Allele Specific shRNA for Nanog, and Its Use to Treat Cancer
Posted Jan 19 2011 7:00pm
Description of Invention: Cancer stem cells are currently thought to be major participants in resistance to radiation therapy and chemotherapy; they are also thought to drive the spread of cancer through metastasis. It has been postulated that genes involved in early embryogenesis, primarily transcription factor Nanog but also Oct4 and SOX2, may be reactivated to maintain the properties of cancer stem cells, any treatment that inhibits such genes may therefore inhibit the progression of cancer and lead to improved survival and other clinical outcomes.
The NIH investigators discovered that the expression of NanogP8, a pseudogene of Nanog, is upregulated in human colorectal cancer spheroids formed in serum-free medium. NanogP8 has also been reported to be upregulated in human prostate cancer and glioblastomas. An inhibitory RNA molecule was identified by the investigators to knock down expression of NanogP8, without interfering with expression of Nanog. The discovery may improve the safety of a shRNA-based gene therapy and improve its chances for acceptance as a clinical therapy.
Applications: This invention may provide a new therapy to target colorectal cancer as well as a few other cancers for treatment.
Development Status: Pre-clinical stage of development.
Collaborative Research Opportunity: The National Cancer Institute, Laboratory of Experimental Carcinogenesis is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize this specific gene therapy to target colorectal and other human carcinomas. Please contact John Hewes, Ph.D. at 301-435-3121 or firstname.lastname@example.org for more information.
Portfolios: Cancer Cancer - Therapeutics Gene Based Therapies Gene Based Therapies - Therapeutics
For Licensing Information Please Contact: Betty Tong Ph.D. NIH Office of Technology Transfer 6011 Executive Blvd. Suite 325, Rockville, MD 20852 United States Email: email@example.com Phone: 301-594-6565 Fax: 301-402-0220