Therapeutic Targeting of CSN5, a Negative Regulator of p53 and p27, in Human Hepatocellular Carcinoma
Description of Invention:
Hepatocellular carcinoma (HCC) represents an extremely poor prognostic cancer that remains one of the most common and aggressive malignancies worldwide. Elevated expression of COP9 complex homolog subunit 5 (CSN5) in early HCC indicates that CSN5 is one of the early markers of malignant conversion. COP9 complex homolog subunit 5 (CSN5) is a multifunctional protein that interacts with a variety of proteins and targets p53 for cell degradation.
Available for licensing are CSN5 siRNAs and nucleic-acid lipid siRNA particles as cancer therapies. HCC cells treated CSN5 siRNAs inhibited HCC progression and increased apoptosis in vitro and in vivo suggesting that CSN5 is an effective target for the development of cancer treatments.
Applications:
siRNA cancer therapeutics
Nucleic-acid lipid siRNA particles for targeted drug delivery
Method to treat cancer
Development Status:
Early-stage of development
Market:
HCC is the most frequent primary malignant tumor of the liver with a world incidence of 1 million new cases per year.
The global cancer therapeutic market is expected to grow from $23.1 billion in 2004 to $60.6 billion in 2011. The targeted therapy segment is providing the growth of the entire market with an expected compound annual growth rate of 24.1 percent for 2004-2011.
Relevant Publication: JS Lee et al. Classification and prediction of survival in hepatocellular carcinoma by gene expression profiling. Hepatology 2004 Sept;40(3):667-676. [PubMed abs]
Licensing Status: Available for non-exclusive licensing.
Portfolios: Gene Based Therapies Cancer
Cancer -Therapeutics-Gene Therapy-Delivery Systems Cancer -Therapeutics Cancer -Research Materials Gene Based Therapies -Therapeutics
For Additional Information Please Contact: Jennifer Wong
NIH Office of Technology Transfer
6011 Executive Blvd, Suite 325
Rockville, MD 20852-3804
Phone: (301)435-4633
Email: wongje@mail.nih.gov
Fax: (301)402-0220
