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An NCI-designated Comprehensive Cancer Center, affiliated with the University of Pittsburgh School of Medicine
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Dr. Daley is a junior faculty physician scientist in the Division of Pediatric Hematology-Oncology with a research focus on the immunobiology of pediatric sarcomas. Her current research focuses on Ewing sarcoma and understanding the tumor immune microenvironment of this rare, aggressive adolescent and young adult cancer. In addition to her translational research in Ewing sarcoma, Dr. Daley also helps to lead the Adolescent and Young Adult oncology working group, a shared program between UPMC Children's and Hillman Cancer Center aiming to improve the care of adolescent and young adult patients with cancer at our institution.
My research interests are in translational science. Specifically, I am interested in designing early-phase clinical trials based on an improved understanding of tumor immunobiology and host-tumor-microenvironment interactions. Additionally, I am interested in the mechanisms underlying non-response to checkpoint inhibition and novel approaches to overcome this non-response. My clinical interests are in the management of advanced melanoma and the development of early phase studies to test novel immunotherapeutic approaches singly and in combination in patients with advanced cancer.
Dr. Davis is a Professor in the Departments of Neurobiology and Medicine at the University of Pittsburgh. During his 35 years of running his own laboratory he as developed three main research programs. The first research program explores normal function of visceral afferents primarily in the colon, bladder and pancreas and how afferent function changes with disease. The second project uses optogenetics to study communication between colon sensory neurons, enteric neurons, interstitial cells of Cajal (ICC), colon epithelium and postganglionic sympathetic neurons with the goal of developing a comprehensive connectome. The third program employs a genetic mouse model of human pancreatic ductal adenocarcinoma (PDAC) to study the role of the nervous system in pancreatic cancer (Cancer Res. 2014, 74:1718) and was the first to show that sensory denervation of the pancreas can slow or halt development of tumors (PNAS 2016, 113:3078). Dr. Jami Saloman, his collaborator, went on to show that depletion NGF could prevent metastasis in PDAC (Pancreas, 2018, 47:856). In separate studies his lab reported that sensory neurons express immune checkpoint proteins (J. Neurosci, 2020, 40:7216), and Dr. Salomon has shown that PDL1 signaling is present in sensory neurons and modulates responses to nociceptive stimuli (Brain, Behav and Immun. 2022, 106:233). The unifying theme of all of three projects is that studying any one cell system (e.g., neural, immune, vasculature) in isolation is unlikely to produce robust findings because these systems evolved together, in an integrated manner.
I investigate longitudinal patterns of drug use and reproductive health in pregnant and parenting people. I take a developmental approach, meaning that I am interested in the timing of behavior within the context of important life events such as puberty, adolescence, young adulthood, pregnancy, and menopause. I am also interested in better understanding health-risk behaviors within the context of families, systems, and communities, including the impact of pervasive structural racism and discrimination, sexism, and heterosexism.
The Deiters Lab works in the areas of Chemical Biology and Synthetic Biology, with the goal of developing novel approaches toward a better understanding of human health and disease. This includes 1) the discovery of small organic molecules that inhibit or activate specific biological pathways. Our discovered microRNA inhibitors have therapeutic implications in cancer and viral infections. 2) We are developing methods for specific covalent modification of proteins and cell surfaces with applications in inhibition of protein function and immunotherapy. 3) We are genetically re-wiring the circuitry of cells in order to give new functions to proteins and organisms. Our approach is based on the expansion of the genetic code with synthetic, unnatural amino acids. 4) Light is a unique control element that enables the regulation of biological processes with high spatial and temporal resolution. We are engineering light-responsive nucleic acids and proteins and are applying them to the optical control of cell signaling, gene editing, and protein degradation.
My research interests include:
1. Immune-oncology and immune microenvironment in Hepatocellular Carcinoma
2. Role of scaffold proteins (e.g., IQGAP1) in liver disease and regeneration.
3. Developing a more accurate model of Hepatocellular Carcinoma that efficiently replicates the human disease.
My overall goal is to challenge the unmet need of effective targeted therapies for Hepatocellular Carcinoma (HCC) by studying the immune landscape to develop personalized immunotherapies for HCC. Additionally, it is my goal to develop a model of HCC that better represents the human disease such that novel therapeutic strategies are easily translated into patients. Finally, to tie these goals together, I aim to better understand the molecular mechanisms that contribute to hepatocellular carcinogenesis. For example, I plan to continue studying IQGAP1, a scaffold protein, and its role in hepatocellular biology. Investigating protein-protein interactions regulated by IQGAP1 will expand the current knowledge of HCC and position me as an independent investigator focusing HCC biology and therapeutics.
In recent years, the decades-long promise of tumor immunotherapy has finally begun to come to fruition. Checkpoint blockade, for example, represents a critically important intervention for potentiating the antitumor immune response. In these therapies, blockade of T cell intrinsic negative regulators (such as CTLA-4 and PD-1 signaling) releases the brake on effector T cells in the tumor, resulting in substantial, durable antitumor immunity, and clinical responses.
While negative regulators on the effector T cells can be relieved through these interventions, effector T cells still face a variety of cell extrinsic modes of immune suppression, notably through suppression via regulatory T (Treg) cells. Treg cells play critical roles in preventing autoimmune responses to self tissues as well as limiting immunopathology during exuberant immune responses. However, Treg cells represent a major barrier to antitumor immunity. Many tumors recruit, activate, and expand large numbers of Treg cells, which can be specific for any number of normal, self antigens expressed by the tumor. While depletion of total Treg cells can result in autoimmune pathologies, inhibition of Treg cell stability or function has been shown to allow for local inhibition of Treg cell suppression in the tumor, while sparing normal tissues from an autoimmune response.
Thus, finding phenotypic, signaling, or functional parameters that distinguish intratumoral Treg and conventional T (Tconv) cells could shed light on mechanisms by which Treg cells could be targeted to allow for a greater antitumor response. Recent studies have found that Tconv and Treg cells have distinct metabolic requirements. Not unlike cancer cells, conventional T cells undergo aerobic glycolysis (the 'Warburg effect') when undergoing robust expansion. However, regulatory T cells utilize alternative sources of fuel. Our initial findings in the laboratory suggest that not only do intratumoral Treg cells utilize distinct fuel from their conventional brethren, but engage different metabolic pathways from Treg cells in normal tissues and lymphoid organs. This suggests that metabolic pathways, or their downstream targets, could be targeted in order to inhibit intratumoral Treg cells specifically, releasing a crucial cell extrinsic brake on the antitumor immune response. The goal is to provide alternative modalities of therapy that could be utilized alone or in combination with other immunotherapeutic strategies, to allow for robust and durable immune responses for the eradication of cancer.
My training is in molecular cancer and environmental epidemiology. Through my doctoral and postdoctoral research, I developed skills in advanced statistical analysis and programming, genetics, epigenomics, and cancer registry analysis. Given my data science skills and ability to translate data results to practice (e.g. grants, research directions, clinic), I was hired to serve as collaborator and resource for HCC investigators and as bridge between the epidemiology and biostatistics groups at HCC. My research interests focus on 1) utilizing cancer registry data to explore socio-economic, racial, and environmental disparities in cancer incidence and mortality and 2) exploring the interplay among toxicants, aging, and dynamic genomic features (e.g., telomeres, DNA methylation and somatic mutations) and the effect of this interplay on cancer development and prognosis. My current research profile at HCC includes characterizing cancer incidence, mortality, and survival disparities and trends in western PA, examining radon and fracking exposures on cancer risk in PA, and evaluating genetic predictors associated with head and neck cancer survival. I plan to become more involved in projects related to environmental somatic mutational signatures in cancer, DNA methylation biomarkers in cancer detection, risk, and prognosis, and other epigenomic and genomic studies of cancer risk and survival.
Terence S. Dermody is the Vira I. Heinz Distinguished Professor and Chair of Pediatrics at the University of Pittsburgh School of Medicine and physician-in-chief and scientific director at UPMC Children’s Hospital of Pittsburgh. He also is professor of microbiology and molecular genetics at the University of Pittsburgh School of Medicine.
With over 36 years of experience in basic virology and viral pathogenesis research, at his core, Dermody is a virologist. Most of his research has focused on reovirus, an important experimental model for studies of viral encephalitis in the young. His research contributions have enhanced an understanding of how these viruses enter into host cells and cause organ-specific disease.
Learn more about Dr. Dermody's work.
The purpose of my laboratory’s research is to investigate the effects of environmental exposure on the host. We are particularly interested in infection and immunity on the lung and its associated pathophysiological response during injury, repair, and regeneration. The primary focus of my current research is the cellular and molecular actions of exposures to toxic chemicals and microorganisms that underlie the pathogenesis of chronic human diseases. Areas of research: 1. Lung epithelial cell phenotype, differentiation, and function upon exposure; 2. Inflammation-associated tissue remodeling and lung tumorigenesis; 3. Development of novel antibiotics to overcome antimicrobial resistance (AMR).
Dr. Diergaarde's research examines the role of diet, lifestyle and genetic variation in the development, progression and treatment of cancer, including cancers of the lung, head and neck, colon, ovaries and breast, and aims to identify markers for risk stratification, early detection and response to treatment. She is currently Co-Leader of Project 2 of the UPCI Specialized Program of Research Excellence (SPORE) in Lung Cancer. This project seeks to establish the relationship between vitamin D exposure, pulmonary inflammation and lung cancer risk and so provide strong rationale for a vitamin D-based approach to lung cancer prevention. She is also Leader of Project 1 of the UPCI SPORE in Head and Neck Cancer. Using data and samples from a large, clinic-based case-control study, this project investigates the role of genetic variation and gene-environment interactions in the development, progression and treatment of head and neck squamous cell carcinoma.
Dr. Vera Donnenberg is an Associate Professor of Cardiothoracic Surgery in the School of Medicine at the University of Pittsburgh with a secondary appointment in the Department of Pharmaceutical Sciences in the School of Pharmacy. Dr. Donnenberg’s research focuses on tumorigenic stem cells in lung cancer, esophageal cancer, and breast cancer; pleural metastases; therapeutic resistance; interaction of tumor cells and regenerating tissue; lung immunology; and pleural immuno-oncology. Dr. Donnenberg has written over 395 publications, abstracts, book chapters, and other scientific presentations. Throughout her career she has received numerous awards for her academic and service efforts including the Nathaniel Kwitt Distinguished Service Award from the ACCP, the Marylou Ingram Woman in Science Award from the Coulter Foundation, the Governor’s Distinguished Citizenship Award, Maryland, and the Service Award from the National Society of Black Engineers.
Dr. Donovan’s research interests are in the development and testing of interventions to improve symptoms and quality of life among individuals with cancer and their family caregivers (NINR R01NR010735; NR01370; 90RTGE0002). She has specific expertise in the integration of theory and evidence to design and test e-health interventions to improve self-management for families facing chronic and life threatening illnesses and disabilities. Her work has been grounded in the Representational Approach (RA) to patient education, an intervention theory that she co-developed. The RA has been used to guide a wide range of interventions in cancer symptom management, family caregiving, heart failure, end stage renal disease and palliative care. Currently, she is the corresponding PI and co-Director of the National Rehabilitation Research and Training Center on Family Support (NCFS; 90RTGE0002; www.caregiving.pitt.edu). NCFS’ mission is to partner with government, academia, and the broad family support stakeholder community to translate state-of-the-art research and training into services and support programs to improve the care, health, and quality of life of all persons with disabilities and the families who support them. Her current research within NCFS is focused on integrating family caregiver assessments and interventions into an established platform to be relevant to caregivers across a wide range of care recipient illnesses and disabilities.
Dr. Dorritie was previously involved in laboratory research focused on the development of novel therapeutic agents for acute myeloid leukemia. More recently, she has shifted her focus to early phase clinical trials in hematologic malignancies, specifically immune therapies for lymphoma and multiple myeloma. She is a member of the Cancer Therapeutics Team. She has played a key role in the development of the chimeric antigen receptor (CAR) T-cell and bispecific antibody programs at UPMC and serves as lead or co-investigator on several clinical clinical trials.
My research is directed towards the development of new therapies for primary and secondary brain tumors using targeted drugs, inhibitors of angiogenesis, and immunotherapies. I am also interested in the identification of molecular markers of prognosis in patients with malignant glioma and other primary brain tumors.
Dr. Du's research is centered on pathophysiology of hematologic diseases such as bone marrow (BM) failure and leukemia. She has a broad background in hematopoiesis, stem cell biology & aging, cellular metabolism and tumor microenvironment, with specific training and expertise in DNA damage response/repair, metabolite profiling, and in vivo disease modeling. Her early research covered understanding the mechanism of hematopoietic stem cell (HSC) mobilization and BM niche engraftment as well as the factors implicated in cell proliferation and apoptosis; identification of functional interactions between certain factors implicated in cell polarity, adhesion/migration, stem cell metabolism and aging. Her current research interests include: 1) Define the molecular and functional collaboration between a major cell signaling (FA) pathway and immunometabolic regulation in HSCs; 2) Target stem cell-niche interaction for improved therapy for patients with bone marrow failure and leukemia; 3) Study a novel interplay between DDR and immune responses in FA leukemogenesis; 4) Study on the systemic immune effects of persistent DNA damage using mouse and human models of DNA repair deficiency and aging; and 5) Mechanistic and functional elucidation of the role of a novel paracrine Wnt5a-Prox1 signaling axis in regulating HSC regeneration under conditions of injury and aging.
My clinical and research interests are in the study of improved diagnostics and treatments for patients afflicted with pancreatic cancer. Specifically, in collaboration with researchers at UPMC Hillman Cancer Center and at the University of Pittsburgh, I am active in the following research projects: 1) using surgical drain fluid to perform liquid biopsy for improved staging of patients with PDAC; 2) gamma-delta TIL therapy for patients with metastatic PDAC; 3) radiomics for improved pre-operative staging and risk-stratification for patients with PDAC; 4) novel drug delivery systems for improved regional therapy in patients with metastatic GI malignancies.
Research in the Duncan Lab focuses on liver development, homeostasis, and regeneration. Polyploidy is a defining feature of the adult liver. Hepatocytes are either mononucleated or binucleated, and ploidy is determined by the number of nuclei per cell as well as the ploidy of each nucleus. Although hepatic polyploidy has been described for well over 100 years, the functional role of hepatic polyploidization is unclear. Dr. Duncan’s lab recently showed that regenerating polyploid hepatocytes undergo specialized cell divisions to form aneuploid daughter cells, generating a high degree of genetic diversity within the liver. Moreover, in rodent models, chromosome-specific aneuploid hepatocytes were shown to play a specialized role in liver regeneration, promoting adaptation and resistance to different forms of chronic liver injury.
