Government-Owned Inventions; Availability for Licensing, 21431-21434 [05-8287]

Download as PDF Federal Register / Vol. 70, No. 79 / Tuesday, April 26, 2005 / Notices obtained by contacting Ms. Farrar or by accessing the Web site managed by OMH at https://www.omhrc.gov/acmh. SUPPLEMENTARY INFORMATION: Pursuant to Public Law 105–392, the Secretary of Health and Human Services established the Advisory Committee on Minority Health (ACMH). The Committee shall provide advice to the Deputy Assistant Secretary for Minority Health in carrying out the duties stipulated under Public Law 105–392. This includes providing advice to improve the health of each racial and ethnic minority group and in the development of goals and specific activities of the OMH, which are: (1) Establish short-range and longrange goals and objectives and coordinate all other activities within the Public Health Service that relate to disease prevention, health promotion, service delivery, and research concerning such individuals; (2) Enter into interagency agreements with other agencies of the Public Health Service; (3) Support research, demonstrations, and evaluations to test new and innovative models; (4) Increase knowledge and understanding of health risk factors; (5) Develop mechanisms that support better information dissemination, education, prevention, and service delivery to individuals from disadvantaged backgrounds, including individuals who are members of racial or ethnic minority groups; (6) Ensure that the National Center for Health Statistics collects data on the health status of each minority group; (7) With respect to individuals who lack proficiency in speaking the English language, enter into contracts with public and nonprofit private providers of primary health services for the purpose of increasing the access of the individuals to such services by developing and carrying out programs to provide bilingual or interpretive services; (8) Support a national minority health resource center to carry out the following: (a) Facilitate the exchange of information regarding matters relating to health information and health promotion, preventive health services, and education in appropriate use of health care; (b) facilitate access to such information; (c) assist in the analysis of issues and problems relating to such matters; (d) provide technical assistance with respect to the exchange of such information (including facilitating the development of materials for such technical assistance); and (9) Carry out programs to improve access to health care services for VerDate jul<14>2003 11:52 Apr 25, 2005 Jkt 205001 individuals with limited proficiency in speaking the English language. Activities under the preceding sentence shall include developing and evaluating model projects. Management and support services for the ACMH are provided by the OMH, which is a program office within the OPHS. Nominations The OPHS is requesting nominations for vacant positions on the ACMH. The Committee is composed of 12 voting members, in addition to non-voting ex officio members. This announcement is seeking nominations for voting members. Voting members of the Committee are appointed by the Secretary from individuals who are not officers or employees of the Federal Government and who have expertise regarding issues of minority health. To qualify for consideration of appointment to the Committee, an individual must possess demonstrated experience and expertise working on issues/matters impacting the health of racial and ethnic minority populations. The charter stipulates that the racial and ethnic minority groups shall be equally represented on the Committee membership. Individuals selected for appointment to the Committee shall be invited to serve four year terms. Committee members who are not officers or employees of the United States Government will receive a stipend for attending Committee meetings and conducting other business in the interest of the Committee, including per diem and reimbursement for travel expenses incurred. Nominations should be typewritten. The following information should be included in the package of material submitted for each individual being nominated for consideration: (1) A letter of nomination that clearly states the name and affiliation of the nominee, the basis for the nomination (i.e., specific attributes which qualify the nominee for service in this capacity), and a statement that the nominee is willing to serve as a member of the Committee; (2) the nominator’s name, address, and daytime telephone number, and the home and/ or work address, telephone number, and e-mail address of the individual being nominated; and (3) a current copy of the nominee’s curriculum vitae. The names of Federal employees should not be nominated for consideration of appointment to this Committee. The Department makes every effort to ensure that the membership of DHHS Federal advisory committees is fairly balanced in terms of points of view PO 00000 Frm 00043 Fmt 4703 Sfmt 4703 21431 represented and the committee’s function. Every effort is made to ensure that a broad representation of geographic areas, females, ethnic and minority groups, and the disabled are given consideration for membership on DHHS Federal advisory committees. Appointment to this Committee shall be made without discrimination on the basis of age, race, ethnicity, gender, sexual orientation, disability, and cultural, religious, or socioeconomic status. Nominations must state that the nominee is willing to serve as a member of ACMH and appears to have no conflict of interest that would preclude membership. An ethics review is conducted for each selected candidate. Therefore, individuals selected for nomination will be required to provide detailed information concerning such matters as financial holdings, consultancies, and research grants or contracts to permit evaluation of possible sources of conflict of interest. Dated: April 13, 2005. Garth N. Graham, Deputy Assistant Secretary for Minority Health. [FR Doc. 05–8250 Filed 4–25–05; 8:45 am] BILLING CODE 4150–29–P DEPARTMENT OF HEALTH AND HUMAN SERVICES National Institutes of Health Government-Owned Inventions; Availability for Licensing National Institutes of Health, Public Health Service, DHHS. ACTION: Notice. AGENCY: 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. E:\FR\FM\26APN1.SGM 26APN1 21432 Federal Register / Vol. 70, No. 79 / Tuesday, April 26, 2005 / Notices Composition and Methods for Diagnosis and Treatment of Metastatic Disease Xin Wei Wang and Anuradha Budhu (NCI). U.S. Provisional Application filed 8 Mar 2005 (DHHS Reference No. E–127– 2005/0–US–01). Licensing Contact: Michelle A. Booden; 301/451–7337; boodenm@mail.nih.gov. Liver cancer, particularly hepatocellular carcinoma (HCC), is a leading cause of cancer deaths worldwide. In spite of recent progress in therapeutic strategies, prognosis of patients with advanced HCC remains very poor. Although routine screening of individuals at risk for developing HCC may extend the life of some patients, many are still diagnosed with advanced HCC and have little chance of survival. A small subset of HCC patients qualifies for surgical intervention, but the consequent improvement in longterm survival is only modest. The extremely poor prognosis of HCC is largely the result of a high rate of recurrence after surgery or of intrahepatic metastases that develop through invasion of the portal vein or spread to other parts of the liver; extra-hepatic metastases are less common. The present invention describes tools to determine a unique gene expression profile present in either liver parenchyma through needle biopsy or blood that can aid diagnosis or prognosis of HCC patients with or without metastatic potential. This method also provides a signaturederived polymerase chain reaction or serological screening method to identify drug candidates to treat metastatic or recurrent HCC. In addition to licensing, the technology is available for further development through collaborative research opportunities with the inventors. Aminoglycosides and Ribosome Inhibitors as Inhibitors of TyrosylDNA-Phosphodiesterase Drs. Yves Pommier and Zhi-Yong Liao (NCI). DHHS Reference No. E–117–2005/0– US–01. Licensing Contact: John Stansberry; 301/ 435–5236; stansbej@mail.nih.gov. Cancer has long been a leading cause of mortality in the United States. DNAdamaging therapies, such as radiotherapy and chemotherapy, are the methods of choice for treating subjects with metastatic cancer or subjects with diffuse cancers such as leukemias. However, radiotherapy can cause substantial damage to normal tissue in VerDate jul<14>2003 11:52 Apr 25, 2005 Jkt 205001 the treatment field, resulting in scarring and, in severe cases, loss of function of the normal tissue. Although chemotherapy can provide a therapeutic benefit in many cancer subjects, it often fails to treat the disease because cancer cells may become resistant to the chemotherapeutic agent. To overcome these limitations additional antineoplastic strategies, such as enhancing the antineoplastic effect of existing therapies, are needed. This invention discloses a method for enhancing an antineoplastic effect of a DNA-damaging therapy. The method includes administering to a subject having a neoplasm a therapeutically effective amount of the DNA-damaging therapy and a ribosome inhibitor that inhibits tyrosyl-DNA phosphodiesterase 1 (Tdp1) activity, wherein the ribosome inhibitor is administered in a sufficient amount to enhance the DNA-damaging therapy. This disclosure also provides pharmaceutical compositions that include at least one chemotherapeutic agent and at least one ribosome inhibitor that inhibits Tdp1 activity, wherein the chemotherapeutic agent and the ribosome inhibitor are present in a therapeutically effective amount for the ribosome inhibitor to enhance an antineoplastic effect of the chemotherapeutic agent. In addition to licensing, the technology is available for further development through collaborative research opportunities with the inventors. Inhibition of Proteosome Function to Potentiate the Proapoptotic and Antitumor Activity of Cytokines Jon Wigginton et al. (NCI). U.S. Provisional Patent Application filed 23 Mar 2005 (DHHS Reference No. E–072–2005/0–US–01). Licensing Contact: Michelle A. Booden; 301/451–7337; boodenm@mail.nih.gov. Protein degradation via the ubiquitinproteosome pathway is an important regulator of cell cycle progression and survival. Thus, inhibitors of this pathway can be directly cytotoxic and can sensitize several tumor cell types to cytotoxic chemotherapy and radiation. Neuroblastoma is the most common extracranial solid tumor in children, and the development of clinical resistance to cytotoxic therapies is a major therapeutic obstacle in these patients. Several apoptosis abnormalities, which result from decreased expression of pro-apoptotic proteins, are associated with increased resistance to standard therapeutic interventions. In addition, PO 00000 Frm 00044 Fmt 4703 Sfmt 4703 neuroblastoma cells also show increased expression of several pro-survival proteins such as Bcl-2, FLIP, and AKT. Preclinical models suggest that IFNgamma/TNF-alpha cytokines including IL–2, IL–12 and IL–18 among others may have potent antitumor efficacy in several preclinical models, and that these regimens may act by inducing an adaptive cell-mediated immune response. Although some single agent cytokine regimens have achieved modest efficacy in the clinical setting, the utility of some approaches has been limited overall by side effects that can be associated with high-dose cytokine therapy. The present invention describes a method for combining ubiquitinproteosome inhibitors with various cytokines to overcome mechanisms of tumor self-defense and sensitize both tumor and/or endothelial cell populations to apoptosis. These combination approaches may not only offer the prospect for improved therapeutic efficacy, but achieve these effects at lower, more clinically tolerable doses than can be achieved utilizing either respective agent alone. It is anticipated that this therapeutic intervention could be directed towards multiple human carcinomas, and potentiate the efficacy of multiple different cytokines both in the setting of oncology and infectious disease applications. In addition to licensing, the technology is available for further development through collaborative research opportunities with the inventors. Methods for Inhibiting or Treating Cancer Ernest Hamel (NCI), et al. U.S. Provisional Application No. 60/ 616,347 filed 05 Oct 2004 (DHHS Ref. No. E–323–2004/0–US–01). Licensing Contact: Thomas P. Clouse; 301/435–4076; clouset@mail.nih.gov. This invention describes novel arylthioindole derivatives having enhanced interaction with tubulin and increased effectiveness in growth inhibition of MCF–7 breast cancer cells as well as other cell types. Antitubulin drugs have an established role in the treatment of cancer, parasitic diseases and inflammatory disorders. These new chemical compounds have the potential to result in more effective therapeutics for the treatment of neoplastic, inflammatory and parasitic diseases. In addition to licensing, the technology is available for further development through collaborative research opportunities with the inventors. E:\FR\FM\26APN1.SGM 26APN1 Federal Register / Vol. 70, No. 79 / Tuesday, April 26, 2005 / Notices Regulation of ATG7 Beclin 1 Program of Autophagic Cell Death by Caspase-8 Michael Lenardo and Yu Li (NIAID), et al. U.S. Provisional Application No. 60/ 556,857 filed 30 May 2004 (DHHS Reference No. E–318–2004/0–US–01). Licensing Contact: Mojdeh Bahar; 301/ 435–2950; baharm@mail.nih.gov. The invention discloses the role of autophagy in regulation cell death. Further it teaches a method of inducing autophagic cell death by administering a caspase inhibitor. The invention also discloses that autophagic cell death can be induced by caspase-8 inhibition and requires the genes ATG7 and Beclin 1. In addition to licensing, the technology is available for further development through collaborative research opportunities with the inventors. Cancer Specific SPANX–N Markers Natalay Kouprina et al. (NCI). DHHS Reference No. E–212–2004/0– US–01. Licensing Contact: Mojdeh Bahar; 301/ 435–2950; baharm@mail.nih.gov. The invention provides SPANX–N polypeptides, nucleic acids and antibodies that could be useful for detecting and treating prostate or other cancers. The SPANX–N genes are a family of related genes that are expressed in normal testis and in tumor cells in humans including melanoma, bladder carcinomas and myelomas. The SPANX cancer/testis antigens thus represent good candidates for diagnosis or treatment of several cancers. In addition to licensing, the technology is available for further development through collaborative research opportunities with the inventors. Methods for Inhibiting or Treating Cancer Srividya Swaminathan, Shyam Sharan (NCI). U.S. Provisional Application No. 60/ 588,918 filed 16 Jul 2004 (DHHS Reference No. E–160–2004/0–US–01). Licensing Contact: Thomas P. Clouse; 301/435–4076; clouset@mail.nih.gov. This invention describes a novel role for BRCA2 in the repair of O6alkylguanine adducts and provides evidence that after treatment with O6benzylguanine, tumor cells with intact BRCA2, are susceptible to ionizing radiations. In this invention the essential and novel function of BRCA2 in the repair of O6-methylguanine is described and demonstrated. BRCA2 physically interacts with alkylated-AGT and undergoes repair-associated VerDate jul<14>2003 11:52 Apr 25, 2005 Jkt 205001 degradation. Treatment with O6benzylguanine renders cell radiation hypersensitive due to degradation of BRCA2. Radio-sensitization of tumors by O6-benzylguanine should have a significant impact on cancer therapeutics. The elucidation of the mechanism of action for the chemotherapeutic agent O6benzylguanine relative to BRCA2 may potentially improve the success rate of treating BRCA2 expressing tumors. In addition to licensing, the technology is available for further development through collaborative research opportunities with the inventors. Chinese Hamster Ovary Cells Resistant to Colcemid With Altered beta-Tubulin Michael M. Gottesman and Fernando R. Cabral (NCI). DHHS Reference No. E–156–2004/0— Research Tool. Licensing Contact: Thomas P. Clouse; 301/435–4076; clouset@mail.nih.gov. The invention is Chinese hamster ovary cells (CHO) resistant to colcemid with altered beta-tubulin. These mutants establish the essential role of tubulin in forming mitotic spindles and identify beta-tubulin as the target for colcemid toxicity. Cloning and Characterization of an Avian Adeno-Associated Virus and Uses Thereof Ioannis Bossis (NIDCR). U.S. Provisional Application No. 60/ 472,066 filed 19 May 2003 (DHHS Reference No. E–105–2003/0–US–01); PCT Application No. PCT/US04/ 15534 filed 18 May 2004, which published as WO 2005/017101 A2 on 24 Feb 2005 (DHHS Reference No. E– 105–2003/0–PCT–02). Licensing Contact: Jesse S. Kindra; 301/ 435–5559; kindraj@mail.nih.gov. Currently, adeno-associated virus (AAV) represents the gene therapy vehicle of choice because it has many advantages over current strategies for therapeutic gene insertion. AAV is less pathogenic than other virus types; stably integrates into dividing and nondividing cells; integrates at a consistent site in the host genome; and shows good specificity towards various cell types for targeted gene delivery. To date, eight AAV isolates have been isolated and characterized, but new serotypes derived from other animal species may add to the specificity and repertoire of current AAV gene therapy techniques. This invention describes vectors derived from an avian AAV. These vectors have innate properties related to PO 00000 Frm 00045 Fmt 4703 Sfmt 4703 21433 their origin that may confer them with a unique cellular specificity in targeted human gene therapy. Therefore, vectors derived from this avian AAV are likely to find novel applications for gene therapy in humans and fowl. This research has been described, in part, in Bossis and Chiorini (2003) J. Virol. (77)12:6799–6810. ´ Identification of Novel Birt-Hogg-Dube (BHD) Gene Laura S. Schmidt (NCI). U.S. Patent Application No. 10/514,744 filed 16 Nov 2004 (DHHS Reference No. E–190–2002/2–US–02). Licensing Contact: John Stansberry; 301/ 435–5236; stansbej@mail.nih.gov. ´ Birt-Hogg-Dube (BHD) syndrome is an inherited autosomal dominant neoplasia syndrome characterized by benign hair follicle tumors and is associated with a higher risk for developing renal cancer, spontaneous pneumothorax and /or lung cysts. The present invention describes identification of the BHD syndrome associated germline mutations in a novel human gene, herein called BHD gene. This gene encodes for the protein, folliculin, functions of which remain currently unknown. This discovery makes possible the development of a diagnostic method for BHD syndrome using a simple blood test. The test is particularly useful in detecting BHD mutations in asymptomatic carriers within BHD families. Patients with kidney tumors can be evaluated for BHD gene mutations using a similar genetic diagnostic test, which will allow for a more accurate diagnosis of a kidney cancer and improved patient prognosis. The BHD encoding sequence is the third gene found to be responsible for inherited kidney cancer, and mutation testing allows for a correct diagnosis and initiation of the proper treatment, which is different for each of the types of kidney cancer caused by the three genes. Since BHD is the first gene found to be associated with chromophobe renal cancer or renal oncocytoma, this invention will enable the development of specific treatments or therapies for these particular histologic types of kidney cancer. Methods of using BHD encoding sequence also allows for a differential genetic diagnosis of spontaneous pneumothorax, or collapsed lung. Since collapsed lung can be caused by several factors, a BHD diagnostic test allows a physician to determine predisposition to and possible recurrence of additional spontaneous pneumothoraces due to mutation(s) in the BHD gene. E:\FR\FM\26APN1.SGM 26APN1 21434 Federal Register / Vol. 70, No. 79 / Tuesday, April 26, 2005 / Notices The discovery should also lead to the development of novel pharmaceutical products and methods for treating BHD skin lesions using creams containing the BHD gene product, folliculin. Such products and methods of treatment are expected to reduce the size and appearance of the benign hair follicle tumors. The disclosed technology will provide new and exciting methodologies to correctly diagnose BHD syndrome and should lead to the development of novel pharmaceutical reagents for treatment of BHD skin lesions as well as other skin diseases. This research is also described in: MB Warren et al., Mod Pathol. (2004 Aug) 17(8):998–1011; ML Nickerson et al., Cancer Cell (2002 Aug) 2(2):157–164; B Zbar et al., Cancer Epidem. Bio. Prev. (2002 Apr) 11(4):393–400; LS Schmidt et al., Am. J. Hum. Genet. (2001 Oct) 69(4):876–882; Toro et al., Arch. Dermatol. (1999 Oct) 135(10): 1195– 1202. In addition to licensing, the technology is available for further development through collaborative research opportunities with the inventors. Compositions Of Transforming Growth Factor Beta (TGF-beta) Which Promotes Wound Healing and Methods for Their Use Michael Sporn et al. (NCI). U.S. Patent No. 5,104,977, granted April 14, 1992, entitled ‘‘Purified Transforming Growth Factor Beta’’ (DHHS Ref. No. E–070–1982/2-US– 05); U.S. Patent No. 5,656,587, granted August 12, 1997, entitled ‘‘Promotion Of Cell Proliferation By Use Of Transforming Growth Factor Beta (TGF-Beta)’’ (DHHS Ref. No. E–070– 1982/2-US–07); and U.S. Patent No. 5,705,477, granted January 6, 1998, entitled ‘‘Compositions Of Transforming Growth Factor Beta (TGF-Beta) Which Promotes Wound Healing And Methods For Their Use’’ (DHHS Ref. No. E–070–1982/2-US–08). Licensing Contact: Jesse S. Kindra; 301/ 435–5559; kindraj@mail.nih.gov. There is a continuing need for the promotion of rapid cell proliferation at the site of wounds, burns, diabetic and decubitus ulcers, and other traumata. Prior to this invention, a number of ‘‘growth factors’’ were known to promote the rapid growth of cells. None of these growth factors, however, had been found to be pharmaceutically acceptable agents for the acceleration of wound healing. VerDate jul<14>2003 11:52 Apr 25, 2005 Jkt 205001 This invention relates to compositions of Transforming Growth Factor beta (TGF-beta) which promote repair of tissue, particularly fibroblast cells, in animals and human beings. This invention also relates to a method of treating wounds by the topical or systemic administration of the compositions. The discovery of this invention initiated a worldwide field of research aimed at the characterization and development of TGF-beta in wound healing and disease. It is now known that TGF-beta’s role in wound healing is complex. Its diverse effects on the many individual participating cell types in a wound are integrated into a specific temporal sequence of events within a defined tissue architecture. In addition to its many roles in wound healing, TGF-beta is also implicated in the pathogenesis of diseases such as autoimmune disease, fibrosis, and cancer. Current research in TGF-beta biology is leading to the development of novel wound healing and disease therapies related to the growth factor and its signaling pathways. Dated: April 18, 2005. Steven M. Ferguson, Director, Division of Technology Development and Transfer, Office of Technology Transfer, National Institutes of Health. [FR Doc. 05–8287 Filed 4–25–05; 8:45 am] BILLING CODE 4140–01–P DEPARTMENT OF HEALTH AND HUMAN SERVICES National Institutes of Health National Institute of Nursing Research; Notice of Meeting Pursuant to section 10(d) of the Federal Advisory Committee Act, as amended (5 U.S.C. appendix 2), notice is hereby given of a meeting of the National Advisory Council for Nursing Research. The meeting will be open to the public as indicated below, with attendance limited to space available. Individuals who plan to attend and need special assistance, such as sign language interpretation or other reasonable accommodations, should notify the Contact Person listed below in advance of the meeting. The meeting will be closed to the public in accordance with the provisions set forth in sections 552b(c)(4) and 552b(c)(6), Title 5 U.S.C., as amended. The grant applications and/or contract proposals and the discussions could disclose confidential trade secrets or commercial property PO 00000 Frm 00046 Fmt 4703 Sfmt 4703 such as patentable material, and personal information concerning individuals associated with the grant applications and/or contract proposals, the disclosure of which would constitute a clearly unwarranted invasion of personal privacy. Name of Committee: National Advisory Council for Nursing Research. Date: May 17–18, 2005. Open: May 17, 2005, 1 p.m. to 5 p.m. Agenda: For discussion of program issues and initiatives. Place: National Institutes of Health, Building 31, 31 Center Drive, Bethesda, MD 20892. Closed: May 18, 2005, 9 a.m. to 2 p.m. Agenda: To review and evaluate grant applications and/or proposals. Place: National Institutes of Health, Building 31, 31 Center Drive, Bethesda, MD 20892. Contact Person: Mary E. Kerr, FAAN, RN, PhD, Deputy Director, National Institute of Nursing, National Institutes of Health, 31 Center Drive, Room 5B–05, Bethesda, MD 20892–2178, 301/496–8230, kerrme@mail.nih.gov. Any member of the public interested in presenting oral comments to the committee may notify the Contact Person listed on this notice at least 10 days in advance of the meeting. Interested individuals and representatives of organizations may submit a letter of intent, a brief description of the organization represented, and a short description of the oral presentation. Only one representative of an organization may be allowed to present oral comments and if accepted by the committee, presentations may be limited to five minutes. Both printed and electronic copies are requested for the record. In addition, any interested person may file written comments with the committee by forwarding their statement to the Contact Person listed on this notice. The statement should include the name, address, telephone number and when applicable, the business or professional affiliation of the interested person. Information is also available on the Institute’s/Center’s home page: https:// www.nih.gov/ninr/a_advisory.html, where an agenda and any additional information for the meeting will be posted when available. (Catalogue of Federal Domestic Assistance Program Nos. 93.361, Nursing Research, National Institutes of Health, HHS) Dated: April 15, 2005. Anna Snouffer, Acting Director, Office of Federal Advisory Committee Policy. [FR Doc. 05–8288 Filed 4–25–05; 8:45 am] BILLING CODE 4140–01–M E:\FR\FM\26APN1.SGM 26APN1

Agencies

[Federal Register Volume 70, Number 79 (Tuesday, April 26, 2005)]
[Notices]
[Pages 21431-21434]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: 05-8287]


-----------------------------------------------------------------------

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.

-----------------------------------------------------------------------

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.

[[Page 21432]]

Composition and Methods for Diagnosis and Treatment of Metastatic 
Disease

Xin Wei Wang and Anuradha Budhu (NCI).
U.S. Provisional Application filed 8 Mar 2005 (DHHS Reference No. E-
127-2005/0-US-01).
Licensing Contact: Michelle A. Booden; 301/451-7337; 
boodenm@mail.nih.gov.

    Liver cancer, particularly hepatocellular carcinoma (HCC), is a 
leading cause of cancer deaths worldwide. In spite of recent progress 
in therapeutic strategies, prognosis of patients with advanced HCC 
remains very poor. Although routine screening of individuals at risk 
for developing HCC may extend the life of some patients, many are still 
diagnosed with advanced HCC and have little chance of survival. A small 
subset of HCC patients qualifies for surgical intervention, but the 
consequent improvement in long-term survival is only modest. The 
extremely poor prognosis of HCC is largely the result of a high rate of 
recurrence after surgery or of intra-hepatic metastases that develop 
through invasion of the portal vein or spread to other parts of the 
liver; extra-hepatic metastases are less common.
    The present invention describes tools to determine a unique gene 
expression profile present in either liver parenchyma through needle 
biopsy or blood that can aid diagnosis or prognosis of HCC patients 
with or without metastatic potential. This method also provides a 
signature-derived polymerase chain reaction or serological screening 
method to identify drug candidates to treat metastatic or recurrent 
HCC.
    In addition to licensing, the technology is available for further 
development through collaborative research opportunities with the 
inventors.

Aminoglycosides and Ribosome Inhibitors as Inhibitors of Tyrosyl-DNA-
Phosphodiesterase

Drs. Yves Pommier and Zhi-Yong Liao (NCI).
DHHS Reference No. E-117-2005/0-US-01.
Licensing Contact: John Stansberry; 301/435-5236; 
stansbej@mail.nih.gov.

    Cancer has long been a leading cause of mortality in the United 
States. DNA-damaging therapies, such as radiotherapy and chemotherapy, 
are the methods of choice for treating subjects with metastatic cancer 
or subjects with diffuse cancers such as leukemias. However, 
radiotherapy can cause substantial damage to normal tissue in the 
treatment field, resulting in scarring and, in severe cases, loss of 
function of the normal tissue. Although chemotherapy can provide a 
therapeutic benefit in many cancer subjects, it often fails to treat 
the disease because cancer cells may become resistant to the 
chemotherapeutic agent. To overcome these limitations additional 
antineoplastic strategies, such as enhancing the antineoplastic effect 
of existing therapies, are needed.
    This invention discloses a method for enhancing an antineoplastic 
effect of a DNA-damaging therapy. The method includes administering to 
a subject having a neoplasm a therapeutically effective amount of the 
DNA-damaging therapy and a ribosome inhibitor that inhibits tyrosyl-DNA 
phosphodiesterase 1 (Tdp1) activity, wherein the ribosome inhibitor is 
administered in a sufficient amount to enhance the DNA-damaging 
therapy.
    This disclosure also provides pharmaceutical compositions that 
include at least one chemotherapeutic agent and at least one ribosome 
inhibitor that inhibits Tdp1 activity, wherein the chemotherapeutic 
agent and the ribosome inhibitor are present in a therapeutically 
effective amount for the ribosome inhibitor to enhance an 
antineoplastic effect of the chemotherapeutic agent.
    In addition to licensing, the technology is available for further 
development through collaborative research opportunities with the 
inventors.

Inhibition of Proteosome Function to Potentiate the Proapoptotic and 
Antitumor Activity of Cytokines

Jon Wigginton et al. (NCI).
U.S. Provisional Patent Application filed 23 Mar 2005 (DHHS Reference 
No. E-072-2005/0-US-01).
Licensing Contact: Michelle A. Booden; 301/451-7337; 
boodenm@mail.nih.gov.

    Protein degradation via the ubiquitin-proteosome pathway is an 
important regulator of cell cycle progression and survival. Thus, 
inhibitors of this pathway can be directly cytotoxic and can sensitize 
several tumor cell types to cytotoxic chemotherapy and radiation.
    Neuroblastoma is the most common extracranial solid tumor in 
children, and the development of clinical resistance to cytotoxic 
therapies is a major therapeutic obstacle in these patients. Several 
apoptosis abnormalities, which result from decreased expression of pro-
apoptotic proteins, are associated with increased resistance to 
standard therapeutic interventions. In addition, neuroblastoma cells 
also show increased expression of several pro-survival proteins such as 
Bcl-2, FLIP, and AKT. Preclinical models suggest that IFN-gamma/TNF-
alpha cytokines including IL-2, IL-12 and IL-18 among others may have 
potent antitumor efficacy in several preclinical models, and that these 
regimens may act by inducing an adaptive cell-mediated immune response. 
Although some single agent cytokine regimens have achieved modest 
efficacy in the clinical setting, the utility of some approaches has 
been limited overall by side effects that can be associated with high-
dose cytokine therapy.
    The present invention describes a method for combining ubiquitin-
proteosome inhibitors with various cytokines to overcome mechanisms of 
tumor self-defense and sensitize both tumor and/or endothelial cell 
populations to apoptosis. These combination approaches may not only 
offer the prospect for improved therapeutic efficacy, but achieve these 
effects at lower, more clinically tolerable doses than can be achieved 
utilizing either respective agent alone. It is anticipated that this 
therapeutic intervention could be directed towards multiple human 
carcinomas, and potentiate the efficacy of multiple different cytokines 
both in the setting of oncology and infectious disease applications.
    In addition to licensing, the technology is available for further 
development through collaborative research opportunities with the 
inventors.

Methods for Inhibiting or Treating Cancer

Ernest Hamel (NCI), et al.
U.S. Provisional Application No. 60/616,347 filed 05 Oct 2004 (DHHS 
Ref. No. E-323-2004/0-US-01).
Licensing Contact: Thomas P. Clouse; 301/435-4076; 
clouset@mail.nih.gov.

    This invention describes novel arylthioindole derivatives having 
enhanced interaction with tubulin and increased effectiveness in growth 
inhibition of MCF-7 breast cancer cells as well as other cell types. 
Antitubulin drugs have an established role in the treatment of cancer, 
parasitic diseases and inflammatory disorders. These new chemical 
compounds have the potential to result in more effective therapeutics 
for the treatment of neoplastic, inflammatory and parasitic diseases.
    In addition to licensing, the technology is available for further 
development through collaborative research opportunities with the 
inventors.

[[Page 21433]]

Regulation of ATG7 Beclin 1 Program of Autophagic Cell Death by 
Caspase-8

Michael Lenardo and Yu Li (NIAID), et al.
U.S. Provisional Application No. 60/556,857 filed 30 May 2004 (DHHS 
Reference No. E-318-2004/0-US-01).
Licensing Contact: Mojdeh Bahar; 301/435-2950; baharm@mail.nih.gov.

    The invention discloses the role of autophagy in regulation cell 
death. Further it teaches a method of inducing autophagic cell death by 
administering a caspase inhibitor. The invention also discloses that 
autophagic cell death can be induced by caspase-8 inhibition and 
requires the genes ATG7 and Beclin 1.
    In addition to licensing, the technology is available for further 
development through collaborative research opportunities with the 
inventors.

Cancer Specific SPANX-N Markers

Natalay Kouprina et al. (NCI).
DHHS Reference No. E-212-2004/0-US-01.
Licensing Contact: Mojdeh Bahar; 301/435-2950; baharm@mail.nih.gov.

    The invention provides SPANX-N polypeptides, nucleic acids and 
antibodies that could be useful for detecting and treating prostate or 
other cancers. The SPANX-N genes are a family of related genes that are 
expressed in normal testis and in tumor cells in humans including 
melanoma, bladder carcinomas and myelomas. The SPANX cancer/testis 
antigens thus represent good candidates for diagnosis or treatment of 
several cancers.
    In addition to licensing, the technology is available for further 
development through collaborative research opportunities with the 
inventors.

Methods for Inhibiting or Treating Cancer

Srividya Swaminathan, Shyam Sharan (NCI).
U.S. Provisional Application No. 60/588,918 filed 16 Jul 2004 (DHHS 
Reference No. E-160-2004/0-US-01).
Licensing Contact: Thomas P. Clouse; 301/435-4076; 
clouset@mail.nih.gov.

    This invention describes a novel role for BRCA2 in the repair of 
O6-alkylguanine adducts and provides evidence that after 
treatment with O6-benzylguanine, tumor cells with intact 
BRCA2, are susceptible to ionizing radiations. In this invention the 
essential and novel function of BRCA2 in the repair of O6-
methylguanine is described and demonstrated. BRCA2 physically interacts 
with alkylated-AGT and undergoes repair-associated degradation. 
Treatment with O6-benzylguanine renders cell radiation 
hypersensitive due to degradation of BRCA2. Radio-sensitization of 
tumors by O6-benzylguanine should have a significant impact 
on cancer therapeutics. The elucidation of the mechanism of action for 
the chemotherapeutic agent O6-benzylguanine relative to 
BRCA2 may potentially improve the success rate of treating BRCA2 
expressing tumors.
    In addition to licensing, the technology is available for further 
development through collaborative research opportunities with the 
inventors.

Chinese Hamster Ovary Cells Resistant to Colcemid With Altered beta-
Tubulin

Michael M. Gottesman and Fernando R. Cabral (NCI).
DHHS Reference No. E-156-2004/0--Research Tool.
Licensing Contact: Thomas P. Clouse; 301/435-4076; 
clouset@mail.nih.gov.

    The invention is Chinese hamster ovary cells (CHO) resistant to 
colcemid with altered beta-tubulin. These mutants establish the 
essential role of tubulin in forming mitotic spindles and identify 
beta-tubulin as the target for colcemid toxicity.

Cloning and Characterization of an Avian Adeno-Associated Virus and 
Uses Thereof

Ioannis Bossis (NIDCR).
U.S. Provisional Application No. 60/472,066 filed 19 May 2003 (DHHS 
Reference No. E-105-2003/0-US-01); PCT Application No. PCT/US04/15534 
filed 18 May 2004, which published as WO 2005/017101 A2 on 24 Feb 2005 
(DHHS Reference No. E-105-2003/0-PCT-02).
Licensing Contact: Jesse S. Kindra; 301/435-5559; kindraj@mail.nih.gov.

    Currently, adeno-associated virus (AAV) represents the gene therapy 
vehicle of choice because it has many advantages over current 
strategies for therapeutic gene insertion. AAV is less pathogenic than 
other virus types; stably integrates into dividing and non-dividing 
cells; integrates at a consistent site in the host genome; and shows 
good specificity towards various cell types for targeted gene delivery.
    To date, eight AAV isolates have been isolated and characterized, 
but new serotypes derived from other animal species may add to the 
specificity and repertoire of current AAV gene therapy techniques.
    This invention describes vectors derived from an avian AAV. These 
vectors have innate properties related to their origin that may confer 
them with a unique cellular specificity in targeted human gene therapy. 
Therefore, vectors derived from this avian AAV are likely to find novel 
applications for gene therapy in humans and fowl.
    This research has been described, in part, in Bossis and Chiorini 
(2003) J. Virol. (77)12:6799-6810.

Identification of Novel Birt-Hogg-Dub[eacute] (BHD) Gene

Laura S. Schmidt (NCI).
U.S. Patent Application No. 10/514,744 filed 16 Nov 2004 (DHHS 
Reference No. E-190-2002/2-US-02).
Licensing Contact: John Stansberry; 301/435-5236; 
stansbej@mail.nih.gov.

    Birt-Hogg-Dub[eacute] (BHD) syndrome is an inherited autosomal 
dominant neoplasia syndrome characterized by benign hair follicle 
tumors and is associated with a higher risk for developing renal 
cancer, spontaneous pneumothorax and /or lung cysts.
    The present invention describes identification of the BHD syndrome 
associated germline mutations in a novel human gene, herein called BHD 
gene. This gene encodes for the protein, folliculin, functions of which 
remain currently unknown.
    This discovery makes possible the development of a diagnostic 
method for BHD syndrome using a simple blood test. The test is 
particularly useful in detecting BHD mutations in asymptomatic carriers 
within BHD families.
    Patients with kidney tumors can be evaluated for BHD gene mutations 
using a similar genetic diagnostic test, which will allow for a more 
accurate diagnosis of a kidney cancer and improved patient prognosis. 
The BHD encoding sequence is the third gene found to be responsible for 
inherited kidney cancer, and mutation testing allows for a correct 
diagnosis and initiation of the proper treatment, which is different 
for each of the types of kidney cancer caused by the three genes. Since 
BHD is the first gene found to be associated with chromophobe renal 
cancer or renal oncocytoma, this invention will enable the development 
of specific treatments or therapies for these particular histologic 
types of kidney cancer.
    Methods of using BHD encoding sequence also allows for a 
differential genetic diagnosis of spontaneous pneumothorax, or 
collapsed lung. Since collapsed lung can be caused by several factors, 
a BHD diagnostic test allows a physician to determine predisposition to 
and possible recurrence of additional spontaneous pneumothoraces due to 
mutation(s) in the BHD gene.

[[Page 21434]]

    The discovery should also lead to the development of novel 
pharmaceutical products and methods for treating BHD skin lesions using 
creams containing the BHD gene product, folliculin. Such products and 
methods of treatment are expected to reduce the size and appearance of 
the benign hair follicle tumors.
    The disclosed technology will provide new and exciting 
methodologies to correctly diagnose BHD syndrome and should lead to the 
development of novel pharmaceutical reagents for treatment of BHD skin 
lesions as well as other skin diseases.
    This research is also described in: MB Warren et al., Mod Pathol. 
(2004 Aug) 17(8):998-1011; ML Nickerson et al., Cancer Cell (2002 Aug) 
2(2):157-164; B Zbar et al., Cancer Epidem. Bio. Prev. (2002 Apr) 
11(4):393-400; LS Schmidt et al., Am. J. Hum. Genet. (2001 Oct) 
69(4):876-882; Toro et al., Arch. Dermatol. (1999 Oct) 135(10): 1195-
1202.
    In addition to licensing, the technology is available for further 
development through collaborative research opportunities with the 
inventors.

Compositions Of Transforming Growth Factor Beta (TGF-beta) Which 
Promotes Wound Healing and Methods for Their Use

Michael Sporn et al. (NCI).
U.S. Patent No. 5,104,977, granted April 14, 1992, entitled ``Purified 
Transforming Growth Factor Beta'' (DHHS Ref. No. E-070-1982/2-US-05);
U.S. Patent No. 5,656,587, granted August 12, 1997, entitled 
``Promotion Of Cell Proliferation By Use Of Transforming Growth Factor 
Beta (TGF-Beta)'' (DHHS Ref. No. E-070-1982/2-US-07); and
U.S. Patent No. 5,705,477, granted January 6, 1998, entitled 
``Compositions Of Transforming Growth Factor Beta (TGF-Beta) Which 
Promotes Wound Healing And Methods For Their Use'' (DHHS Ref. No. E-
070-1982/2-US-08).
Licensing Contact: Jesse S. Kindra; 301/435-5559; kindraj@mail.nih.gov.

    There is a continuing need for the promotion of rapid cell 
proliferation at the site of wounds, burns, diabetic and decubitus 
ulcers, and other traumata. Prior to this invention, a number of 
``growth factors'' were known to promote the rapid growth of cells. 
None of these growth factors, however, had been found to be 
pharmaceutically acceptable agents for the acceleration of wound 
healing.
    This invention relates to compositions of Transforming Growth 
Factor beta (TGF-beta) which promote repair of tissue, particularly 
fibroblast cells, in animals and human beings. This invention also 
relates to a method of treating wounds by the topical or systemic 
administration of the compositions. The discovery of this invention 
initiated a worldwide field of research aimed at the characterization 
and development of TGF-beta in wound healing and disease. It is now 
known that TGF-beta's role in wound healing is complex. Its diverse 
effects on the many individual participating cell types in a wound are 
integrated into a specific temporal sequence of events within a defined 
tissue architecture. In addition to its many roles in wound healing, 
TGF-beta is also implicated in the pathogenesis of diseases such as 
autoimmune disease, fibrosis, and cancer.
    Current research in TGF-beta biology is leading to the development 
of novel wound healing and disease therapies related to the growth 
factor and its signaling pathways.

    Dated: April 18, 2005.
Steven M. Ferguson,
Director, Division of Technology Development and Transfer, Office of 
Technology Transfer, National Institutes of Health.
[FR Doc. 05-8287 Filed 4-25-05; 8:45 am]
BILLING CODE 4140-01-P
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