Center for Diabetes and Endocrine Research (CeDER)



Active Members
Jennifer W. Hill, PhD.
Beata Lecka-Czernik, PhD.
Abraham D. Lee, PhD, PT.
Marcia F. McInerney, PhD.
Nikolai Modyanov, PhD.
Sonia M. Najjar, PhD.
Joshua J. Park, PhD.
Edwin R. Sanchez, PhD.
Cynthia M. Smas, DSc.
Stanislaw M. Stepkowski, PhD.
Guillermo Vazquez, PhD.

Associate Members
Cara Gatto-Weis, MD.

A. Active Members

Jennifer W. Hill, PhD. Assistant Professor in the Department of Physiology and Pharmacology.
Dr. Jennifer Hill received her PhD degree in Neuroscience from Northwestern University where she studied the role of neuropeptide Y in reproduction in the laboratory of Dr. Jon Levine. Her postdoctoral work investigating the hypothalamic regulation of food intake and glucose homeostasis began at Harvard University's Beth Israel Deaconess Medical center and was completed at UT Southwestern Medical Center (Dallas) in the laboratory of Dr. Joel Elmquist. Her primary interest is nutritional infertility and the impact of energy balance on the hypothalamic control of reproduction.

The brain blocks reproduction in animals under metabolic stress. About 5% of women of reproductive age suffer from infertility related to eating disorders. On the opposite end of the spectrum, obesity and diabetes also negatively affect fertility. As rates of these diseases rise, the need to unravel the hypothalamic homeostatic mechanisms controlling body weight and fertility and the interactions between these two systems is clear.

Within the hypothalamus, GnRH neurons maintain fertility and receive input from surrounding neurons involved in the regulation of food intake. The goal of research in the Hill laboratory is to (1) identify the circulating metabolic factors that are perceived directly or indirectly by GnRH neurons and convey information influencing GnRH release, and (2) to develop a clear picture of how the GnRH neuron interacts with surrounding neuronal subtypes leading to reproduction appropriately timed for periods of energy availability. Among other techniques, the laboratory uses interventional genetic studies to analyze the function of specific neuronal populations within the hypothalamus. By deleting receptors for adiposity signals only from POMC neurons, her laboratory has recently identified overlapping intracellular signals responsible for the maintenance of normal reproductive function.

Dr. Hill has authored 22 peer-reviewed articles. Her laboratory is funded from grants from the NIH and institutional funds. Top

Beata Lecka-Czernik, PhD. Professor in the Department of Orthopaedic Surgery and Head of CeDER Steering Committee.

Dr. Lecka-Czernik received her PhD degree from the Institute of Biochemistry and Biophysics, Polish Academy of Sciences in Warsaw, Poland. She then carried out her post-doctoral fellowship at the University of Arkansas for Medical Sciences in Little Rock, Arkansas, and moved up the academic rank there in the Department of Geriatrics and Reynolds Institute on Aging until she moved to the University of Toledo College Of Medicine in 2007.

Dr. Lecka-Czernik’s research focuses on diabetes, obesity, and osteoporosis. These diseases are major public health concerns due to their prevalence in our increasingly sedentary and aging society. At the cellular level, these pathologies share several features including a genetic predisposition, molecular controls and a common cell progenitor. Diabetics have display higher incidence of bone fractures and the process of fracture healing is affected. In addition, the use of antidiabetic TZD drugs increases fracture risk and causes bone loss in older diabetic postmenopausal women. Dr. Lecka-Czernik pioneered these findings and was the first to demonstrate that the anti-diabetic drugs TZDs cause loss of bone and affect fracture healing in animals. This has enabled her to lead the investigation of the underlying molecular mechanisms. She has also demonstrated that the side effect of TZDs on bone could be prevented by a slight modification, and is currently investigating the means by which diabetic bone homeostasis is improved by bone-specific gene and stem cell therapies, as well as pharmacological therapies with anti-osteoporotic drugs commonly used in clinics.

Dr. Lecka-Czernik has authored 45 peer-reviewed articles. Her laboratory has been funded from grants from the NIH and the American Diabetes Association. Top

Abraham D. Lee, PhD, PT. Associate Professor in the Department of Physical Therapy, College of Health Science and Human Service.

Dr. Lee received his MS in Exercise Physiology and Cardiac Rehabilitation from Northeastern Illinois University, MS in Physical Therapy from Texas Woman’s University and his Ph.D. from Arizona State University. Dr. Lee carried out his post-doctoral training on glucose uptake at the laboratory of Dr. J. Holloszy at Washington University in St. Louis prior to joining the University of Toledo as Assistant Professor in 2002.

The area of Dr. Lee’s research interest is the regulation of glucose and fat metabolism in normal or genetically modified animals during acute exercise and exercise training. More specifically, Dr. Lee is interested in identifying biological mechanisms underlying training-induced improvement in insulin sensitivity of skeletal muscle and other peripheral tissues. He is also interested in the role of genetics in improvement in glucose and fat metabolism with exercise training. Overall the purpose of his research is to advance exercise-based preventive measures against diabetes, heart disease, hypertension, and the metabolic syndrome.

Dr. Lee has authored more than 10 peer-reviewed articles. His research interest is fundamental to the growth of translational research in this institution. Top

Marcia F. McInerney, PhD. Distinguished University Professor of Medicinal and Biological Chemistry and Associate Dean for research and Graduate Studies in the College of Pharmacy and Pharmaceutical Sciences.

Major research interest of Dr. McInerney is in elucidating the underlying immunopathological mechanisms in diabetes with the hope that a better understanding of the molecular and cellular basis for the disease will lead to better diagnostic, preventative and therapeutic strategies.

A prime interest of her laboratory has been on studying the role of inflammation and cytokines in diet –induced obesity and diabetes. The work on obesity and type 2 diabetes was a USDA-funded research project with collaborator Dr. Sonia Najjar (Physiology and Pharmacology). Type 2 Diabetes is a complex disease usually involving abnormal metabolism resulting from both genetic predisposition and environmental factors. Diet and lack of exercise play critical roles in obesity, which may progress to diabetes and its complications. By identifying dietary and other environmental factors that act upon genetic predisposition, strategies may be developed and implemented to prevent obesity, diabetes and its associated diseases. As of November, 2005, 20.8 million Americans have diabetes and the cost to society has increased to $150 billion a year making the impact of diabetes highly significant in the United States. Recently, the American Diabetes Association indicated that of the live births in 2000, 1 out of every 3 will be diabetic in their lifetime and for minorities this is 1 in 2. These are horrendous statistics making the work on diabetes highly significant. The USDA work has resulted in five publications and one submitted paper, numerous meeting presentations, and seminars.

Another major basic science focus involves assessment of innate immune responses to oral pathogens in diabetes. Diabetes is a risk factor for severe periodontal disease caused by gram negative anaerobes. Previous studies suggest that both innate and adaptive immunity are involved in protection against periodontal infection. Innate immune responses are the first line of defense against infection. Innate immune system cells, such as macrophages, react to common microbial surface molecules through newly discovered receptors on the macrophage cell surface called Toll-like receptors (TLRs). Our purpose is to determine the role of TLRs in the initiation of host immune responses against oral pathogens in periodontal infection, using   the nonobese diabetic (NOD) mouse model of type 1 diabetes as well as animal models for type 2 diabetes. Macrophages respond to live bacteria and/or lipolysaccharide (LPS), derived from gram negative bacteria,by producing cytokines, expressing costimulatory molecule(s), fluctuating the TLR mRNA and protein levels and promoting TLR signal transduction. These events are essential for macrophage activation and initiation of specific adaptive immune responses for the generation of antigen specific cells. Macrophage activation in response to bacteria or LPS from oral pathogens will be compared in diabetic and nondiabetic mice. The working hypothesis is that a defect in innate immunity in diabetes contributes to the susceptibility to periodontal infection since it is likely that the interaction between the TLR and the oral pathogen initiates immune responses.   This work was funded by NIH.

Innate immunity was also the focus of my 2008 sabbatical at the University of Michigan in the Department of Internal Medicine, the Division of Metabolism, Endocrinology and Diabetes. Two review papers on innate immunity and diabetes were generated associated with this sabbatical.

Another major aspect of Dr. McInerney's research is focused on the autoimmune aspects of Type 1 or insulin-dependent diabetes, using the nonobese diabetic (NOD) mouse as a primary model. In humans and the NOD mouse, insulin-dependent diabetes is inherited. Autoantibodies to insulin and islet cells are produced, and T lymphocytes invade the islets in the pancreas. T-cell invasion or insulitis is associated with destruction of the insulin-secreting beta cells. In the NOD mouse, insulitis begins at 4-6 weeks of age, however the mice do not spontaneously become diabetic until 3 to 6 months of age, at which time sufficient beta cells have been destroyed to result in the loss of insulin secretion. Other investigators have shown that the insulin receptor (IR) can function as a chemotactic receptor capable of directing cell movement in response to a gradient of insulin. Published data from my laboratory has shown that flow cytometry sorted T lymphocytes, from diabetic NOD mice, expressing a high density of insulin receptors (IR+ T cells) aggressively transfer insulitis and diabetes while T cells with low to negative IR expression (IR- T cells) are capable of neither. An association of IR+ T cells with an increased risk for diabetes would provide a new target for drug therapy. Furthermore, chemotactic signaling and metabolic signaling are mediated by distinct parts of the insulin receptor and could therefore, be selectively targeted for therapeutic intervention prior to diabetes onset. Current research in my laboratory involves the development of flag tagged, T cell specific, IR transgenic mouse on a background that does not spontaneously become diabetic to determine if movement of T cells into an islet can be based on IR expression. We have been successful in two new transgenic models and now wish to make a transgenic mouse that has IR expression on the surface of Tregs to prevent the development of type 1 diabetes. Translational work has indicated increased number s of IR+ T cells in high risk relatives and further collaborative translational work is in development. Over time, this work has received funding nationally by NIH, American Diabetes Association, and Juvenile Diabetes Research Foundation.

Collaborative work with Dr Quinn (Biological Sciences) has been on autoantigens and cytokines in Type 1 Diabetes in animal models. New collaborations with Drs Quinn, Wall (Medicinal and Biological Chemistry) and Sucheck (Chemistry) involve construction of a bioconjugate platform containing autoantigenic peptides to screen mouse models and diabetic patient’s pheripheral blood for responses to specific autoantigens in diabetes and the use of altered peptide ligands to examine possible turn off of responsiveness. This work could produce possible future peptide therapy (customized medicine) based on an individual person’s responses.   Early work on autoantigens was funded by a Career Development Award from the American Diabetes Association.

Collaborative work with Joslin Diabetes Center/Harvard University involves beta cell surrogates for islet transplantation.|

Dr. McInerney has authored 26 peer-reviewed articles, her research has been supported by NIH, USDA, American Diabetes Association, Juvenile Diabetes Research Foundation, Central Ohio Diabetes Association, Diabetes Action Research and Education Foundation, The Iacocca Foundation, and the Ohio Board of Regents. Top

Nikolai N. Modyanov Ph.D., D.Sc, Professor in the Department of Physiology and Pharmacology

Dr. Modyanov received his PhD in from the Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry , Moscow, Russia in 1973, where he subsequently was doing research for 25 years. Professor Modyanov was a Head of Laboratory of Membrane Biochemistry since1986. In 1994 he joined the University of Toledo College of Medicine as Professor of Pharmacology.

For more than 30 years Dr.Modyanov's research was focused on the molecular aspects of ion transport across biological membranes, and primarily on the structure-function relationship of the ion-transporting ATPases that are receptors for cardiotonic drugs (Na,K-ATPase) and antiulcer drugs (H,K-ATPase).

New direction of his research resulted in discovery of the unique BetaM proteins encoded by ATP1B4 genes, members of X,K-ATPase gene family. He determined that ATP1B4 genes represent a rare instance of orthologous vertebrate gene co-option that created fundamental changes in the physiological roles and functional properties of the encoded proteins. In lower vertebrates BetaM is a subunit of Na,K-ATPase. In placental mammals BetaM-proteins lost their ancestral functions and acquired entirely new functions as proteins in the inner nuclear membrane of heart and skeletal muscle, which regulate gene expression and signal transduction acting specifically during a critical period of perinatal development and adult muscle regeneration.

These findings clearly indicate that placental mammals should have a hitherto unknown physiologically important necessity, which did require evolutionary forces to trigger co-option of the X-chromosome gene ATP1B4 and fundamental changes in the functional properties of the BetaM proteins.

To better understand the physiological role of the mammalian BetaM, Dr.Modyanov developed Atp1b4 knockout mouse model and determined that BetaM deficiency sharply decreased level of expression of a major myogenic regulatory factor MyoD and slow down mouse general body development and growth. Moreover, the survival rate of Atp1b4-/Y males and homozygous Atp1b4-/- females is significantly lower than that of male wild type and heterozygous female littermates, respectively.

Most importantly, Atp1b4 knockout males, which survived to adulthood, upon feeding by a high-fat diet showed far less weight gain, are resistant to   diet-induced obesity, exhibit enhanced insulin sensitivity and improved glucose tolerance compared with wild type littermates. Studies on the molecular basis of these beneficial effects of BetaM ablation on dietary fat metabolism are now in progress.

Dr.Modyanov has authored more than 150 peer-reviewed articles. His current research is supported by CeDER. Top

Sonia M. Najjar, PhD. Professor in the Department of Physiology and Pharmacology and Director of the Center for Diabetes and Endocrine Research (CeDER).
Dr. Najjar earned a PhD degree in Physiology at Stanford University School of Medicine in 1989, and completed her post-doctoral fellowship training at the Diabetes Branch at the NIH in 1994. Subsequently, she joined the faculty of the Department of Pharmacology at the University of Toledo College of Medicine at the Assistant Professor rank. In 2006, she became Founding Director of CeDER.

Dr. Najjar’s research focuses on identifying the genetic and environmental interactions underlying obesity, type 2 diabetes and their cardiovascular complications.

The laboratory pioneered the finding that CEACAM1 plays a key role in regulating insulin action by promoting insulin clearance in liver. By generating mouse models of loss- or gain-of function of this protein, the Najjar team observed that genetic inactivation/deletion of this protein causes insulin resistance, obesity and fatty liver disease, in addition to predisposing to type 2 diabetes and Non-alcoholic steatohepatitis (NASH) in response to high-fat diet. Current studies focus on the role of CEACAM1 in the pathogenesis of atherosclerosis and common types of cancer.

The Najjar laboratory also investigates the central role of CEACAM2 proteins in insulin secretion and energy balance.

Dr. Najjar has published more than 60 peer-reviewed original research articles with seminal work in leading journals and more than 10 book chapters on diabetes and insulin action.

Dr. Najjar has attained an international acclaim, delivering lectures in major national and international meetings.
Her research has been continuously funded by the National Institutes of Health and other funding agencies. Top

Joshua J. Park, PhD. Assistant professor, Department of Neurosciences

Dr. Park received his Ph.D. from Johns Hopkins University and did his postdoctoral training in the National Institute of Health (NIH). During his postdoctoral work at NIH, he worked in the laboratory of Dr. Y. Peng Loh who is an authority in the field of the metabolic diseases, type 2 diabetes and obesity. Under Dr. Loh’s guidance, he extended his expertise in microtubule-based vesicle and protein transport in the context of metabolic diseases and won several research awards. He joined the Department of Neurosciences at the University of Toledo College of Medicine in 2009. His research focuses on characterization of the molecular mechanism(s) by which the regulated secretion of neuropeptides in the hypothalamus and hippocampus is disrupted by dietary pattern, environments, and genetic predisposition.

Obliteration of secretion of hypothalamic anorexigenic neuropeptides contributes to the development of type 2 diabetes (T2D) and obesity in adults and children. The molecular mechanism(s) by which anorexigenic neuropeptide secretion in the hypothalamus is regulated are poorly understood. Similarly, little is known about how anorexigenic neuropeptide secretion becomes impaired during high-calorie food diet (HFD) and early in T2D. Our research goals are to provide a fundamental understanding of the regulated secretion of anorexigenic neuropeptides in hypothalamic neurons and how pre-diabetic conditions disrupt the hypothalamic neuropeptide secretion, resulting in exacerbation of T2D and development of obesity. The outcome of our research will advance scientific knowledge to find a therapeutic targetfor effective treatment of type 2 diabetes and obesity.

Dr. Park has authored 17 peer-reviewed articles and book chapter. His research has been funded from grants from the NIH and University of Toledo. Top

Edwin R. Sanchez, PhD. Professor in the Department of Physiology and Pharmacology and Vice Director of CeDER.

Dr. Sanchez received his PhD in Human Genetics from the University of Michigan in 1983, where he subsequently carried out a post-doctoral fellowship and served as Assistant Research Scientist in the Department of Pharmacology until he joined the University of Toledo College of Medicine at the rank of Assistant Professor in 1989.

Dr. Sanchez’s research focuses on the steroid hormone receptors, with an emphasis on the tetratricopeptide repeat (TPR) proteins that act as molecular chaperones to the receptors. These chaperone proteins include: FK506-binding protein 52 (FKBP52), FKBP51, protein phosphatase 5 (PP5) and cyclophilin 40 (Cyp40).

Steroid hormones are a large class of cholesterol-derived molecules, which serve to control the functional states of a variety of cells and target tissues. These hormones include progestins, estrogens, androgens, mineralocorticoids and glucocorticoids. Many important endocrine and physiological processes are controlled by these hormones, including immunity and inflammation, glucose and fatty acid metabolism, male and female reproduction, and blood pressure. The central thrust of the research program is to understand how the TPR chaperones described above contribute to the actions of steroid receptors at the molecular, cellular and physiological levels.

The most recent findings at the Sanchez laboratory suggest that the TPR chaperones act as tissue-selective modulators of steroid receptor physiology. FKBP52 was found to exert a stimulatory effect on progesterone receptor action only in the uterus and not in other female reproductive organs. Similarly, FKBP52 is needed for the androgen receptor contribution to embryonic development of select male reproductive organs, such as the prostate gland, but not others. Both FKBP51 and Cyp40 were found to be critically important to androgen receptor action in the adult prostate gland, and may be key factors necessary for the onset and progression of prostate cancer.

Most recently, the laboratory has uncovered an interesting and unique reciprocal relationship between FKBP52 and FKBP51 on the activity of glucocorticoid receptors in liver, muscle and adipose tissues. Reciprocal modulation of the glucocorticoid receptor is such that these two chaperones serve to either increase or decrease the involvement of glucocorticoid receptors in development of metabolic syndrome and propensity to type 2 diabetes.

Taken as a whole, this investigative effort has identified TPR proteins as novel and potentially important targets for drug development against male and female infertility, prostate cancer, and metabolic disorders, such as diabetes and obesity.

Dr. Sanchez has authored 68 peer-reviewed articles. His research has been continuously funded by grants from the NIH. Top

Cynthia M. Smas, DSc. Associate Professor in the Department of Biochemistry and Cancer Biology.

Dr. Smas received her D.Sc. in Nutritional Biochemistry from Harvard University in 1994, and completed her postdoctoral training at the Division of Nutritional Sciences and Toxicology, University of California, Berkeley, in 2000 when she joined the University of Toledo at the Assistant Professor rank.

Dr. Smas is studying adipogenesis and the molecular basis of visceral obesity. The laboratory has identified novel gene products with adipose tissue-specific expression and hormonal regulation. Characterization of their function in the pathogenesis of obesity and its co-morbidities is underway.

Dr. Smas has authored 34 peer-reviewed articles. Her research has been funded by grants from the NIH. Top

Stanislaw M. Stepkowski, PhD. Professor in the Department of Medical Microbiology and Immunology.

Dr. Stepkowski received his Ph.D. and D.Sc. from the Polish Academy of Sciences, Warsaw, Poland. He carried out his post-doctoral training at Radium Hospital, Oslo, Norway and at Dalhousie University, Halifax, Nova Scotia, Canada. He began his academic career at the rank of Assistant Professor at the University of Texas Medical School, Houston, where he remained until he joined UT College of Medicine in 2007.

Dr. Stepkowski’s research interests are in cell and organ transplantation, with focus on improvement of long-term allograft survival and development of new immunosuppressive modalities. More specifically, the laboratory focuses on the cytokine-mediated Jak3/Stat-dependent signals leading to proliferation and differentiation of activated T cells. Based on screening of multiple compounds from NIH database, the laboratory has developed a selective Jak3 inhibitor (NC1153), which may inhibit kidney allograft rejection in rats and cynomolgus monkeys. Most of this work has been published in the Journal of Immunology, Blood, and Transplantation.

Dr. Stepkowski had investigated a sphingosin-1-phosphate receptor (S1P) agonist, FTY720 (2-amino-2-2-[4[octylphenyl]ethyl)propane-1,3-diol hygrochloride), which inhibits allograft rejection. However, this promising compound was abandoned following clinical kidney trials because of its side effects, and in particular bradycardia and hypertension, which occurred because of poor selectivity of this compound. Over the last 2 years, the laboratory has tested a novel compound, KRP203 (2-amino-2-propanediol hydrochloride), with selective agonist activity on S1P1. Recent results showed that KRP203 not only extends allograft survival of kidney allografts but also induces transplantation tolerance to pancreatic islet allografts when combined with local infusion of T regulatory cells. One cannot overemphasize the implication of this work on type 1 diabetes.

More recently, the laboratory showed that a short therapy with anti-T cell receptor (TCR) monoclonal antibody prevented development of Type 1 Diabetes (T1D) as well as blocked onset of the disease in two mouse models. These results correlated with significant expansion of CD4+Foxp3+ regulatory T (Treg) cells. Furthermore, the laboratory has shown that anti-TCR mAb did not produce a cytokine storm similar to anti-CD3 mAb, the latter therapy is currently used in clinical trials. The plan is to produce humanized anti-human TCR mAb, which will be tested in vivo in humanized mouse model of islet and vascularized artery transplantation.

Dr. Stepkowski has developed multiple collaborations with other members of CeDER to investigate the role of the immune response in the pathogenesis of obesity and obesity-induced diseases, including diabetes, non-alcoholic steatohepatitis (NASH) and atherosclerosis.

Dr. Stepkowski has authored more than 150 peer-reviewed articles. His research has been continuously funded by grants from the NIH. Top

Guillermo Vazquez, PhD. Assistant Professor in the Department of Physiology and Pharmacology.

Dr. Vazquez received his Ph.D. from the Universidad Nacional del Sur in Bahia Blanca, Argentina. Before he joined the University of Toledo College of Medicine in February 2007, he was a Research Fellow in the Calcium Regulation Group in the Laboratory of Signal Transduction at the National Institute of Environmental Health Sciences in North Carolina.

Dr. Vazquez focuses on the role of Ca2+-dependent signaling via Transient Receptor Potential Canonical (TRPC) channels in endothelial dysfunction/inflammation associated with atherosclerosis, a chronic inflammatory vascular disease that represents the leading cause of death in western societies and the main vascular complication of diabetes, metabolic syndrome and obesity. Mammalian TRPC proteins (TRPC1 through TRPC7) form channels typically activated downstream receptor-dependent stimulation of phosphoinositide-specific phospholipase C (PLC). They take part in the action of various PLC-coupled receptors for transmitters, peptides and growth factors that modulate diverse vascular functions, such as vascular tone and permeability, secretion, endothelial cell proliferation and apoptosis. Whereas the importance of the role of Ca2+ channels in endothelial cell physiology and pathophysiology has received increasing appreciation over the last decade, the current understanding of its role in the signaling pathways underlying inflammatory vascular disease is in its infancy. Dr. Vazquez’s group has recently pioneered the demonstration that endothelial TRPC3 is fundamental within the signaling underlying regulated expression of VCAM-1 and monocyte adhesion in response to pro-atherogenic factors, two critical events in early and advanced stages of atherosclerotic lesion development. These findings led to the generation of two novel mouse models of atherosclerosis with endothelial-specific gain- and loss-of-function for TRPC3. These new mouse models are essential in elucidating the impact of Ca2+ channel expression/function in the pathogenesis of atherosclerosis.

Dr. Vazquez has authored 56 peer-reviewed articles. His laboratory has been funded from grants from the American Heart Association and promises upcoming funding by the NIH. Top

B. Associate Members

Cara Gatto-Weis, MD. Assistant Professor in the Department of Pathology.

Dr. Cara Gatto-Weis received her MD degree from the University of Medicine and Dentistry of New Jersey - Robert Wood Johnson Medical School, New Jersey. She carried out her residency training in Anatomic and Clinical Pathology, as well as fellowships in Surgical Pathology and Cytopathology, at Drexel University College of Medicine in Philadelphia, Pennsylvania. She then served as Chief Resident in Pathology, until she joined the University of Toledo College of Medicine in 2003.

Dr. Gatto-Weis’ special clinical interests include fine needle aspiration and diagnosis of palpable lesions, in addition to oncologic surgical pathology. She has been actively involved with CeDER, serving as its pathology director and collaborating with several CeDER investigators in the interpretation of mouse histology for the past 3 years. Her current collaborations with Dr. Najjar include investigation of the role of PTEN and CEACAM1 genes as tumor suppressor genes in multiple organ systems, including endometrium, prostate and lymphoid tissues, and how these pathways mediate the link between these types of cancer and metabolic and inflammatory disorders such as non-alcoholic steatohepatitis (NASH).

Dr. Gatto-Weis has authored 3 peer-reviewed journal articles and more than 5 clinical articles and book chapters. Her research interest is fundamental to the growth of translational research in this institution. Top

Last Updated: 10/29/15