Identifying Novel Combination Therapeutic Targets for Pancreatic Cancer
1,294 views
|
March 2, 2016
Pancreatic cancer is presently a largely incurable disease. Increasing evidence suggests that effective treatment strategies will need to simultaneously target multiple molecular mediators of critical functions in pancreatic ductal adenocarcinoma cells (PDAC). In this webinar Dr. Melissa L. Fishel from the Indiana University School of Medicine (Indianapolis, IN) discusses the use of ACEA Bioscience’s xCELLigence® system, in conjunction with other cell/molecular biology tools, to elucidate the mechanism by which APE1 regulates STAT3 activity. The studies described in this webinar set a framework for future clinical studies on pancreatic cancer using dual-targeting APE1-STAT3 approaches. The webinar specifically addresses:
• Dual-targeting of APE1 and STAT3 as a novel approach in pancreatic cancer chemotherapy
• Advantages of monitoring the kinetic profiles of cell proliferation and migration
• Benefits of integrating the xCELLigence® system with other cell/molecular biology tools
Dr. Melissa L. Fishel is an assistant research professor of Pediatrics and Pharmacology & Toxicology at the Indiana University School of Medicine. Her research projects focus on novel combinations of therapeutics to enhance treatment of pediatric, pancreatic and ovarian cancers. In addition to testing these combinations in pediatric, pancreatic and brain cancer cell lines, she also uses ectopic and orthotopic mouse models to look at their efficacy in vivo. From 2001 to 2004 she was a postdoctoral fellow with M. Eileen Dolan at the University of Chicago, where she discovered connections between multiple DNA repair pathways/proteins in sensitizing cancer cells to chemotherapy. She obtained her Ph.D. in Biochemistry from Indiana University in 2001.
For more information, please visit: http://www.aceabio.com/products/xcelligence-rtca/
REFERENCES:
Cardoso AA, Jiang Y, Luo M, Reed AM, Shahda S, He Y, Maitra A, Kelley MR, Fishel ML. APE1/Ref-1 regulates STAT3 transcriptional activity and APE1/Ref-1-STAT3 dual-targeting effectively inhibits pancreatic cancer cell survival. PLoS One. 2012;7(10):e47462.
