Research Interest: Cancer Signaling & Biochemistry
| Name | PhD Program | Research Interest | Publications |
|---|---|---|
| Schrank, Travis PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
I am a surgeon-scientist specialized in head and neck cancers. My goal is to address translationalquestions with genomic data and bioinformatic methods, as well as benchtop experimentation. My clinical practice as a head and neck cancer surgeon also influences my research by helping me seek solutions to problems that will directly inform gaps in the current treatment protocols. I have developed a strong interest in HPV genomics as well as HPV/host genome integrations, as these factors are intrinsically related to transcriptional diversity and patient outcomes in HPV-associated head and neck cancers. Our work has helped to demonstrate that a novel mechanism of HPV-mediated oncogenesis requiring NF-kB activation is present in nearly 50% of oropharyngeal tumors. In this vein, we are aggressively investigating the cellular interplay between the NF-kB pathway and persistent HPV infection, tumor radiation response, NRF2 signaling, and more. Another outgrowth of this work has been investigating APOBEC3B and its non-canonical roles in regulating transcription. Our preliminary work has demonstrated that APOBEC3B has surprisingly strong transcriptional effects in HPV+ HNSCC cells and may promote oncogenesis and tumor maintenance by suppressing the innate immune response and influencing the HPV viral lifecycle. Our group also have a strong interest in translational genomic studies. Our group is working to develop methods that will make gene expression-based biomarkers more successful in the clinic, as well as studying many aspects of genomic alterations that contribute to the development of squamous cell carcinomas. |
| Chung, Kay WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
The Chung lab is engineering immune cells, particularly T cells, to achieve maximum therapeutic efficacy at the right place and timing. We explore the crossroads of synthetic biology, immunology, and cancer biology. Particularly, we are employing protein engineering, next-gen sequencing, CRISPR screening, and bioinformatics to achieve our objectives: (1) Combinatorial recipes of transcription factors for T cell programming. (2) Technologies for temporal regulation and/or rewiring of tumor and immune signal activation (chemokine, nuclear, inhibitor receptors). (3) Synthetic oncolytic virus for engineering tumor-T cell crosstalk. |
| Peng, Aimin WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
Our overarching goal is to delineate how cells respond to cancer therapeutics that induce DNA damage, and, accordingly, to develop new strategies that overcome treatment resistance in cancer, including head and neck cancer. To achieve this goal, we study new mechanisms of the cell cycle and DNA repair using comprehensive experimental systems; we investigate the involvement of these mechanisms in oral cancer progression and resistance; and we develop new therapeutics using cellular, biochemical, and pharmacological approaches. |
| Yates, Melinda PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
Our translational research lab is focused on the earliest changes that occur in the uterus (endometrium) during cancer development related to obesity and hereditary DNA repair defects. We use preclinical tools (rodents, organoids, and cell lines) to probe mechanisms of endometrial cancer pathogenesis, in parallel with human tissue studies. Our overall goal is to understand how environmental factors, including obesity, hormones, and other exposures, influence endometrial cancer development and disparities so that we can use pharmacologic agents to prevent or reverse cancer development. |
| Starbird, Chrystal PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
Our lab is interested in understanding the structural basis for activation of cell surface receptors. Using a combination of biochemistry, structural biology and cell biology, we seek to understand how the membrane environment and receptor:ligand interactions are modulated to generate the wide diversity of signaling regulated by these receptors, and how these interactions are modified in disease. |