[Federal Register Volume 74, Number 68 (Friday, April 10, 2009)]
[Notices]
[Pages 16405-16406]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: E9-8212]


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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, HHS.

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.

Selective Killing of Cancer Cells by Inhibition of Geminin

    Description of Technology: The current strategy for developing 
cancer therapeutics is to identify unique differences between cancer 
cells and normal cells that can serve as specific targets for 
chemotherapeutic drugs, thereby allowing elimination of cancer cells 
with minimal toxicity to normal tissues. Geminin, an inhibitor of DNA 
replication, is typically undetectable in normal cells while rapidly 
proliferating cancer cells express geminin and hence could be targeted 
for cancer treatment. The NIH researchers have discovered that 
inhibition of geminin expression induced DNA re-replication in most of 
the tested cancer cell lines, but not in matched non-cancer cell lines 
from the same tissues. DNA re-replication occurs when DNA synthesis is 
initiated multiple times from the same replication origin during one 
cycle of cell division resulting in DNA damage which halts cell 
proliferation and induces apoptosis in a wide variety of cancer cells. 
The researchers also analyzed the effect of suppression of geminin 
expression on apoptosis and cell survival in cancer and non-cancer cell 
lines. They found that the geminin siRNA induced apoptosis in a colon 
carcinoma cell line, but not in a normal skin fibroblast cell line. 
Furthermore, suppression of geminin expression markedly reduced cell 
survival of several cancer cell lines, but not non-cancer cell lines. 
Therefore, suppressing the level of geminin expression can be 
potentially used to selectively kill cancer cells.
    Applications: Therapeutic for treating breast, colon and rectal, 
kidney (renal cell), lung, brain, and bone cancers.
    Advantages: Targeted therapeutic; No requirement for use of other 
cell cycle inhibitors
    Market: Cancer continues to be a burden to the public health of 
Americans. After heart disease, cancer is the most common cause of 
death in the United States. For 2008, it was estimated that about 
565,650 Americans were expected to die of cancer. The incidence of 
cancer has been dropping over the years but it is estimated that over 
1.4 million Americans would be diagnosed with cancer in 2008. 
Therefore, there is a continued need for the development of new 
therapies to effectively treat this disease.
    Inventors: Wenge Zhu and Melvin L. DePamphilis (NICHD)
    Publications: Paper accepted for publication in Cancer Research.
    Patent Status: U.S. Provisional Application No. 61/106,465 filed 17 
Oct 2008 (HHS Reference No. E-324-2008/0-US-01)
    Licensing Status: Available for licensing.
    Licensing Contact: Betty Tong, PhD; 301-594-6565; 
[email protected].

Transgenic Mice in Which the Gene for MCP-1 Is Deleted

    Description of Technology: Dr. Yoshimura has developed a transgenic 
mouse which does not express the chemokine MCP-1 due to a deletion of 
the gene for MCP-1. MCP-1 is a CC chemokine which is responsible for 
recruiting monocytes into sites of

[[Page 16406]]

inflammation and cancer. Using a thioglycollate challenge as a measure 
of the impact of the deletion of MCP-1, MCP-1 deficient mice exhibit a 
60% reduction in the number of monocytes/macrophages at 96 hours 
compared to wild type mice. Unlike previously generated MCP-1 deficient 
mice in which the expression of the neighboring gene for MCP-3 is down-
regulated (our own data), the expression of MCP-3 is up-regulated in 
this mouse model.
    Applications: This mouse may be useful as an in vivo model for 
evaluating the role of MCP-1 and MCP-3 in cancer or other diseases 
associated with inflammation due to the accumulation of monocytes.
    Inventor: Teizo Yoshimura (NCI)
    Patent Status: HHS Reference No. E-241-2005/0--Research Tool. 
Patent protection is not being pursued for this technology.
    Licensing Status: Available for licensing under a Biological 
Materials License Agreement.
    Licensing Contact: Betty Tong, PhD; 301-594-6565; 
[email protected].
    Collaborative Research Opportunity: The National Cancer Institute, 
Center for Cancer Research, Laboratory of Molecular Immunoregulation, 
Cancer and Inflammation Program, is seeking statements of capability or 
interest from parties interested in collaborative research to further 
develop, evaluate, or commercialize agents useful to treat patients 
with inflammation or cancer. Please contact John D. Hewes, PhD at 301-
435-3121 or [email protected] for more information.

DU145 Camptothecin (CPT)-Resistant Cell Line

    Description of Technology: Drug resistance is a major limitation of 
chemotherapy. Understanding how drug resistance develops may lead to 
more effective treatments. This invention describes the DU145 
Camptothecin (CPT)-resistant prostate cancer cell line that can be used 
to study mechanisms of drug resistance.
    Inventor: Yves G. Pommier (NCI)
    Related Publication: Y Urasaki et al. Characterization of a novel 
topoisomerase I mutation from a camptothecin-resistant human prostate 
cancer cell line. Cancer Res. 2001 Mar 1;61(5):1964-1969.
    Patent Status: HHS Reference No. E-159-2005/0--Research Tool. 
Patent protection is not being pursued for this technology.
    Licensing Status: Available for licensing under a Biological 
Materials License Agreement.
    Licensing Contact: Betty Tong, PhD; 301-594-6565; 
[email protected].

Creation and Characterization of Carcinogen-Altered Mouse Epidermal 
Cell Lines

    Description of Technology: The invention relates to the creation of 
three (3) cell lines that may be used as models of putative initiated 
cancer cells. The cell lines can be used in basic research assays and 
low/high throughput screening assays.
    Cell line 308 evolved from a calcium-resistant focus from adult 
mouse epidermis that was exposed to the carcinogen, 7,12-
dimethylbenz[a]anthracene (DMBA). Cell lines F and D were derived by 
treating primary newborn mouse epidermal cells in culture with N-
methyl-N[iacute]-nitro-N-nitrosoguanidine (MNNG) and DMBA, 
respectively. These three (3) noncancerous cell lines derived from 
differentiation-resistant, carcinogen-induced foci may be considered to 
be putative initiated cells.
    Inventor: Stuart H. Yuspa (NCI)
    Related Publications:
    1. SH Yuspa and DL Morgan. Mouse skin cells resistant to terminal 
differentiation associated with initiation of carcinogenesis. Nature 
1981 Sep 3;293(5287):72-74.
    2. H Hennings et al. Response of carcinogen-altered mouse epidermal 
cells to phorbol ester tumor promoters and calcium. J Invest Dermatol. 
1987 Jan;88(1):60-65.
    Patent Status: HHS Reference No. E-154-2004/0--Research Tool. 
Patent protection is not being pursued for this technology.
    Licensing Status: Available for licensing under a Biological 
Materials License Agreement.
    Licensing Contact: Betty Tong, PhD; 301-594-6565; 
[email protected].

A Mouse Model for Conditional Gene Deletion of c-Met Receptor

    Description of Technology: c-Met oncogene has been implicated in a 
variety of human cancers as well as degenerative diseases. Signaling 
via the c-Met receptor is essential for survival as evidenced by the 
embryonal death of mice in which the c-Met has been deleted. Further 
analysis of the role of the signaling pathway supported by c-Met 
receptor in the adult organism is hindered by its embryonic lethality. 
The establishment of a mouse model for the conditional c-Met gene 
deletion will provide a unique opportunity to explore the function of 
c-Met in the adult mouse by selectively deleting the receptor gene in 
various tissues. Such a mouse model is established at the National 
Institutes of Health and available for licensing.
    Applications:
     Animal model to study the physiological role of the c-Met 
receptor.
     Animal model for testing potential drug targeted to the c-
Met signal transduction pathway.
    Inventor: Snorri S. Thorgeirsson (NCI)
    Patent Status: HHS Reference No. E-048-2003/0--Research Tool. 
Patent protection is not being pursued for this technology.
    Licensing Status: c-Met receptor conditional KO mice are available 
for licensing.
    Licensing Contact: Betty Tong, PhD; 301-594-6565; 
[email protected].

    Dated: April 6, 2009.
Richard U. Rodriguez,
Director, Division of Technology Development and Transfer, Office of 
Technology Transfer, National Institutes of Health.
 [FR Doc. E9-8212 Filed 4-9-09; 8:45 am]
BILLING CODE 4140-01-P