A Novel PARP Inhibitor Resistance Mechanism Mediated by the RNA-Binding Protein HuR

Authors

Saswati N. Chand, Thomas Jefferson UniversityFollow
Nicole Meisner-Kober, Novartis Institute for Biomedical Research, Basel, SwitzerlandFollow
Shruti Lal, Thomas Jefferson UniversityFollow
Charles J. Yeo, MD, Thomas Jefferson UniversityFollow
Jordan M. Winter, MD, Thomas Jefferson UniversityFollow
Jonathan R. Brody, MD, Thomas Jefferson UniversityFollow

Document Type

Poster

Publication Date

4-9-2014

Comments

Presented at: 2014 CSHL The PARP Family and Friends: Gene Regulation and Beyond at Cold Spring Harbor, NY.

Abstract

Abstract

Pancreatic ductal adenocarcinoma (PDA) is the 4th leading cause of cancer-related deaths in the United States, and ranks as the third most common cancer associated with BRCA mutations, not including Fanconi Anemia gene mutations such as PALB2. Current combinations of chemotherapeutics have significant toxicities and only minimally extend overall patient survival. Poly-ADP ribose polymerase (PARP) inhibitors (PARPi), which target the DNA damage repair (DDR) pathway, have delivered promising preclinical and clinical results. Although synthetic lethality conferred by PARPi is a promising approach, still “selected” patients with DNA repair-deficient tumors (e.g., BRCA2 mutated) that initially respond to such molecular-targeted therapies ultimately develop resistance. Therefore, optimizing PARPi therapy requires a thorough understanding of associated drug resistance mechanisms.

Recommended Citation

Chand, Saswati N.; Meisner-Kober, Nicole; Lal, Shruti; Yeo, MD, Charles J.; Winter, MD, Jordan M.; and Brody, MD, Jonathan R., "A Novel PARP Inhibitor Resistance Mechanism Mediated by the RNA-Binding Protein HuR" (2014). Department of Surgery Faculty Papers. Paper 119.
https://jdc.jefferson.edu/surgeryfp/119