Pathogenesis and Kaposi's Sarcoma Development in HIV+ Patients.
Pathogenesis of vulvar squamous carcinogenesis and pathognesis and classification of endometrial carcinoma.
My research focuses on the molecular genetics of longevity and age-associated diseases. I was trained in genetics, and turned to C. elegans as a model system in which to define and characterize genes that govern longevity. Using novel gene-mapping methods we developed, we discovered over 27 highly-significant loci for lifespan, resistance to stresses, and Darwinian fitness.
Primary areas of investigation are aimed at enhancing our understanding of cancer biology to discover and develop improved methods for cancer treatment. Our major future objective is to significantly and positively contribute to translational research and clinical practice.
The overall goal of my research is to elucidate the role of stress-induced molecular pathways on the skeletal effects of sex steroid deficiency and old age. Our work combines the use of genetic and pharmacological approaches in mice, with biochemical and molecular testing in cultured bone cells, to discover critical pathophysiological mechanisms and potential anti-osteoporotic therapies.
Skin cancer and inflammatory skin disease. Primary a clinical physician, but interested in and collaborate with translational research efforts. Not accepting students as a major advisor.
My research is focused on defining the mechanisms underlying the dynamics and combinatorial relationships of regulatory pathways implicated in the biology and pathobiology of the mammary gland and the uterus. We have a specific interest in elucidating the signaling pathways by which steroid hormone receptors, growth factors, cytokines and dietary components are engaged in the pathogenesis of breast cancer and uterine-associated diseases. We employ diverse cellular and molecular techniques and experimental models including gene arrays for gene discovery, cell lines for analyses of signaling pathways, and human and mouse models of diseases to address basic goals with translational potential.
The activity of primary sensory neurons is critical for the development and maintenance of persistent pain states. Following peripheral injury, primary sensory neurons show complex activity-dependent plasticity as a result of prolonged noxious stimuli and ectopic discharges. This altered activity in the primary sensory neurons is transmitted to spinal dorsal horn neurons and ultimately to the brain which results in persistent pain in a proportion of patients. While genetic studies have advanced our knowledge of nociceptive pathways, our current understanding does not explain variations in the susceptibility of individuals to the development of this cancer-related persistent pain. Common genetic variations in pain phenotypes show inconsistencies across studies6 and have not facilitated the development of new treatments. Epigenetic variations within the genome are known to cause misregulation of protein at a cellular level which may modulate nociception. My long term goal is to determine the contribution of epigenetic pathways to enhanced pain sensitivity and the establishment of cancer-related persistent pain. Specific research questions that I am eager to explore include (1) the association between altered chromatin structure in the dorsal root ganglion and cancer-related pain, and (2) cell-type specific changes in chromatin accessibility associated with chemotherapy-induced peripheral neuropathy.
My laboratory focuses on histone epigenetic mechanisms that regulate gene transcription and that are coupled to melanoma progression. We utilize a suite of techniques in our studies including proteomics of human biopsies, immunohistochemistry, cell culture, tumorigenicity assays, ChIPseq, biochemical and proteomic approaches for analyses of protein complexes, and cutting-edge mass spectrometry for the analysis of histone post-translational modifications.
We are using ‘third generation sequencing technology’ (such as Oxford Nanopore flow cells) to do metagenomics of clinical isolates and environmental samples.
My research focuses on the role of circulating blood platelets, in thrombosis, inflammation, and cancer
According to the CDC, more than 1 billion people, or one-sixth of the world’s population, is suffering from one or more Neglected Tropical Diseases with many of these diseases affecting the poorest populations in the developing world. Our lab focuses on the parasitic disease that results from Leishmania infection. We use a combination of mouse models and in vitro culture to define the cellular and molecular mechanisms that are important in the development of disease and the resolution of inflammation. More specifically, we are interested in the balance between the vascular and immune responses that lead to parasite control and those that promote lesion pathology.
In my lab, I conduct federally funded research that focuses on the Replication stress response and DNA damage repair mechanisms in normal and tumor cells after radiation therapy or chemotherapy. Understanding the interplay between defective DNA repair and cancer cell growth, as well as normal cell injury could lead to new avenues for both cancer prevention and personalized cancer treatment. My research team and I are motivated by an unyielding desire to find answers.
Young-Chen William Lu research focuses on the development of effective T cell-based immunotherapies for patients with metastatic cancers. Lu has played a pivotal role in the successful cancer treatments using the T-cell therapies targeting shared cancer antigens or patient-specific mutated antigens. More recently, he also utilizes single-cell sequencing technologies to facilitate the development of new T-cell therapies against cancer.
We are interested in the pathophysiology of multiple myeloma (MM), a B cell cancer characterized by proliferation of malignant plasma cells in the bone marrow, presence of a monoclonal serum immunoglobulin, and osteolytic lesions. We are investigating roles/mechanisms of PTH axis (PTH signal transduction) in MM development and therapeutic agents that target this axis. Additionally we are exploring the roles of Hypoxia (low oxygen tension) and microRNA (miRNA) in MM.
Dr. Zhan is interested in understanding how the genetic alterations in cancer cells contribute to tumor progression, alter treatment response and create vulnerabilities that may be targeted therapeutically.