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