01-20424. Government-Owned Inventions; Availability for Licensing

AGENCY:

National Institutes of Health, Public Health Service, DHHS.

ACTION:

Notice.

SUMMARY:

The inventions listed below are owned by agencies 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.

ADDRESSES:

Licensing information and copies of the U.S. patent applications listed below may be obtained by contacting Wendy R. Sanhai, Ph.D., at the Office of Technology Transfer, National Institutes of Health, 6011 Executive Boulevard, Suite 325, Rockville, Maryland 20852-3804; telephone: [phone] ext. 244; fax: [phone]; e-mail: [e-mail]. A signed Confidential Disclosure Agreement will be required to receive copies of the patent applications.

A Mouse Model of von-Hippel Lindau Disease

Laura S. Schmidt et al. (NCI)

DHHS Reference No. E-264-01/0

The current invention embodies a mouse model which has been rendered a conditional homozygous knockout at the murine chromosome 6 VHL locus, homologous to the human VHL locus at chromosome 3p25. Mutations in VHL, a tumor suppressor gene, lead to the clinical manifestations of von Hippel-Lindau disease, a rare autosomal dominant syndrome characterized by tumor formation in multiple organs, including the brain and kidneys. Using Cre/lox site-specific recombination, this invention allows for homozygous deletion of wild-type VHL only in specified tissues, thereby circumventing the embryonic lethality seen in the VHL knockout mouse. The model embodied in this invention therefore appears to represent a valuable research tool for understanding how inactivation of both copies of the VHL gene lead to tumor formation, and ultimately should aid in the testing of possible therapeutic approaches to von Hippel-Lindau disease.

A Mouse Model of Multiple Endocrine Neoplasia, Type I

Judy S. Crabtree, Francis S. Collins (NHGRI)

DHHS Reference No. E-243-01/0

The current invention embodies a mouse model which is heterozygous for a null allele at the Men1 locus of murine chromosome 19. Men1 has similar exon-intron organization and amino acid identity compared with its human analog MEN1, which has been implicated in the pathogenesis of multiple endocrine neoplasia, type I (MENI). This mouse model has been shown to develop features remarkably similar to those of MEN1, which include tumors of the endocrine pancreas, pituitary, and parathyroids. The model embodied in this invention appears to represent a valuable research tool for use in elucidating the role of the wild-type Men1 allele in tumor formation, and ultimately should aid in the testing of possible therapeutic approaches to human MEN1.

Dated: August 8, 2001.

Jack Spiegel,

Director, Division of Technology Development and Transfer, Office of Technology Transfer, National Institutes of Health.