[Federal Register: August 14, 2001 (Volume 66, Number 157)]
[Notices]               
[Page 42671-42672]
From the Federal Register Online via GPO Access [wais.access.gpo.gov]
[DOCID:fr14au01-91]                         

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DEPARTMENT OF HEALTH AND HUMAN SERVICES

National Institutes of Health

 
Government-Owned Inventions; Availability for Licensing

AGENCY: National Institutes of Health, Public Health Service, DHHS.

ACTION: Notice.

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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,

[[Page 42672]]

National Institutes of Health, 6011 Executive Boulevard, Suite 325, 
Rockville, Maryland 20852-3804; telephone: 301/496-7736 ext. 244; fax: 
301/402-0220; e-mail: sanhaiw@od.nih.gov. 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.
[FR Doc. 01-20424 Filed 8-13-01; 8:45 am]
BILLING CODE 4140-01-P