[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]
BILLING CODE 4140-01-M