UW Medicine Pathology has a strong focus on basic science and clinical research. Our research principle, followed since the establishment of the University of Washington School of Medicine, is that research based on the most modern methods and the up to date knowledge of basic sciences is an essential component of an academic department of pathology. This is particularly true at the present time when new discoveries generated by basic biomedical research are applied to pathology practice. The research done by our faculty has received high recognition both nationally and internationally.
Below is a roster of Department of Pathology research laboratories:
The Akilesh lab uses functional genomic, 3D culture systems and digital spatial profiling methods to study kidney disease and kidney cancer.
The Alpers Laboratory of Renal Pathology has research interests which include experimental renal disease, diagnostic human renal pathology, developmental renal biology, and solid organ transplant rejection.
The Bornfeldt Laboratory is dedicated to understanding the cellular and molecular mechanisms of diabetes-accelerated cardiovascular disease, so that these complications can be effectively treated or prevented.
The focus of the Byers Research Laboratory is to identify and characterize the molecular bases and disease mechanisms responsible for heritable disorders of bone, blood vessels, and skin. The major genetic disorders studied in the lab include all forms of osteogenesis imperfecta (OI) and Ehlers-Danlos syndrome (EDS); Loeys-Dietz syndrome, familial aneurysm syndromes and other similar disorders. The Byers Research Lab is housed alongside the Collagen Diagnostic Laboratory, a certified clinical laboratory that provides testing and consultation for patients and their families with suspected connective tissue disorders and the associated clinicians.
The Chen Lab's main research interest is in understanding pathogenesis of cancer using zebrafish and mammalian experimental systems. Their current research focuses on dissecting cellular and molecular mechanisms underlying the pathogenesis of pediatric rhabdomyosarcoma, in particular the key events regulating tumor differentiation, relapse and metastasis. Chen laboratory utilizes the strategies of chemical genetics, functional genomics and genome engineering to identify key driver events of rhabdomyosarcoma.
The mission of the Crispe lab is to understand liver immunology. Therefore, the Crispe lab investigates both innate immunity and T cell immunity in the liver, and the way both kinds of immune processes can lead to or protect against liver injury, cell death and liver fibrosis.
The Darvas Research Laboratory focuses on brain circuits as well as structural and molecular bases of learning and memory, the study of mouse brains in aging and Alzheimer’s disease models, investigation of pharmacological therapeutics aimed at preventing or reversing dementia and pathologic processes associated with progressive Alzheimer’s disease, and development of state-of-the-art quantitative neuropathology assays for Alzheimer’s disease pathologic changes in frozen and formalin-fixed autopsy tissue.
The Davis Lab is focused on uncovering the mechanistic basis for how the heart heals, repairs, and remodels in response to injury and disease. We are tackling the fundamental problem in which contractile muscle is replaced by fibrotic scarring by resolving the cellular and molecular basis for fibrotic scar formation. In addition, we have demonstrated that intracellular and extracellular biomechanical signals are central determinants of maladaptive cardiac remodeling. In lieu of this result, our lab seeks to understand how cell and tissue forces are sensed and transduced into changes in cell geometry, differentiation, and proliferation.
The goal of the Disteche Lab is to understand the mechanisms of dosage compensation by X up-regulation of the single active X chromosome of males and females in terms of molecular processes.
Neurotoxicology associated with heavy metal exposure
The Horwitz Lab employs genetic mapping and sequencing strategies to identify genes responsible for familial predisposition to leukemia, lymphoma, and bone marrow failure syndromes. This lab has successfully identified genes responsible for human cyclic neutropenia, canine cyclic neutropenia, severe congenital neutropenia (Kostmann syndrome), Hodgkin’s lymphoma, myelodysplasia and acute myeloid leukemia, and, recently, acute lymphocytic leukemia.
Research in the Kaeberlein Lab is focused on developing therapies for age-associated diseases by targeting the pathways that regulate aging.
The Keene Lab focuses on Alzheimer's disease, Parkinson's disease and toxicity.
The Kennedy Lab's main interest is the intersection of aging and the accumulation of somatic mutations (in both mitochondrial and nuclear genomes) in age-related diseases
Over the last 15 years, the HPV research group has conducted a variety of studies focused on HPV and HPV related cancers.
The Latimer Lab studies the molecular mechanisms that underlie resilience and resistance to Alzheimer’s disease neuropathologic change
The Loeb's Lab research is centered on the molecular biology of mutagenesis, and our goal is to understand the relationships between DNA damage, mutations and cancer. Our current work involves the study of the fidelity of DNA replication, an analysis of mutator phenotypes in human cancers, the creation of new enzymes for cancer gene therapy, the relationship of mutations to aging, and the prevention of HIV replication by mutagenic nucleoside analogs.
The Martin and Oshima Lab investigates mechanisms of biological aging.
The Mendenhall Lab is working to understand the fundamental aspects of gene expression regulation. They are focused on understanding how epigenetic and stochastic differences in gene expression affect the manifestation of traits like lifespan and cancer. Understanding the basic biology of gene expression will allow us to collectively affect change in human health and disease.
The Monnat Lab is located in the UW Departments of Pathology and Genome Sciences in Seattle. Our research is focused on the mechanisms that ensure human genomic stability and determine cancer therapeutic response. We also develop and apply genome engineering tools to advance biology and disease treatment or prevention.
The Murphy Lab is dedicated to studying the biology of Plasmodium parasites that cause malaria and our immune response against them in order to make highly effective and long-lasting malaria vaccines. To study these infections, the laboratory uses specialized immunology and diagnostic techniques in mice, non-human primates, and humans.
Since 1996, the Murry Lab has worked to understand the mechanisms that underlie cardiovascular disease and to develop new treatments. We have a longstanding interest in the biology of myocardial infarction (heart attacks), and in particular, how the heart heals after infarction. The lab has a major focus in stem cell biology and tissue engineering, where we seek to understand the molecular basis for cardiovascular differentiation, and to harness the potential of stem cells to repair the heart. Recently, our group has begun to use stem cell approaches to study genetically based cardiomyopathies.
Najafian Lab research strives to better understand pathobiology of kidney diseases.
The Oshima Laboratory is interested in the genetic mechanisms of aging and age-related disorders with a special emphasis on the progeroid syndromes. In the past 15 years, our main focus has been the genetics and pathogenesis of Werner syndrome.
The Promislow Lab works on the evolutionary genetics of life history strategies and sexual selection, bringing a systems biology perspective to the study of natural genetic variation for traits relevant to fitness and disease. We use empirical, epidemiological, bioinformatic and theoretical approaches in studies on a variety of organisms, from flies and mice to dogs, marmosets and humans.
The primary focus of the Rabinovitch Laboratory's research is on the use of genetically altered mouse models to examine the effects of cell signaling and reactive oxygen species (ROS) on lifespan and healthspan. Transgenic mice that overexpress catalase have been found to be protected against multiple health challenges, including cardiac aging, sarcopenia and some cancers. A second area of lab interest is studies of neoplastic progression. These focus on precancerous human gastrointestinal diseases and the hope that a better understanding of these disease processes will yield improved management of individual patients and their cancer risk.
The Rea Lab is working to define the fundamental molecular causes of aging and makes use of several model organisms ranging from worms to mice. Areas of special emphasis include mitochondrial dysfunction and retrograde signaling, human cellular senescence and life extending interventions.
The Risques Lab studies the early steps of cancer progression and works on translating this knowledge into biomarkers for early cancer detection and prediction. We are especially interested in alterations that link cancer and aging including somatic mutation, telomere shortening, and mitochondrial dysfunction. We have developed and optimized genetic methods to quantify these alterations with high sensitivity with the ultimate goal of understanding early cancer progression and enabling cancer prediction and prevention.
The Stewart & Shi Lab's research focuses on understanding the molecular mechanisms of development and progression of neurodegenerative disorders (including Alzheimer's and Parkinson's diseases), and exploring unique biomarkers for diagnosing the diseases and monitoring their progression.
The focus of the lab, in collaborative projects, is to identify and determine the clinical importance of novel phenotypes of prostate cancer, using open top light sheet microscopy and immunohistochemistry.
The primary research in this laboratory is focused on delineating the mechanisms of transcriptional regulation of voltage-gated cardiac ion channel underlying ventricular tachycardia/fibrillation in ischemic heart disease (IHD). Ongoing studies in the lab are focused on defining the suppressive effect of enhanced Wnt/b-catenin signaling on cardiac NaV1.5 expression, leading to decreased Na+ channel activity, decelerated depolarization and development of VT/VF in IHD.
The Young lab is interested in determining the molecular and cellular mechanisms behind genetic risk for late-onset sporadic Alzheimer’s disease (SAD), the most common neurodegenerative disorder.