National Institutes of Health, Public Health Service, HHS.
The inventions listed below are owned by an agency of the U.S. Government and are available for licensing in the U.S. in accordance with 35 U.S.C. 207 to achieve expeditious commercialization of results of federally-funded research and development. Foreign patent applications are filed on selected inventions to extend market coverage for companies and may also be available for licensing.
Licensing information and copies of the U.S. patent applications listed below may be obtained by writing to the indicated licensing contact at the Office of Technology Transfer, National Institutes of Health, 6011 Executive Boulevard, Suite 325, Rockville, Maryland 20852-3804; telephone: 301/496-7057; fax: 301/402-0220. A signed Confidential Disclosure Agreement will be required to receive copies of the patent applications.
An Improved Chromosomal Comparative Genomic Hybridization (CGH) Microarray for the Detection of Cancer Associated Genome Amplification and Deletion Events
Description of Technology: The progression and therapeutic response of cancer is closely associated with chromosomal instability (i.e. genomic amplifications and deletions). The most widely used technique to detect these small changes in the genome is CGH. CGH utilizes nucleic acid hybridization to oligonucleotide features corresponding to specific, predetermined regions of the genome to detect DNA copy number changes. Due to the size of the human genome, it is necessary to have high-density features to detect small amplification and deletion events within the genome.
The current invention is based on a CGH microarray with oligonucleotide features that provides a high-density coverage. More specifically, the inventors have used 60-mer oligonucleotide features within a previously shown set of 36 tumor associated genes/genomic regions and have successfully detected small changes in DNA copy number with high density coverage (1 feature per 400bp). Furthermore, the inventors have used a fade-out design for coverage of the flanking regions and cover the remainder of the genome at an average density of 1 feature per 100kb.
1. CGH microarray can be used to detect small regions of genomic instability within cancer associated genes, while larger events can also be detected with similar efficacy.
2. Gene amplification and deletion profiles of patient samples can be used in diagnosis and therapeutic decision making.
1. Easy to use, CGH microarray technique, based on current technology.
2. Technology detects small changes in tumor associated genomic instability Start Printed Page 45253more efficiently than current available technologies.
3. The average coverage of Agilent oligoarray is 1 per 35kb of human genome, while the average coverage of the currently described technology is 1 per 400bp.
Developmental Status: The technology is ready for use.
Benefits: More than 600,000 cancer deaths are estimated to occur in 2007. Efficient diagnosis and informed decision making will aid in improved clinical management of cancer. This technology can rapidly diagnose cancer and thus help in proper clinical management leading to improved overall survival and quality of life of patients suffering from cancer. The current in-vitro diagnostics market is valued at $30 billion dollars and expected to grow.
Inventors: Xiaolin Wu, David Munroe, Ester Rozenblum, Hongling Liao (NCI/SAIC).
Patent Status: U.S. Provisional Application No. 60/911,411 filed 12 April 2007 (HHS Reference No. E-122-2007/0-US-01).
Licensing Contact: Thomas P. Clouse, J.D.; 301/435-4076; email@example.com.
Collaborative Research Opportunity: The National Cancer Institute Laboratory of Molecular Technology is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize CGH microarrays. Please contact John D. Hewes, PhD at 301-435-3121 or firstname.lastname@example.org for more information.
Methods and Compositions for Treating Diseases and Disorders Associated with Natural Killer T-Cells
Description of Technology: The invention relates to the discovery that C12 beta-D-galactosyl ceramide may be used to deplete or inactivate NKT cell populations. These findings suggest methods for using C12 beta-D-galactosyl ceramide to treat conditions that would benefit from depletion of NKT cells, such as certain autoimmune diseases (e.g. lupus, MS) and AIDS.
The presence of NKT cells can be associated with either beneficial effects or pathology. Deficiencies in NKT cells are associated with at least some types of autoimmune disease, including type 1 diabetes and autoimmune gastritis in mice. In contrast, NKT cells augment autoantibody secretion and lupus development in lupus-prone mouse models and therefore lupus patients may benefit from the depletion of NKT cells. The remission state of multiple sclerosis (MS) is also associated with decreased levels of NKT cells, suggesting NKT cell depletion as a method of treatment for MS.
Inventors: John R. Ortaldo and Robert H. Wiltrout (NCI).
U.S. Provisional Application No. 60/488,339 filed 17 July 2003 (HHS Reference No. E-282-2002/0-US-01).
PCT Application No. PCT/US2004/22913 filed 16 Jul 2004, which published as WO 2005/014008 on 17 Feb 2005 (HHS Reference No. E-282-2002/0-PCT-02).
European Application No. 04778424.4 filed 16 Jul 2004, which published as 1653977 on 10 May 2006 (HHS Reference No. E-282-2002/0-EP-03).
Licensing Status: Available for exclusive or non-exclusive licensing.
Licensing Contact: Jennifer Wong; 301/435-4633; email@example.com.
P53 and VGEF Regulate Tumor Growth of NO2 Expressing Cancer Cells
Description of Technology: The increased expression of nitric oxide synthase 2 (NOS2), an inducible enzyme that produces nitric oxide (NO), has been found in a variety of human cancers. It also has been shown that NOS2-specific inhibitors can reduce the growth of experimental tumors in mice. These findings suggest a pathophysiological role for NO in the development and progression of cancer. However, the function of NO and NOS2 in carcinogenesis is uncertain. NO had been found to either inhibit or stimulate tumor growth, and high concentrations of NO also are known to induce cell death in many cell types including tumor cells. On the other hand, the lower concentrations of NO that are found in human tissue can have an opposite effect and protect against programmed cell death, or apoptosis, from various stimuli. The role of NO and NOS2 in tumor progression, particularly with respect to p53, therefore need to be further defined.
This invention comprises methods of screening for modulators of NOS2 expression in p53 mutant cells, both in vivo and in vitro, as well as methods for predicting the chemotherapeutic benefit of administering NOS2-inhibitors to cancer patients. It has been demonstrated that NOS2-expressing cancer cells with wild-type p53 have reduced tumor growth in athymic nude mice whereas NOS2-expressing cancer cells with mutated p53 have accelerated tumor growth. Therefore, this invention has potential application for a number of cancers that overexpress NOS2 and have a high frequency of p53 mutations, including breast, brain, head, neck, lung and colon cancers.
1. Method to treat cancer with NOS2 inhibitors.
2. Method to screen for NOS2 modulators.
3. Method to predict therapeutic benefits of NOS2 inhibitors in patients.
1. An estimated 1,444,920 new cancer diagnoses in the U.S. in 2007.
2. 600,000 deaths caused by cancer in the U.S. in 2006.
3. Cancer is the second leading cause of death in United States.
4. It is estimated that market for cancer drugs would double to $50 billion a year in 2010 from $25 billion in 2006.
Development Status: The technology is currently in the pre-clinical stage of development.
Inventors: Stefan Ambs and Curt Harris (NCI).
1. JE Goodman et al. Nitric oxide and p53 in cancer-prone chronic inflammation and oxyradical overload diseases. Environ Mol Mutagen. 2004;44(1):3-9.
2. LJ Hofseth et al. Nitric oxide in cancer and chemoprevention. Free Radic Biol Med. 2003Apr 15;34(8):955-968.
U.S. Patent Application No. 11/195,006 filed 01 Aug 2005 (HHS Reference No. E-223-1998/0-US-04).
U.S. Patent Application No. 09/830,977 filed 02 May 2001 (HHS Reference No. E-223-1998/0-US-03).
PCT Patent Application No. PCT/US1999/27410 filed 17 Nov 1998 (HHS Reference No. E-223-1998/0-PCT-02).
U.S. Provisional Patent Application No. 60/109,563 filed 23 Nov 1998 (HHS Reference No. E-223-1998/0-US-01).
Licensing Status: Available for exclusive or non-exclusive licensing.
Licensing Contact: Jennifer Wong; 301/435-4633; firstname.lastname@example.org.Start Signature
Dated: August 3, 2007.
Steven M. Ferguson,
Director, Division of Technology Development and Transfer, Office of Technology Transfer, National Institutes of Health.
[FR Doc. E7-15749 Filed 8-10-07; 8:45 am]
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