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My research interests are investigating the molecular mechanisms through which the microenvironment promotes tumor initiation, progression and therapeutic resistance.
My interest in elucidating the role of the microenvironment in tumorigenesis began with my graduate studies under Dr. Terry Van Dyke (UNC-Chapel Hill), where I designed and created a new transgenic mouse model of prostate cancer based on retinoblastoma gene (RB) family inactivation. Interestingly, I uncovered that tumor initiation due to pRb family inactivation in the epithelium created selective pressure for p53 loss in the surrounding stromal cells, identifying a critical role for p53 in the mesenchyme. Most importantly, this stromal alteration aided further tumor progression.
This underscored the importance of the microenvironment in tumor progression and supported the emerging concept of targeting the tumor microenvironment as a valid therapeutic strategy.
As a Damon Runyon postdoctoral fellow with Dr. Hong Wu (UCLA), I chose to focus on an area of research with a largely unmet need for translational research. Pancreatic cancer (PDAC) has a high mortality rate, dismal prognosis and few therapeutic options. This pointed to a dire need for novel therapeutic and chemopreventative strategies, and for relevant research models of disease development. I played a central role in establishing mouse models based on PTEN loss of function that recapitulated human PDAC and worked to translate these findings to the human disease.
PDAC is the 3rd leading cause of cancer-related deaths in the United States and has a 5-year survival rate of 9%. This dismal prognosis shows an urgent need for novel therapeutic strategies. A prominent desmoplastic reaction, when the microenvironment surrounding epithelial tumors expands due to infiltration of fibroblasts, pancreatic stellate cells, immune cell populations, and endothelial cells, is one of the hallmarks of PDAC. This dense stromal layer can account for up to 90% of the tumor bulk and is believed to serve as a physical impediment to effective pharmacological treatment and to play an important role in the aggressive nature of the disease. Thus, full understanding of disease development will require experimental assessment of the mechanisms through which the microenvironment can affect the course of disease progression.
The Hill lab uses novel mouse models, human clinical samples, and newly-established assay systems to elucidate how the microenvironment or inflammation contributes to all three stages of tumorigenesis: initiation, progression to metastasis, and therapeutic resistance.
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