Reginald Hill Email & Phone Number

Los Angeles, Ca, Us

Founder and lead consultant of Lab Lift-Off, a consulting group that specializes in transforming research labs by applying teamwork and communication principles inspired by Crew Resource Management (CRM) training from aviation. Major duties include delivering customized workshops and one-on-one consulting, guiding labs in improving communication, leadership, and efficiency.

Greater Los Angeles Area

Reginald is an Assistant Professor of Medicine at the Keck School of Medicine of USC and the Lawrence J. Ellison Institute for Transformative Medicine at USC. The Pancreatic Cancer Laboratory, under the direction of Dr. Reginald Hill, uses novel mouse models, human clinical samples, and newly-established assay systems to elucidate the molecular mechanisms through which the microenvironment or inflammation contributes to all three stages of tumorigenesis: initiation, progression to metastasis, and therapeutic resistance.

South Bend, Indiana

Pancreatic Ductal Adenocarcinoma (PDAC) is the 4th leading cause of cancer-related deaths in the United States and has a 5-year survival rate of less than 4%.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. My 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, and therapeutic resistance. Our current focus is on three questions which have implications beyond pancreatic cancer research: (i) How does the microenvironment influence cancer stem cell development? (ii) How does the endoplasmic reticulum (ER) stress contribute to tumor growth and maintenance? (iii) What factors or signals from the microenvironment are responsible for mediating chemoresistance?Novel therapeutic targets and strategies identified from these projects will have immediate clinical relevance and could potentially change the current treatment strategies for patients with advanced stage pancreatic cancer.

Ucla

Unraveling the mechanisms by which PI3K and COX-2 controlled signaling pathways contribute to pancreatic cancer initiation and progression.• Developed a transgenic mouse model of pancreatic cancer based on Kras mutation and abrogation of the PTEN signaling pathway. Discovered that loss of PTEN function promotes pancreatic tumor initiation and progression by increasing the rate of development of acinar-to-ductal metaplasias, lesions which were shown to express markers consistent with those of purported cancer stem cells. Examined the role that COX-2 mediated inflammatory response plays in pancreatic tumor initiation and progression, and identified cell intrinsic and cell non-intrinsic mechanisms through which COX-2 promotes tumor development.• Performed microarray data analysis in order to identify key pathways which are responsible for pancreatic tumor progression and invasiveness. Collaborated with surgeons at UCLA with access to human tumor samples in order to perform comprehensive array analysis to identify genes linked to poor prognosis in human patients with pancreatic cancer.

Uncoupling the contributions of the RB family, PTEN, and p53 in prostate tumorigenesis. • Created a transgenic mouse model of prostate cancer based on RB family inactivation utilizing a truncated version of the Large T-antigen. Discovered that RB family members (p107 and p130) play a critical role in suppression of prostate tumor formation.• Discovered that selective pressure for Pten LOH leads to accelerated tumor progression and enhanced tumor survival. Identified that tumor initiation in the epithelial cell compartment creates selective pressure for p53 loss in the surrounding stromal cells, establishing the important role genetic changes in the microenvironment play in tumorigenesis.

Ph.D., Genetics And Molecular Biology

Activities and Societies: Associate Member, American Association for Cancer Research (AACR)

Bs, Biology

Activities and Societies: President, Society of Biological Sciences Fellow, BIONR