Dr. Bao is a member of the Hillman Cancer Center (HCC) Cancer Biology Program and Co-Director of the UPMC HCC Cancer Bioinformatics. Using a combination of multi-omics data integration, machine learning, and computer vision-assisted pathology image recognition, Dr. Bao’s work bridges methodological advances and biomedical applications with a direct impact on accelerating the knowledge discovery to new clinical trials that could benefit patients. Her lab focuses on the data-driven discovery of resistance mechanisms to cancer immunotherapy, with major contributions to the identification of WNT/ß-catenin activation as the first tumor-intrinsic mechanism that drives immune exclusion, commensal microbiome as the modulator of anti-PD1 efficacy, and systemic discovery of oncogenic pathways that contribute to the absence of immune infiltration across human solid tumors. Those findings are of particular importance because they provide the scientific rationale to new trials that combine therapeutic targets, such as IDH1 inhibitors, with anti-PD1. Dr. Bao is Co-Leader of Bioinformatics/Biostatistics in the Melanoma and Skin Cancer SPORE and Head and Neck Cancer SPORE programs. She also serves as the the UPMC HCC Informatics Committee, providing critical advice on data accessibility, analysis, integration, and infrastructure for translational research across the Cancer Center. Dr. Bao is a member of The American Association of Immunologists, Society for Immunotherapy of Cancer, and Medical Image Computing and Computer Assisted Intervention.

Dr. Hicks' research addresses computational challenges in single-cell genomics, epigenomics, and spatial transcriptomics leading to an improved understanding of human health and disease. Specifically, she develops computational methods using statistics and machine learning. She implements these methods in open-source software for the analysis of biomedical data.

​

Her research philosophy is problem-forward: she develops computational methods and software that are motivated by concrete problems, often with real-world, messy data. This philosophy permeates into her contributions to statistics and data science education, and service to the profession including being an advocate for diversity, equity, and inclusion.

​

She is also a co-host of the The Corresponding Author podcast, member of the Editorial Board for Genome Biology, an Associate Editor for Reproducibility at the Journal of the American Statistical Association, and co-founder of R-Ladies Baltimore.

Dr. Bajaj's research focuses on poorly differentiated aggressive myeloid diseases are often resistant to standard therapy and associated with significantly poor survival in both children and adults. There is thus a significant need for a better understanding of the mechanisms that drive disease progression and for finding novel therapeutic targets. While intrinsic signals that drive myeloid cancer progression are well described, the role of interactions with the surrounding microenvironment on leukemic growth remain poorly understood. Our primary goal is to define the role of cancer stem cell interactions with their bone marrow niche in disease progression. To address these questions, we use genetic mouse models of human disease and primary human patient samples, single cell technologies, as well as metabolomic approaches. In the long term, these studies will not only add to our understanding of the tumor microenvironment in the development and progression of hematological malignancies, but may also contribute to the design of novel therapies.

I obtained an MD/PhD (microbiology) from the State University of New York at Buffalo, completed a residency in medicine at Yale New Haven Hospital, and a medical oncology fellowship at Memorial Sloan Kettering Cancer Center (MSKCC). As a medical oncology fellow during my training at MSKCC, I initiated the initial pre-clinical studies demonstrating the potential clinical application of autologous T-cells genetically modified to target the CD19 antigen through the retroviral gene transfer of artificial T-cell receptors termed chimeric antigen receptors (CARs).

​

Following the completion of my medical oncology training, I became the principal investigator of my own laboratory. As a PI, I successfully translated these studies to the clinical setting treating patients with relapsed CD19+ tumors including chronic lymphocytic leukemia (CLL) and B cell acute lymphoblastic leukemia (B-ALL). Ongoing pre-clinical research in the laboratory is focused on the further development of CAR modified T-cells designed to overcome the hostile immunosuppressive tumor microenvironment through the generation of “armored CAR T-cells” currently being translated to the clinical setting as second-generation CAR modified T-cell clinical trials. Additionally, work in the Brentjens’ lab has expanded this CAR technology to target additional tumor antigens expressed on other malignancies including solid tumors

​

In 2024, I was one of four recipients of the prestigious Warren Alpert Foundation Prize for my role in the creation of chimeric antigen receptor (CAR) T cells. 

Research efforts in the David lab apply core techniques in chemical biology, biochemistry, and cell biology to address fundamental questions in the epigenetic regulation of transcription. Epigenetic regulation relies on the dynamic modification of the two building blocks of chromatin: DNA and histone packaging proteins, to establish and maintain cell identity and fate. We develop and utilize chemical methods to synthesize site-specifically modified histones in vitro and in vivo and study the roles that these modifications play in disease states, with the ultimate goal of targeting them for therapeutics.