Bark Lab
David Bark, PhD
The overarching goal of our lab is to identify how mechanical stress impacts upon cell and protein function in the cardiovascular system, while advancing tools to diagnose and treat disease.
Bednarski Lab
Jeffrey J. Bednarski, MD, PhD
My research has centered on understanding the signals that direct early B cell development. Specifically, over the last several years, we have focused on understanding how signals induced by DNA damage impact developmental signals in B cells. B cell development occurs through a carefully regulated process that centers on the generation of a mature, non-autoreactive antigen receptor. To produce a mature antigen receptor, B cells must intentionally generate and repair DNA breaks in the antigen receptor genes. The creation of these DNA breaks is highly regulated by cooperative signaling from two surface proteins, the pre-B cell receptor (pre-BCR) and the interleukin-7 receptor. Together these two signals control cell cycle proliferation and arrest, induction of genes required for antigen receptor gene rearrangement, and cell viability.
Brossier Lab
Nicole M. Brossier, MD, PhD
Patients with the genetic disorder Neurofibromatosis Type 1 (NF1) are at increased risk for multiple neurodevelopmental abnormalities, including brain tumor development and impaired cognition. In the Brossier lab, we are interested in identifying how genetic, neurodevelopmental and environmental factors modulate risk of developing these phenotypes in NF1, as well as in the broader pediatric population. We utilize murine models of NF1 as platform for investigation, with an eye towards developing new patient risk assessment strategies and identifying new targets for therapeutic intervention. Using this approach, we have identified maternal exposure to an obesogenic Western-style diet as a risk factor for glioma formation and growth.
Child Health and Education Lab
Allison King, MD, MPH, PhD
The Child Health and Education Laboratory focuses on children with chronic illness, specifically those with Sickle Cell Disease (SCD) or brain tumors.
Di Paola Lab
Jorge Di Paola, MD
The Di Paola lab, headed by Jorge Di Paola, MD, comprises a diverse group of physician scientists, geneticists, bioinformaticists, and basic scientists. Advances in technology and decreases in costs of whole-genome sequencing have enabled us to pursue innovative approaches to discovering the genetic and biological determinants of a variety of conditions. We extend the scope of our research through both national and international collaboration. Using state of the art equipment and techniques, we aim to set the stage for the development of novel therapies to improve quality of life for those living with bleeding and thrombotic disorders.
Green Lab
Abby Green, MD
Division of Infectious Diseases
Cancer develops through accumulation of DNA mutations and structural aberrations collectively known as genome instability. Genome damage in adult-onset malignancies can be traced to exogenous carcinogens or simply the process of aging. However, pediatric cancers do not arise as a result of aging or exogenous genotoxic agents. We are interested in the etiology of genome instability in pediatric cancers and the resulting genome-protective responses — also called DNA damage responses — that are activated. Our long-term goal is to identify predictors of mutagenesis and therapeutic vulnerabilities within DNA damage response pathways in order to develop new treatment options for children with cancer.
Magee Lab
Jeffrey Magee, MD, PhD
The Magee lab is working to answer several important questions that surround the causes of childhood leukemia. How do childhood leukemias arise from normal blood forming stem cells? How do leukemia cells hijack normal stem cell programs? Why do childhood and adult leukemias have different mutations? Can we identify and target programs that maintain leukemia cells that are unique to childhood leukemia?
Mavers Lab
Melissa Mavers, MD, PhD
Work in our lab focuses on immune regulation of graft-versus-host disease (GVHD), a debilitating and potentially fatal complication of hematopoietic stem cell transplantation (HSCT). HSCT can cure high-risk malignancies and other diseases of the blood and bone marrow, yet success is limited as many patients develop this devastating complication.
We aim to elucidate the biological mechanisms underlying immune tolerance in HSCT and develop approaches to enhance regulatory immune cells for GVHD prevention and treatment. Our goal is to use a bench-to-bedside approach to develop a cellular therapy for GVHD, engineering viable approaches to prevention and cure, and thereby make HSCT a safer way to cure cancer and other blood diseases, giving survivors long, healthy lives.
Schuettpelz Lab
Laura G. Schuettpelz, MD, PhD
The Schuettpelz Lab is interested in understanding how inflammatory signals regulate hematopoietic stem cells (HSC). In particular, we are studying the role of toll-like receptor (TLR) signaling in HSCs. Our lab is currently using mouse models to better define the role of individual TLRs in regulating HSC function. In addition, we are exploring the connection between enhanced TLR signaling and myelodysplastic syndrome (MDS) through the use of various mouse models of this disease.
Schwartz Lab
Alan L. Schwartz, MD, PhD
Our laboratory focuses on the cell and molecular biology of intracellular protein targeting and degradation.
Shenoy Lab
Shalini Shenoy, MD, MBBS
My academic focus is on the development of safer less toxic methods of hematopoietic stem cell transplantation in children. Toward this, I am investigating reduced intensity transplantation for children with hemoglobinopathy (sickle cell disease and thalassemia) using the best available related or alternate donors.
Sykes Lab
Stephen Sykes, PhD
The principal objective of my laboratory is to identify and define those molecular features that drive leukemogenesis and then use that information to develop rational therapeutic strategies for improving outcomes in acute leukemia.
The lab is most interested in molecular pathways that: 1) are differentially regulated between malignant cells and their healthy counterparts; 2) promote resistance to conventional chemotherapies; and 3) support leukemia stem cell biology.