2238 Brody, Jonathan - Thomas Jefferson University - Thomas Jefferson University
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Jonathan Brody, PhD

Contact Dr. Brody

1015 Walnut Street
Room 623
Philadelphia, PA 19107

(215) 955-2693

Most Recent Peer-reviewed Publications

  1. Delivery of Therapeutics Targeting the mRNA Binding Protein HuR Using 3DNA Nanocarriers Suppresses Ovarian Tumor Growth
  2. The landscape of pancreatic cancer therapeutic resistance mechanisms
  3. Analysis of 13 cell types reveals evidence for the expression of numerous novel primate- And tissue-specific microRNAs
  4. Selective impact of CDK4/6 suppression on patient-derived models of pancreatic cancer
  5. Novel targets in pancreatic cancer research
  6. Studying RNA-binding protein interactions with target mRNAs in eukaryotic cells: Native ribonucleoprotein immunoprecipitation (RIP) assays
  7. Targeting the mRNA-binding protein HuR impairs malignant characteristics of pancreatic ductal adenocarcinoma cells
  8. MUC1 promoter-driven DTA as a targeted therapeutic strategy against pancreatic cancer
  9. Upgrading gemcitabine with recycled kinase inhibitors
  10. Argonaute CLIP-Seq reveals miRNA targetome diversity across tissue types
  11. HuR posttranscriptionally regulates WEE1: Implications for the DNA damage response in pancreatic cancer cells
  12. Commentary : Fusing transcriptomics to progressive prostate cancer
  13. Targeting PARP-1 allosteric regulation offers therapeutic potential against cancer
  14. PARP inhibitors for chemoprevention - Letter
  15. dCK expression correlates with 5-fluorouracil efficacy and HuR cytoplasmic expression in pancreatic cancer: A dual-institutional follow-up with the RTOG 9704 trial
  16. Structural implications for selective targeting of PARPs
  17. Targeting cell cycle and hormone receptor pathways in cancer
  18. Mitoxantrone targets human ubiquitin-specific peptidase 11 (USP11) and is a potent inhibitor of pancreatic cancer cell survival
  19. HuR is a post-transcriptional regulator of core metabolic enzymes in pancreatic cancer
  20. Dormant cancer cells contribute to residual disease in a model of reversible pancreatic cancer
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