OCT 17, 2013 02:00 PM PDT
Oncoproteins K-Ras and Pim kinases as molecular targets in pancreatic cancer
CONTINUING EDUCATION (CME/CE/CEU) CREDITS: CE
72 44 1715

Speakers:
  • Associate Professor, Department of Biology & the Cancer Research Program , North Carolina Central University, Durham, North Carolina; Adjunct Professor, School of Medicine, Department of
    Biography
      Dr. Antonio T. Baines is an Associate Professor in the Department of Biology at North Carolina Central University (NCCU) and an adjunct professor in the Department of Pharmacology in the School of Medicine at the University of North Carolina (UNC) Chapel Hill. He earned a bachelors degree in biology from Norfolk State University and a doctorate in pharmacology and toxicology from the University of Arizona. Afterwards, Dr. Baines accepted a postdoctoral fellowship at UNC in pharmacology and radiation oncology under Drs. Channing Der and Adrienne Cox. His research focused on understanding the role of the Ras oncogene as a molecular target in pancreatic cancer oncogenesis. In August 2006, Dr. Baines accepted a tenure-track faculty position at NCCU where he currently teaches and conducts research as a cancer biologist. Also, he mentors high school, undergraduate, and graduate students in his laboratory. Pancreatic cancer is the 4th most common cause of cancer deaths in the United States with a high mortality rate and very limited treatment options. The overall focus of Dr. Baines research program is to identify and validate novel molecular targets in pancreatic cancer which can be targeted by potential cancer therapeutics. Additionally, his lab aims to understand the role of these molecular targets in the development and progression of normal cells transforming into cancer cells of the pancreas. Currently, Dr Baines studies the functional significance of the oncogenic Pim kinase family in pancreatic cancer growth and development. He hypothesizes that inhibition of these enzymes will be an effective approach for antagonizing the aberrant growth of pancreatic carcinoma. In addition to working with colleagues in academia, he collaborates with various pharmaceutical companies that are developing Pim inhibitors. Results from his studies will allow for critical validation of these kinases as novel therapeutic targets for pancreatic cancer treatment. Dr. Baines research has been funded by NIH and other grant sources. He has presented his research at various national scientific meetings such as the Society of Toxicology and the American Association for Cancer Research. In addition, Dr. Baines has given invited research seminars at universities such as Duke University, UNC-Chapel Hill, North Carolina Agricultural and Technical (A&T) State University, Indiana University, North Carolina State University, University of Missouri-Kansas City and Massachusetts Institute of Technology (MIT).

    Abstract:
    Pancreatic cancer is the 4th most common cause of cancer deaths in the United States. Due to the aggressive nature of this cancer and the lack of biomarkers for early detection, the incidence and mortality rates for pancreatic cancer are nearly equivalent. The presence of oncogenically mutated K-Ras in 90% of human pancreatic ductal adenocarcinomas (PDAC) strongly suggests a critical role for this genetic mutation in the development of this disease. We and others demonstrate that mutated K-Ras can activate one or more downstream signaling pathways, including the RalGTPase pathway, and lead to transformed growth in PDAC. However, despite many years of research, there are no anti-Ras therapies that have successfully reached the clinic. One of the genes that have been found by microarrays to be overexpressed after oncogenic K-ras is Pim-1 kinase. Most recently, another member of the Pim family, Pim-3 kinase, was shown to be aberrantly expressed and to block apoptosis in PDAC cell lines and patient tumors. With these and other observations implicating Pim kinases as oncogenes and inhibitors of apoptosis, the overall goal of our research is to determine the functional significance of the Pim kinase family in PDAC growth. We hypothesize that inhibition of one or more Pims will be an effective approach for antagonizing the aberrant growth of pancreatic carcinoma. Our results will help to define the role of K-Ras activation in Pim upregulation and determine the consequences of Pim inhibition on PDAC growth. Furthermore, these findings will allow us to critically validate these kinases as novel therapeutic targets for PDAC treatment. Learning objectives: 1. Discuss the importance of oncogenic K-Ras and downstream signaling pathways in the development and progression of pancreatic cancer. 2. Discuss the roles of oncogenic Pim kinases in pancreatic cancer growth and as a potential drug target.

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