[Federal Register Volume 64, Number 37 (Thursday, February 25, 1999)]
[Notices]
[Pages 9341-9342]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 99-4661]
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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.
ADDRESS: Licensing information and copies of the U.S. patent
applications listed below may be obtained by contacting Susan S.
Rucker, J.D., Patent and Licensing Specialist, Office of Technology
Transfer, National Institutes of Health, 6011 Executive Boulevard,
Suite 325, Rockville, Maryland 20852-3804; telephone: 301/496-7057 ext.
245; fax: 301/402-0220; e-mail: [email protected]. A signed Confidential
Disclosure Agreement will be required to receive copies of the patent
applications.
Attenuated and Dominant Negative Varient cDNAs of Stat6: Stat6b and
Stat6c
WJ LaRochelle, BKR Patel, JH Pierce (NCI)
PCT/US98/17821 filed 27 Aug 1998 and based on applications 60/070,397
and 60/056,075.
These application(s) disclose the identification, isolation,
cloning and sequencing of two human variants of a signal transducer and
activator of transcription (STAT) protein known as Stat6. The variants
or isoforms of human Stat6 are designated Stat6b and Stat6c and they
are, respectively, attenuated and dominant negative isoforms of Stat6.
The STAT proteins are a family of signal transduction molecules which
have been shown to play a role in modulating the activity of a variety
of cytokines. In particular, Stat6 has been shown to be involved in
interleukin-4 (IL-4) regulation suggesting that Stat6 may play a role
in inflammatory and cell-mediated immune responses. The dominant
negative isoform, Stat6c, is particularly interesting because of its
ability to down-regulate the IL-4 response. This suggest that it may be
useful alone or in identifying agents which may be useful in treating
diseases linked to the IL-4 response such as asthma. Diagnostic
applications for allergy or asthma may also be possible. In addition to
describing the variants of Stat6 the application describes the promoter
for Stat6 and notes that the gene is located on the long arm of
chromosome 12 at 12q13.3-14.1. Regulation of the Stat6 promoter might
provide insights toward the control of proliferative and inflammatory
processes.
This work has appeared, in part, in PNAS, USA 95(1):172-77 (January
6, 1998) and Genomics 52(2):192-200 (Sept. 1, 1998).
Methods and Compositions for Treatment of Restenosis
AB Mukherjee, GC Kundu, DK Panda (NICHD)
DHHS Reference No. E-163-96/1 filed 07 Aug 98 (PCT/US98/16569) and
claiming priority to 60/054,694 filed 07 Aug 97
This application describes the use of antisense oligonucleotides
designed to inhibit osteopontin production, and their use in treating
restenosis, the reocclusion of an artery following angioplasty.
Utilizing blood samples and coronary artery tissues from patients it
was demonstrated that OPN levels are increased both in the
atherosclearotic tissues as well as in the blood following angioplasty.
Further, using an in vitro system employing human coronary artery
smooth muscle cell culture (CASMC), it has been demonstrated that these
antisense molecules inhibit osteopontin expression.
This research has been published in PNAS USA 94(19):9308-13 (August
18, 1997).
cDNA for a Human Gene Deleted in Liver Cancer
BZ Yuan, NC Popescu, SS Thorgeirsson (NCI)
Serial No. 60/075,952 filed 25 Feb 98
This application discloses the identification, isolation, cloning
and sequencing of a newly discovered gene, DLC-1 (Deleted in Liver
Cancer), which has been localized to the short arm of chromosome 8 at
8p21.3-22 using FISH (fluorescent in situ hybridization). Studies of
human tumors show that DLC-1 is deleted in 50% of primary
hepatocellular carcinomas and is not expressed in 20% of hepatocellular
carcinoma cell lines. This differential expression suggests that
diagnostic applications of DLC-1 may be developed. Other cancers where
preliminary data indicates that DLC-1 may have diagnostic possibilities
are breast and colon cancer. A polyclonal antibody which recognizes
DLC-1 has been characterized. Work to date indicates that DLC-1 is a
tumor suppressor gene suggesting that gene therapy utilizing DLC-1 may
also be possible.
This work has appeared, in part, in Cancer Research 58(10) : 2196-9
(May 15, 1998).
Partial Intron Sequence of Von Hippel-Lindau (VHL) Disease Gene and
Its Use in Diagnosis of Disease
WM Linehan, MI Lerman, F Latif, B Zbar (NCI)
Serial No. 08/623,428 filed 28 Mar 96
This application, in conjunction with patents 5,654,138 (8/5/1997)
and 5,759,790 (6/2/1998), describes the isolation, cloning, and
sequencing of the gene associated with Von Hippel Lindau (VHL)
syndrome. The sequence of VHL includes, in addition to the coding
region, the sequence of the VHL promoter and genomic sequence
information at the intron/exon boundaries of the VHL gene. The VHL gene
is found on the short arm of chromosome 3 at 3p25-26. It functions as a
tumor suppressor and has been associated with sporadic kidney cancer,
[[Page 9342]]
in particular clear cell renal carcinoma (cRCC). In particular,
antibody-based or nucleotide-based diagnostics are contemplated in the
applications. Various techniques have been used to examine VHL
mutations including FISH (fluorescent in situ hybridization), southern
blotting, PCR-SSCP and complete sequencing of the VHL gene.
There are numerous publications detailing the work of Dr. Linehan
and his colleagues regarding the VHL disease gene. Two of these are Hum
Mutat 12(6): 417-23 (1998) and Biochim Biophys Acta 1243 (3): 201-10
(March 18, 1996).
Dated: February 18, 1999.
Jack Spiegel,
Director, Division of Technology Development and Transfer, Office of
Technology Transfer.
[FR Doc. 99-4661 Filed 2-24-99; 8:45 am]
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