[Federal Register Volume 62, Number 191 (Thursday, October 2, 1997)]
[Notices]
[Pages 51670-51671]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 97-26171]
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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, HHS.
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 United States 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 U.S. 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 writing to the indicated
licensing contact at the Office of Technology Transfer, National
Institutes of Health, 6011 Executive Boulevard, Suite 24, 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.
Genes for Niemann-Pick Type C Disease
DA Tagle, ED Carstea, JA Morris, PG Pentchev, WJ Pavan, MA Rosenfeld,
SK Loftus (NINDS/NHGRI)
Serial No. 60/051,682 filed 03 Jul 97
Licensing Contact: Leopold J. Luberecki, Jr., 301/496-7735 ext. 223
Niemann-Pick disease is a class of inherited lipid storage
diseases. Niemann-Pick Type C disease is an autosomal recessive
neurovisceral lipid storage disorder which leads to systemic and
neurological abnormalities including ataxia, seizures, and loss of
speech. Patients with the disease typically die as children. The
biochemical hallmark of Niemann-Pick Type C cells is the abnormal
accumulation of unesterified cholesterol in lysosomes, which results in
the delayed homeostatic regulation of both uptake and esterification of
low density lipoprotein (LDL) cholesterol. Niemann-Pick Type C is
characterized by phenotypic variability. The disease appears at random
in families that have no history of the disorder, making diagnosis
problematic. This invention provides the human gene for Niemann-Pick
Type C disease and the nucleic acid sequences corresponding to the
human gene for Niemann-Pick Type C disease. Also provided is the mouse
homolog of the human gene. The invention could lead to improved
diagnosis and the design of therapies for the disease and improved
means of detection of carriers of the gene. In addition, this invention
may contribute to the understanding and development of treatments for
atherosclerosis, a more common disorder associated with cholesterol
buildup that involves the accumulation of fatty tissue inside arteries
that blocks blood flow, leading to heart disease and stroke. The
invention may also lead to additional discoveries concerning how
cholesterol is processed in the body.
AIB-1, A Steroid Receptor Co-Activator Amplified in Breast and Ovarian
Cancer
PS Meltzer, JM Trent (NHGRI)
OTT Reference No. E-018-97/0 filed 17 Jun 97
Licensing Contact: Ken Hemby, 301/496-7735 ext. 265
Breast cancer is the number one cancer in U.S. women, with over
185,000 cases in 1996 and an estimated 44,560 deaths in the past year.
Breast cancer arises from estrogen-responsive breast epithelial cells.
Estrogen activity is though to promote the development of breast
cancer, and many breast cancers are initially dependent on estrogen at
the time of diagnosis. Anti-estrogen compositions have therefore been
used to threat breast cancer.
AIB-1 (Amplified in Breast Cancer-1) is a novel gene that is
pivotal to a crucial metabolic pathway linked to the growth and
progression of human breast cancer. In many cancers, especially breast
cancer, tumor cells have amplified copies of genes that can give the
cancer a growth advantage. AIB-1, located on the long arm of chromosome
20, is one such amplified gene. High-level AIB-1 amplification and
overexpression have been observed in several estrogen receptor (ER)
positive breast and ovarian cancer cell lines, as well as in uncultured
breast cancer specimens. AIB-1 has also been found to be expressed in
prostate epithelial cells.
AIB-1 is the most recently identified member of a gene family known
as SRC-1 (steroid receptor coactivator), all of which interact with
genes for steroid hormone receptors, ultimately enhancing tumor cell
growth.
This invention provides the gene for AIB-1, a novel steroid
receptor co-activator which is overexpressed in breast cancer cells. It
also encompasses diagnostic assays for steroid hormone-responsive
cancers and screening assays to identify compounds which inhibit
interactions of the co-activator with steroid hormone receptors and
other proteins in this pathway.
Methods and Compositions for Inhibiting Inflammation and Angiogenesis
K Kelly (NCI)
Serial No. 60/027,871 filed 25 Oct 96
[[Page 51671]]
Licensing Contact: J. Peter Kim, 301/496-7056 ext. 264
The invention provides compositions and methods directed to
isolated subunits of the 7TM protein CD97. CD97 is a
heterodimer existing in three isoforms, namely three forms of
subunit and one invariant subunit. The invention provides
compositions and methods for detecting a subunit of CD97, a T-cell
protein which is unregulated in activated T-cells and is involved in
the onset and maintenance of inflammation and angiogenesis. The
invention provides an isolated protein comprising a soluble CD97
subunit, and an isolated nucleic acid encoding a soluble Cd97
subunit protein. The invention also provides methods for
identifying compounds which inhibit soluble CD97 subunit
expression. The invention may be used to inhibit angiogenesis
associated with chronic inflammation in a mammal by administering a
therapeutically effective amount of a CD97 antagonist. Another
application includes determining the degree of inflammation at a site
in a mammal with an antibody composition specifically reactive to a
soluble CD97 subunit. Further, it should be noted that these
compositions and methods further have in vitro utility in the
construction of proteins and subsequences thereof for the construction
of antibodies, and nucleic acids and subsequences thereof for use as
probes.
Peptides With Laminin Activity
Y Yamada, JO Graf, Y Iwamoto, F Robey, HK Kleinman,
M Sasaki, GR Martin (NIDR)
U.S. Patent 5,092,885 issued 03 Mar 92
Licensing Contact: Jaconda Wagner, 301/496-7735, ext. 284
Peptides with laminin activity, including YIGSR, are claimed. These
peptides block angiogenesis, alter the formation of capillary
structures by endothelial cells, prevent the formation of excess blood
vessels in tissue and inhibit in vivo tumor cell colonization of
tissues. These peptides can be used, among other things, to inhibit
metastasis.
This research has been described in B.J. Cancer 73:589, 1996;
Cancer Res 54:5005, 1994; Semin Cancer Biol 1993 Aug; 4(4):259-65;
Cancer Res 1993 Aug 1;53(15):3459-61; Cell 1987 Mar 27;48(6):989-9.
Laminin A Peptides
Y Yamada, HK Kleiman, M Sasaki, GR Martin (NIDR)
U.S. Patent 5,211,657 issued 18 May 93
Licensing Contact: Jaconda Wagner, 301/496-7735, ext. 284
This invention relates to peptides and derivatives thereof having
laminin-like activity, as well as a pharmaceutical composition of the
peptide. The peptides claimed include Serine-Isoleucine-Lysine-Valine-
Alanine-Valine (SIKVAV). Methods for promoting increased adhesion and
migration of epithelial cells is also disclosed. The peptides have wide
usage in research, nerve regeneration and cancer treatment. For
example, this invention may be useful as an adhesion and regeneration
agent for nerve guides and as an adhesion agent for vascular prothesis.
This research had been described in Bioorganic Medinal Chem Lett
5:711, 1995; J Neurosci Res 1995 Oct 15;42(3):314-22; Cancer Res 1995
Jun 1;55(11):2476-80; FEBS Lett 1995 May 29;365(2-3):227-3; J Cell
Physiol 1994 Jul;160(1):185-93; Cell Immunol 1994 Jan; 153(1):94-104.
Dated: September 25, 1997.
Barbara M. McGarey,
Deputy Director, Office of Technology Transfer.
[FR Doc. 97-26171 Filed 10-1-97; 8:45 am]
BILLING CODE 4140-01-M