Nadia Carlesso, M.D. Ph.D. Professor 
Modulation of the bone marrow niche to redirect cellular networks in stress and malignant hematopoiesis.
Dr. Carlesso’ s research interests are in fundamental and translational science and explore how cell-cell communication and the inflamed microenvironment alter the healthy trajectory of hematopoietic stem cells in aging, leukemia and sickle cell disease. Her laboratory studies the role of the bone marrow niche, Notch signaling, NF-kB pathway and non-coding RNAs in regulating hematopoietic homeostasis and in contributing to hematopoietic malignancies.

Michael E. Barish, Ph.D. Professor
At the Intersection of Neurobiology and Immuno-oncology
Our laboratory is applying a developmental neurobiology approach to study of tumorigenesis in brain and cellular heterogeneity in glioblastoma, including design of chimeric antigen receptor (CAR) T cell immunotherapies against novel tumor antigens. We are also employing organoid and organotypic culture models to better understand adaptive reactions of brain tumors to the selection pressures imposed by immunotherapies in the context of normal brain tissue.

Karen S. Aboody, M.D. Professor
Translational Research - Neural Stem Cell as Delivery tool for Cancer Treatment
Dr. Aboody overses a translational research laboratory focused on using neural stem cells (NSCs) as a platform for targeted delivery of anti-cancer agents to invasive and metastatic solid tumors. Therapeutic cargo explored to date includes: pro-drug converting enzymes, therapeutic proteins (interleukins, anti-angiogenic proteins, antibodies), oncolytic viruses, stimuli-responsive nanoparticles, and exosome-encapsulated oligonucleotides. Ongoing are first-in-human NSC-mediated enzyme/prodrug and oncoviral therapy trials for patients with glioblastoma.

Qiang Lu, Ph.D. Professor
Regulation of Neural Progenitor Cell Proliferation and Differentiation in Brain Development and Tumor Formation
Dr. Lu’s research is aimed at understanding the genetic and epigenetic mechanisms that control proliferation vs. differentiation decisions of neural progenitor cells in the developing cerebral cortex. His group is also applying the knowledge gained from these studies to develop novel preclinical models and therapeutics for brain tumors. 

Margarita Gutova, Ph.D. Research Associate Professor
Regenerative medicine for Traumatic Brain Injury
Dr. Gutova’s research program is focused on the integration of regenerative medicine approach from bench-to-bedside directed to improve neurobehavioral recovery and learning after experimental traumatic brain injury (TBI). Her lab is utilizing a neural stem cell in combination with environmental enrichment to restore function and/or attenuate TBI-induced deficits. Dr. Gutova is utilizing 3D culture organoid models and precision medicine approach to develop personalized treatments for patients with brain injury and tumors.  

Paul Salvaterra, Ph.D. Professor Emeritus
Molecular Neurobiology 
Dr. Salvaterra is interested in identifying underlying mechanisms responsible for neurodegenerative diseases such as Alzheimer’s (AD).  No existing AD animal models exhibit clear chronic progressive neurodegeneration an understudied disease phenotype. His lab has developed a human embryonic stem cell model which exhibits Abeta42-dependent neurodegeneration (TALEN editing of one allele of the amyloid precursor protein to directly express Abeta42 peptide). Parallel editing to express Abeta40 peptide does not show neurodegeneration. These cell lines can thus be used to uncover unknown mechanisms of Abeta42 dependent AD-like neurodegeneration in a human genetic context and test potential neurodegenerative blocking treatments.

June-Wha Rhee, M.D., Assistant Professor of Medicine
Tackling Cardio-Oncology with Human iPSCs and Genomics
Our research focuses on understanding the biology underlying cancer therapy-induced cardiovascular complications by leveraging human-induced pluripotent stem cells (iPSCs) as well as patient samples, genomics and leading-edge computational biology. Emerging data suggest that cardiovascular complications related to these therapies can cause treatment interruptions and lead to worse oncologic and cardiovascular outcomes. Therefore, there is a critical need to better understand 1) why and through what mechanisms the cancer therapy-related cardiotoxicity occurs, 2) who is at risk and 3) how to mitigate or prevent this toxicity. Our lab is working toward addressing these questions so that cancer patients can safely be treated with life-saving cancer therapies. Specifically, we believe metabolism and biologic aging are critical in modulating this risk and are working to define their roles by leveraging genome editing technology, multi-omics and advanced bioinformatics utilizing patient-specific iPSCs and patient samples.