[Federal Register Volume 65, Number 146 (Friday, July 28, 2000)]
[Notices]
[Pages 46478-46479]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 00-19153]


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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.

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.

Discovery of a Novel Human Aminopeptidase Which May Regulate 
Cleavage and Shedding of the Human Type-I Tumor Necrosis Factor 
Receptor

Stewart J. Levine (NHLBI)
DHHS Reference No. E-003-00/0 filed 28 Feb 2000
Licensing Contact: Richard U. Rodriguez; 301/496-7056 ext. 287; e-mail: 
[email protected]

    Cytokines are a large and diverse group of molecules which mediate 
interactions between cells. Aberrant regulation of cytokine signaling 
results in a wide variety of hyper-inflammatory, autoimmune and immune-
deficiency pathological conditions. Tumor necrosis factor- 
(TNF-) is a multifunctional cytokine mediating pleiotropic 
biological functions in both healthy and disease states. TNF- 
has been shown to have a role in the following activities: Destroying 
tumors, mediating responses to tissue injury, protecting hosts from 
infections by various microorganisms and activating numerous genes, 
including NF-B and AP-1. TNF- has also been 
implicated in the pathogenesis of a variety of diseases and disorders. 
The present invention provides compositions and methods related to 
regulation of cytokine signaling through the TNF- pathway. 
Specifically, the invention provides a novel gene, polypeptide and 
related compositions and methods for the regulation of TNF Type-I 
receptor ectodomain shedding. It is contemplated that the compositions 
and methods of this invention will find use in therapeutics for the 
treatment of diseases and disorders of the immune system.

Amplification and Overexpression of Multiple Genes at 17q23 in 
Breast Cancer

Anne H Kallioniemi, Olli P Kallioniemi, Juha T Kononen, Maarit Barlund 
(NHGRI)
DHHS Reference No. E-051-00/0 filed 28 Jan 2000
Licensing Contact: Richard U. Rodriguez; 301/496-7056 ext. 287; e-mail: 
[email protected]

    This invention pertains to gene amplification and its role in the 
progression and initiation of many solid

[[Page 46479]]

tumors, including breast cancer. Amplification is a common mechanism 
for upregulation of critical genes involved in cancer development and 
progression. Discovery of HER-2 oncogene amplification in breast cancer 
has led to a specific therapy for breast cancer patients with an 
activated HER-2 gene. Chromosomal region 17q23 is frequently amplified 
in breast cancer but the genes involved in this amplification are not 
yet known. Amplification of four previously known genes, S6K, TBX2, 
PAT1, RAD51C, has been identified in breast cancer cell lines and 
primary breast tumors. The amplification in cell lines leads to 
overexpression at the mRNA level. Thus, these genes represent putative 
targets for the 17q23 amplification and their upregulation may 
contribute to the genesis and progression of breast cancer.

Inhibition of Cell Motility

Donald P. Bottaro, Terrence R. Burke, Jr., Zhu-Jun Yao, Nese S. Atabey, 
Diane E. Breckenbridge, Yang Gao (NCI)
DHHS Reference No. E-265-99/0 filed 22 Oct 1999
Licensing Contact: Richard U. Rodriguez; 301/496-7056 ext. 287; e-mail: 
[email protected]

    The present invention relates to a method of inhibiting cell 
motility induced by hepatocyte growth factor (HGF) and treating various 
diseases in a mammal. HGF stimulates mitogenesis, motogenesis and 
morphogenesis in a wide range of cellular targets including epithelial 
and endothelial cells, hematopoietic cells, neurons, melanoytes, and 
hepatocytes. These pleiotropic effects play important roles during 
development and tissue regeneration, but they are also implicated in 
several human cancers, including colon, breast, lung, thyroid and renal 
carcinomas, several sarcomas and gliolastomas. The ability of HGF to 
initiate a program of cell dissociation and increased cell motility 
coupled with increased protease production promotes aggressive cellular 
invasion and is linked to tumor metastasis. The methods of the present 
invention employ compounds, e.g., phosphotyrosine mimetics, to inhibit 
cell motility. A key advantage of this invention is that the peptides 
are free of cytotoxicity. Further development and use of this invention 
could serve a serious public need.

Fibroblast Growth Factor-5 (FGF-5) Is a Tumor Associated T-cell 
Antigen for Human Renal Cell Cancer and Other Adenocarcinomas

Ken-ichi Hanada and James C. Yang (NCI)
DHHS Reference No. E-243-99/0 filed 02 Oct 1999
Licensing Contact: Elaine Gese; 301/496-7056 ext. 282; e-mail: 
[email protected]

    Renal cell carcinoma (RCC) is a form of kidney cancer caused when 
cells in the lining of the renal tubule undergo cancerous changes. The 
inventors have shown that fibroblast growth factor-5 (FGF-5) is a tumor 
associated antigen (TAA) for RCC and cancers of the breast and 
prostate. TAAs can be used to stimulate cytotoxic T-lymphocytes (CTL) 
which can be directed against specific tumor cells. This can be 
accomplished in at least two ways: (1) Activating a patient's immune 
system by administering a vaccine containing the TAA, or (2) by 
removing a patient's lymphoid cells, activating these cells ex vivo and 
then reintroducing these activated cells back into the patient to 
attack the tumor cells. The invention provides for methods of treating 
RCC and other adenocarcinomas with FGF-5 using the aforementioned 
approaches.

Genetic System in Yeast for Functional Identification of Human p53 
Mutations

Michael A. Resnick, Alberto Inga (NIEHS)
DHHS Reference No. E-183-99/0 filed 30 Jul 1999
Licensing Specialist: Vasant Gandhi; 301/406-7056 ext. 224; e-mail: 
[email protected]

    The tumor suppressor gene p53, a key regulator of cellular 
mechanisms that maintain genome integrity, is the most commonly 
inactivated gene target associated with neoplastic transformation. 
About 50% of all human tumors express a mutated form of p53 and more 
than 80% of these mutations are missense, leading to single amino acid 
changes. This invention relates to human p53 mutants and identification 
methods using screening assays in the yeast Saccharomyces cerevisiae to 
functionally categorize expressed p53 mutant proteins. Additionally, 
the invention relates to methods of detecting or generating novel human 
p53 mutations with properties that can include toxicity in yeast and 
growth suppression in human cells, enhanced or reduced transactivation 
relative to wild type p53, altered promoter selectivity, and 
reactivation of common tumor mutations for the transactivation function 
of major p53 downstream genes. The invention also provides for 
screening of genetic factors, peptides and chemicals that mimic the 
toxic or supertransactivating mutations or inhibit p53 function.

    Dated: July 19, 2000.
Jack Spiegel,
Director, Division of Technology Development and Transfer, Office of 
Technology Transfer, National Institutes of Health.
[FR Doc. 00-19153 Filed 7-27-00; 8:45 am]
BILLING CODE 4140-01-P