[Federal Register Volume 69, Number 91 (Tuesday, May 11, 2004)]
[Notices]
[Page 26173]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 04-10689]


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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.

Mouse Model With Targeted Disruption of the Neurofibromatosis Type-1 
(Nf1) Gene

Neal G. Copeland et al. (NCI).
DHHS Reference No. E-162-2004/0--Research Tool
Licensing Contact: Jesse S. Kindra; 301-435-5559; [email protected].

    This invention relates to a mouse model having a targeted 
disruption of the neurofibromatosis type-1 (NF1) gene. This mouse model 
is useful as a research tool in studying some forms of human neuron 
diseases/injuries in addition to juvenile chronic myelomonocytic 
leukemia (JMML).
    The neurofibromatosis (NF1) gene shows significant homology to 
mammalian GAP and is an important regulator of the Ras signal 
transduction pathway. To study the function of NF1 in normal 
development and to develop a mouse model of NF1 disease, the inventors 
have used gene targeting in ES cells to generate mice carrying a null 
mutation at the mouse Nf1 locus. Although heterozygous mutant mice, 
aged up to 10 months, have not exhibited any obvious abnormalities, 
homozygous mutant embryos die in utero. Embryonic death is likely 
attributable to a severe malformation of the heart. Interestingly, 
mutant embryos also display hyperplasia of neural crest-derived 
sympathetic ganglia. These results identify new roles for NF1 in 
development and indicate that some of the abnormal growth phenomena 
observed in NF1 patients can be recapitulated in neurofibromin-
deficient mice. In addition, lethally-irradiated wild type mice 
transplanted with fetal liver cells taken from NF1 null embryos develop 
a form of juvenile chronic myelomonocytic leukemia (JMML) that is very 
similar to what is seen in children with NF1 disease. This mouse model 
can be used to test various therapeutic treatments for this disease.

Novel Antisense Oligonucleotides Targeting Folate Receptor Alpha

Mona S. Jhaveri, Patrick C. Elwood, Koong-Nah Chung (NCI).
U.S. Patent Application No. 10/093,523 filed 11 Mar 2002, U.S. Pat. 
App. Pub. No. U.S. 2003/0050267 A1 (DHHS Reference No. E-321-2000/0-
EIR-00).
Licensing Contact: Thomas P. Clouse; 301/435-4976; 
[email protected].

    Ovarian cancer is the fifth leading cause of cancer death for women 
in the United States. Drug resistance of ovarian tumors to chemotherapy 
is a common problem resulting in only 20 to 30 percent overall 5-year 
survival rates.
    Folate is a vitamin that is required for cell survival. Some cancer 
cells, including ovarian carcinomas, have an abundance of a folate-
binding protein termed the human alpha folate receptor (ahFR). It is 
believed that elevated levels of ahFR in cancer, relative to normal 
cells, contribute to the cellular malignant phenotype by mediating 
increased folate uptake or by generating positive regulatory growth 
signals.
    This invention comprises a DNA-based therapy that selectively 
targets and diminishes the levels of ahFR using antisense 
oligonucleotides that block the transcription of the ahFR gene. Studies 
have shown that this invention significantly decreases proliferation of 
cultured cancer cells and sensitizes these cells to treatment with 
chemotherapeutic drugs. Further development of ahFR-targeted antisense 
oligonucleotides and related compounds has potential therapeutic value 
for a range of cancers that express increased levels of ahFR, including 
cancers of the ovary, cervix, uterus, and brain.

    Dated: May 5, 2004.
Steven M. Ferguson,
Director, Division of Technology Development and Transfer, Office of 
Technology Transfer, National Institutes of Health.
[FR Doc. 04-10689 Filed 5-10-04; 8:45 am]
BILLING CODE 4140-01-P