[Federal Register Volume 69, Number 173 (Wednesday, September 8, 2004)]
[Notices]
[Pages 54297-54298]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 04-20295]


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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 an agency 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 writing to the indicated 
licensing contact at the Office of Technology Transfer, National 
Institutes of Health, 6011 Executive Boulevard, Suite 325, 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.

Vectors for Wild-Type DDR1b or DDR1b Mutant, and Production of THP-1 
Cell Line Expressing Two DDR1 Isoforms, DDR1a and DDR1b

Teizo Yoshimura (NCI)
    DHHS Reference No.: E-243-2004/0--Research Material.
    Licensing Contact: Jesse S. Kindra; (301) 435-5559; 
[email protected].
    This technology relates to cloning of cDNAs coding for human 
discoidin domain receptor (DDR1) cDNAs (clone 11A for DDR1a and Clone 
11B for DDR1b) from a human lung cDNA library; a mammalian expression 
vector for wild-type DDR1b or DDR1b mutant, and a THP-1 cell line 
expressing two DDR1 isoforms, DDR1a and DDR1b. These materials are 
useful to study the role and signaling pathways of DDR1 and to identify 
agonists or antagonists of these receptors.

[[Page 54298]]

    Additional information regarding these materials is described in: 
Kamohara et al., ``Discoidin domain receptor 1 isoform-a (DDR1a) 
promotes migration of leukocytes in three-dimensional collagen 
lattices,'' FASEB J, 15:2724-2726, 2001; Matsuyama et al., 
``Interaction of discoidin receptor 1 isoform b (DDR1b) with collagen 
activates p38 mitogen-activated protein kinase and promotes 
differentiation of macrophages,'' FASEB J, 17:1286-1288, 2003; 
Matsuyama et al., ``Activation of discoidin receptor 1 facilitates the 
maturation of human monocyte-derived dendritic cells through the TNF 
receptor associated factor 6/TGF-beta-activated protein kinase 1 
binding protein 1beta/p38alpha mitogen-activated protein kinase 
signaling cascade,'' J. Immunol. 171:3520-3532, 2003; Matsuyama et al., 
``Activation of discoidin domain receptor 1 isoform b with collagen up-
regulates chemokine production in human macrophages: Role of p38 
mitogen-activated protein kinase and NF-kB,'' J. Immunol. 172:2332-
2340, 2004.

Method for Ex-Vivo Selection and Expansion of Stimulus-Responding 
Primary Cells Using Selective Reversible Immortalization

Eugene Barsov, David Ott (NCI)
    U.S. Provisional Application No.: 60/528,244 filed 09 Dec 2003 
(DHHS Reference No. E-210-2002/0-US-01).
    Licensing Contact: Mojdeh Bahar; (301) 435-2950; 
[email protected].
    This invention is a gene transfer technique to immortalize primary 
cells (e.g. lymphocytes) that respond to a stimulus, such as a viral 
antigen (e.g. HIV toxoids), a tumor antigen, or a growth factor. The 
antigen or growth factor stimulates a specific subset of primary cells 
within a population of cells to proliferate and divide. Murine leukemia 
virus (MuLV)-based retroviral vectors comprising a gene or genes for 
immortalization are used to transfect primary cells that have been 
stimulated to divide. Since MuLV retroviral vectors will only infect 
dividing cells, only primary cells activated by the antigen or growth 
factor will be infected by this retroviral vector and immortalized, 
thereby creating an ``antigen-specific trap.'' The primary cells to be 
immortalized can be in targeted tissue or in stimulated ex vivo 
culture. The transduced cells are expanded to large numbers without 
differentiating, and brought back to the primary cell stage by removing 
the introduced genes (e.g. by Cre-lox recombination). The expanded 
population of primary cells can then be used.

Hybrid Adeno-Retroviral Vector for the Transformation of Cells

Changyu Zheng, Brian O'Connell, Bruce J. Baum (NIDCR)
    U.S. Provisional Application No.: 60/265,198 filed 30 Jan 2001 
(DHHS Reference No. E-312-2000/0-US-01; PCT Application PCT/US02/02279 
filed 25 Jan 2002, which was published as WO 02/061104 on 30 Jul 2002 
(DHHS Reference No. E-312-2000/0-PCT-02).
    U.S. Patent Application No.: 10/470,784 filed 29 Jul 2003 (DHHS 
Reference No. E-312-2000/0-US-03).
    Licensing Contact: Jesse Kindra; (301) 435-5559; 
[email protected].
    The invention described and claimed in these patent applications 
provides for novel hybrid vectors which may be used for cell 
transformation either in vivo, in vitro, or ex vivo. The hybrid 
vectors, which are capable of integrating into the chromosome of the 
host cell and are capable of transducing dividing and non-dividing 
cells, have an adenoviral serotype 5 backbone and two retroviral 
(Moloney murine leukemia virus) elements upstream and downstream of the 
transgene. These elements include part of the envelope sequence, the 
long terminal repeat (LTR) and the packaging signal sequence 
(upstream), and part of the envelope sequence and LTR (downstream). Due 
to their hybrid nature, these vectors provide a means of efficient, 
reliable, long-term gene expression. Furthermore, unlike other chimeric 
or hybrid vector systems, only a single vector is required to deliver a 
transgene of interest and retroviral functional proteins are not 
required. The vectors are packaged and delivered via an adenoviral 
particle and administered directly to the target cell.
    This research is described, in part, in: Zheng et al., ``Inclusion 
of Moloney murine leukemia virus elements upstream of the transgene 
cassette in an E1-deleted adenovirus leads to an unusual genomic 
integration in epithelial cells,'' Virology 2003 313:460-72, 2003; 
Zheng et al., ``Integration efficiency of a hybrid adenoretroviral 
vector,'' Biochem Biophys Res Commun. 300:115-20, 2003; Zheng & Baum, 
``Long-term expression after infection by the hybrid vector AdLTR-luc 
is from integrated transgene,'' Biochem Biophys Res Commun. 291:34-40, 
2002.

    Dated: August 31, 2004.
Steven M. Ferguson,
Director, Division of Technology Development and Transfer, Office of 
Technology Transfer, National Institutes of Health.
[FR Doc. 04-20295 Filed 9-7-04; 8:45 am]
BILLING CODE 4140-01-P