Government-Owned Inventions; Availability for Licensing, 10945-10948 [E9-5418]
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10945
Federal Register / Vol. 74, No. 48 / Friday, March 13, 2009 / Notices
listed below. This proposed information
collection was previously published in
the Federal Register on December 30,
2008, page 79889–79890 and allowed
60-days for public comment. One
comment was received and appropriate
response was made. The purpose of this
notice is to allow an additional 30 days
for public comment. The National
Institutes of Health may not conduct or
sponsor, and the respondent is not
required to respond to, an information
collection that has been extended,
revised or implemented on or after
October 1, 1995 unless it displays a
current valid OMB control number.
Proposed Collection: Title: Women’s
Health Initiative (WHI) Observational
Study. Type of Information Collection
Request: REVISION: OMB No. 0925–
0414, Expiration date: 05/31/2009. Need
and Use of Information Collection: This
study will be used by the NIH to
evaluate risk factors for chronic disease
among older women by developing and
following a large cohort of
postmenopausal women and relating
subsequent disease development to
baseline assessments of historical,
physical, psychosocial, and physiologic
characteristics. In addition, the
observational study will complement
the clinical trial (which has received
clinical exemption) and provide
additional information on the common
causes of frailty, disability and death for
postmenopausal women, namely,
coronary heart disease, breast and
colorectal cancer, and osteoporotic
fractures. Continuation of follow-up
years for ascertainment of medical
history update forms will provide
essential data for outcomes assessment
for this population of aging women.
Frequency of Response: Annually.
Affected Public: Individuals and
physicians. Type of Respondents:
Women, next-of-kin, and physician’s
office staff. The annual reporting burden
is as follows:
ESTIMATE OF ANNUAL HOUR BURDEN
Number of
respondents
Type of response
Frequency of
response
Average hours
per response
Annual hour
burden
Observational Study Participants
Next of Kin1
Health Care Providers1
63,230
1,163
9
1.1
1
1
.3383
.083
.083
23,509
97
.77
Total
64,402
............................
............................
23,607
1 Annual
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burden is placed on health care providers and respondent relatives/informants through requests for information which will help in the
compilation of the number and nature of new fatal and nonfatal events.
The annualized cost burden to
respondents is estimated at $377,725.
There are no Capital Costs, Operating
Costs and/or Maintenance Costs to
report.
Request for Comments: Written
comments and/or suggestions from the
public and affected agencies should
address one or more of the following
points: (1) Evaluate whether the
proposed collection is necessary for the
proper performance of the function of
the agency, including whether the
information will have practical utility;
(2) Evaluate the accuracy of the agency’s
estimate of the burden of the proposed
collection of information, including the
validity of the methodology and
assumptions used; (3) Enhance the
quality, utility, and clarity of the
information to be collected; and (4)
Minimize the burden of the collection of
information on those who are to
respond, including the use of
appropriate automated, electronic,
mechanical, or other technological
collection techniques or other forms of
information technology.
Direct Comments to OMB: Written
comments and/or suggestions regarding
the item(s) contained in this notice,
especially regarding the estimated
public burden and associated response
time, should be directed to the: Office
of Management and Budget, Office of
Regulatory Affairs,
OIRA_submission@omb.eop.gov or by
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17:55 Mar 12, 2009
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fax to 202–395–6974, Attention: Desk
Officer for NIH. To request more
information on the proposed project or
to obtain a copy of the data collection
plan and instruments, contact: Shari
Eason Ludlam, Project Officer, Women’s
Health Initiative Program Office, 6701
Rockledge Drive, 2 Rockledge Centre,
Suite 10018, MSC 7936, Bethesda, MD
20892–7936, or call (301) 402–2900 or
E-mail your request, including your
address to: ludlams@mail.nih.gov.
Comments Due Date: Comments
regarding this information collection are
best assured of having their full effect if
received within 30-days of the date of
this publication.
Dated: March 2, 2009.
Michael S. Lauer,
Director, Division of Prevention and
Population Sciences, NHLBI, National
Institutes of Health.
Dated: March 3, 2009.
Suzanne Freeman,
Chief, FOIA, NHLBI, National Institutes of
Health.
[FR Doc. E9–5521 Filed 3–12–09; 8:45 am]
BILLING CODE 4140–01–P
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DEPARTMENT OF HEALTH AND
HUMAN SERVICES
National Institutes of Health
Government-Owned Inventions;
Availability for Licensing
AGENCY: National Institutes of Health,
Public Health Service, HHS.
ACTION:
Notice.
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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10946
Federal Register / Vol. 74, No. 48 / Friday, March 13, 2009 / Notices
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Gene Signature for Predicting
Hepatocellular Carcinoma Patient
Prognosis
Description of Technology: A
progressive sequence of somatic
mutations and epigenetic changes of
oncogenes or tumor suppressor genes
are believed to cause tumor
development. However, high genomic
instability in tumors causes the
accumulation of genomic aberrations
that do not contribute to tumor
progression. Therefore it is important to
distinguish between ‘‘driver’’ mutations
which are functionally important and
‘‘passenger’’ mutations which do not
provide a selective advantage to the
tumor cells.
The current invention describes a
driver gene signature for predicting
survival in patients with hepatocellular
carcinoma (HCC). The gene signature
includes ten HCC-associated genes, and
the NIH researchers further discovered
that a decrease in DNA copy number or
mRNA expression of some genes is
associated with a poor prognosis in HCC
tumors, while a decrease in DNA copy
number or mRNA expression of a few
other genes is associated with a good
prognosis.
Available for licensing is a method of
predicting the prognosis of a patient
diagnosed with HCC by detecting
expression of one of more HCCassociated genes, and a method of
identifying an agent for use in treating
HCC.
Applications: Prognosis for
hepatocellular carcinoma (HCC) patient
survival; Potential new method to
identify therapeutic treatment for HCC
patients.
Market: Hepatocellular carcinoma
(HCC) is the most frequent malignant
tumor in the liver and the third leading
cause of cancer death worldwide.
Systemic chemotherapy has been shown
to be ineffective and tumor recurrence
rate after surgical resection is high due
to relapse and metastasis. Therefore, the
development of new drugs will be
crucial to prevent relapse and to prolong
patient survival.
Development Status: Early-stage
development.
Inventors: Xin Wei Wang and
Stephanie Roessler (NCI).
Patent Status: U.S. Provisional
Application No. 61/198,813 filed 10
Nov 2008 (HHS Reference No. E–024–
2009/0–US–01).
Licensing Status: Available for
licensing.
Licensing Contact: Betty Tong, Ph.D.;
301–594–6565; tongb@mail.nih.gov.
Collaborative Research Opportunity:
The National Cancer Institute, Center for
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Cancer Research, Laboratory of Human
Carcinogenesis, is seeking statements of
capability or interest from parties
interested in collaborative research to
further develop, evaluate, or
commercialize Gene Signature for
Predicting Hepatocellular Carcinoma
Patient Prognosis. Please contact John D.
Hewes, Ph.D. at 301–435–3121 or
hewesj@mail.nih.gov for more
information.
Lasonolide Compounds as Reagents for
Inducing Premature Chromosome
Condensation and Methods of Treating
Cancer
Description of Technology:
Lasonolide A is a natural product
initially isolated from an extract of the
shallow water Caribbean marine sponge.
The chemical structure of lasonolide A
was identified in 2002, and it was
chemically synthesized in 2007. The
current invention discloses the
discovery that lasonolide A may be used
as a new reagent for inducing premature
chromosome condensation in nondividing cells; and a novel antiproliferative and anti-metastatic agent
for cancer treatment. Currently, it is
difficult to analyze the cytogenetic
composition of the genome of nondividing cells because the chromosomes
are loosely distributed in the nucleus,
lasonolide A may be useful for
performing cytogenetic studies in cells
by inducing premature chromosome
condensation without inducing mitosis.
In addition, the invention also reveals
that lasonolide A inhibits cancer cell
motility. As such, lasonolide A may be
used as an anti-cancer agent by itself or
in combination with other anti-cancer
agents such as inhibitors of
topoisomerases.
Applications: A new reagent for
inducing premature chromosome
condensation in non-dividing cells; a
novel anti-cancer agent.
Market: Cancer continues to be a
burden to the public health of
Americans. After heart disease, cancer is
the most common cause of death in the
United States. For 2008, it was
estimated that about 565,650 Americans
were expected to die of cancer. The
incidence of cancer has been dropping
over the years but it is estimated that
over 1.4 million Americans would be
diagnosed with cancer in 2008.
Therefore, there is a continued need for
the development of new therapies to
effectively treat this disease.
Development Status: Early-stage
development.
Inventors: Yves G. Pommier (NCI) et
al.
Patent Status: U.S. Provisional
Application No. 61/137,193 filed 28 Jul
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2008 (HHS Reference No. E–247–2008/
0–US–01).
Licensing Status: Available for
licensing.
Licensing Contact: Betty Tong, Ph.D.;
301–594–6565; tongb@mail.nih.gov.
Collaborative Research Opportunity:
The National Cancer Institute, Center for
Cancer Research, Laboratory of
Molecular Pharmacology, is seeking
statements of capability or interest from
parties interested in collaborative
research to further develop, evaluate, or
commercialize Lasonolide Compounds
as Reagents for Inducing Premature
Chromosome Condensation and
Methods of Treating Cancer. Please
contact John D. Hewes, Ph.D. at 301–
435–3121 or hewesj@mail.nih.gov for
more information.
Increased Image Quality for Early
Colon Polyp Detection
Description of Technology: The
invention relates to a method for
improving the specificity and sensitivity
of computer tomographic colonoscopy
(CTC) computer aided detection (CAD).
Currently CTC CAD programs are
capable of delivering high sensitivity
and low false positive results when used
to detect large polyps of 1 cm or greater
in diameter. However, CTC CAD is not
as effective at detecting medium-sized
polyps (6–9 mm in diameter) as it
demonstrates lower sensitivities and
higher false positives in this range.
Since early polyp detection is critical to
the survival of patients with colon
cancer, the ability to accurately detect
medium size polyps could be
advantageous to the outcome of colon
cancer treatment.
The invention uses a wavelet-based
analysis to distinguish true polyps from
false positives in CTC images. The steps
involved include generating a 2D
projection image, computing features of
the 2D images from their Haar wavelet
coefficients, applying the feature
selection algorithm, and training a
classifier using the selected features to
classify CTC CAD.
Using this technology, it will be
possible to create high quality images
for viewing the colon surface in 3D with
reduced false positives in the mediumsized range for colon polyps. The
technology can also be used to locate
anomalies in both medical and nonmedically related image applications
such as endoscopy, microscopy, and
photography.
Applications: High quality images for
early colon polyp detection; Sensitive
and efficient colon cancer diagnosis;
Locating anomalies in several different
image applications.
Development Status: Early stage.
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Inventors: Ronald M. Summers et al.
(CC)
Publications:
1. J Li, R Van Uitert, J Yao, N Petrick,
M Franaszek, A Huang, RM Summers.
Wavelet method for CT colonography
computer-aided polyp detection. Med
Phys. 2008 Aug;35(8):3527–3538.
2. S Greenblum, J Li, A Huang, RM
Summers. Wavelet analysis in virtual
colonoscopy. Proc. SPIE, Vol. 6143,
614336 (March 13, 2006); doi:10.1117/
12.655680.
Patent Status: U.S. Patent Application
No. 11/685,127 filed 12 Mar 2007 (HHS
Reference No. E–314–2006/0–US–02);
No foreign rights available.
Licensing Status: Available for
licensing.
Licensing Contact: Jeffrey A. James,
Ph.D.; 301–435–5474;
jeffreyja@mail.nih.gov.
Microdissection and High-Throughput
Analysis of Biological Samples
Description of Technology: A variety
of techniques have been used to
microdissect specific cells or cell
populations from a histological sample
under direct microscopic visualization.
Original microdissection techniques
involved painstaking (and sometimes
clumsy) manual dissection using
needles or other micro-manipulation
devices to isolate individual cells based
on visible, histological characteristics.
The subject technology is a method of
performing specific target activated
transfer from a biological sample (i.e.,
tissue) for analysis using a device
system that can be automated for high
throughput analysis. The method
employs a localized reagent, such as an
absorbative stain, that specifically
determines the microadhesion of
desired cellular material in a tissue
sample to a transfer surface such as a
thermoplastic polymer film. The energy
from a light or heat source causes the
microadhesion of the target cells or cell
populations to the thermoplastic
transfer surface. Subsequent separation
of the film from the tissue section
selectively removes the adhered target
from the tissue section. The transfer
surface is activated from within the
target to adhere the target to the transfer
surface, for example by heating the
target to adhere or to a thermoplastic
transfer surface. Such in situ activation
can be achieved by exposing the
biological sample to an immunoreagent
that specifically binds to the target (or
a component of the target). The
immunoreagent can alter the transfer
surface directly (for example with a heat
generating enzyme carried by the
immunoreagent), or indirectly (for
example by changing a characteristic of
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the target). In some embodiments, the
immunoreagent deposits a precipitate in
the target that increases its light
absorption relative to surrounding
tissue, such that the biological specimen
can be exposed to light to selectively
heat the target. Alternatively, the
immunoreagent is an
immunofluorescent agent that carries a
fluorophore that absorbs light and emits
heat.
Applications: Microdissection of
specific cells or cell populations from a
histological sample; High throughput
analysis of biological samples.
Advantages: Automated system for
high throughput microdissection and
analysis; Does not require a visual
detection step.
Development Status: In vitro data can
be provided upon request.
Inventors: Michael R. Emmert-Buck
(NCI), Robert F. Bonner (NICHD),
Michael A. Tangrea (NCI), Thomas J.
Pohida (CIT), Rodrigo F. Chuaqui (NCI).
Patent Status:
International Patent Application No.
PCT/US03/23317 filed 23 July 2003,
which published as WO 2004/068104
on 12 Aug 2004 (HHS Reference No. E–
113–2003/0–PCT–02),
U.S. Patent Application No. 10/
543,218 filed 22 Jul 2005 (HHS
Reference No. E–113–2003/0–US–03),
Canadian Patent Application No.
2513646 filed 23 Jul 2003 (HHS
Reference No. E–113–2003/0–CA–05),
Australian Patent Application No.
2003256803 filed 23 Jul 2003 (HHS
Reference No. E–113–2003/0–AU–04),
U.S. Patent Application No. 11/
202,848 filed 12 Aug 2005 (HHS
Reference No. E–113–2003/1–US–01).
Licensing Status: Available for
licensing,
Licensing Contact: Kevin W. Chang,
Ph.D.; 301–435–5018,
changke@mail.nih.gov,
Collaborative Research Opportunity:
The National Cancer Institute, Center for
Cancer Research, Laboratory of
Pathology, is seeking statements of
capability or interest from parties
interested in collaborative research to
further develop, evaluate, or
commercialize Target Activated
Microtransfer—Expression
Microdissection (xMD). Please contact
John D. Hewes, Ph.D. at 301–435–3121
or hewesj@mail.nih.gov for more
information.
Use of Anthrax Lethal Factor To Treat
Cancer and Screening Methods for
MAPK Kinase Protease Activity
Description of Technology: Anthrax
toxin, produced by Bacillus anthracis, is
composed of three proteins: Protective
antigen (PA), edema factor (EF), and
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10947
lethal factor (LF). PA by itself has little
or no toxic effect upon cells, but serves
to bind cell surface receptors and
mediate the entry of EF and LF into the
cell. EF has been identified as an
adenylate cyclase and together with PA
forms a toxin (edema toxin; EdTx)
which can induce edema formation
when injected subcutaneously. LF and
PA together form a toxin (lethal toxin;
LeTx) which can cause rapid lysis of
certain macrophage-derived cell lines in
vitro as well as death when injected
intravenously.
Indirect evidence had suggested that
LF was a metalloprotease. However, the
intracellular target of LF remained
unknown until recently when NIH
scientists discovered that LF
proteolytically inactivates mitogen
activated protein kinase kinase 1 and 2
(MAPKK1, 2). Using oocytes of the frog
Xenopus laevis as well as tumor derived
NIH3T3 (490) cells expressing an
effector domain mutant form of the
human V12HaRas oncogene these
scientists demonstrated that LF induced
proteolysis of MAPKK 1 and 2, resulting
in their irreversible inactivation.
MAPKK 1 and 2 are components of the
mitogen activated protein kinase
(MAPK) signal transduction pathway,
an evolutionarily conserved pathway
that controls cell proliferation and
differentiation in response to
extracellular signals and also plays a
crucial role in regulating oocyte meiotic
maturation. Further, the MAPK pathway
has been shown to be constitutively
activated in many primary human as
well as in tumor-derived cell lines.
Consistent with this, treatment of
V12Ha-Ras transformed NIH 3T3 cells
with LeTx inhibits cell proliferation and
causes their reversion to a nontransformed phenotype.
This invention specifically relates to
in vitro and ex vivo methods of
screening for modulators, homologues,
and mimetics of LF mitogen activated
protein kinase kinase (MAPKK) protease
activity. Applications for this
technology could be:
• A novel tool (LF) for the study of
the cellular role of the MAPK pathway
in normal or tumor cells.
• Investigation of LF for developing
inhibitors for cancer therapy. By
analyzing structural-functional
relationships, additional compounds
with improved specificity, increased
potency, and reduced toxicity can be
generated. Mimetics which block
MAPKK activity or the determination of
mechanisms of regulation of proteases
that target MAPKK at or near the same
site targeted by LF could be developed.
• A protease-based assay for LF by
using a peptide to test for LF cleavage.
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Federal Register / Vol. 74, No. 48 / Friday, March 13, 2009 / Notices
There is no commercial test for anthrax.
This assay could be used for testing
soldiers for anthrax exposure.
Characterization of the interaction
between LF and MAPKK at the amino
acid level may lead to the generation of
inhibitors which may prove useful in
treating anthrax.
Inventors: Nicholas S. Duesbery (NCI),
Craig Webb (NCI), Stephen H. Leppla
(NIDCR), George F. Vande Woude (NCI).
Patent Status:
U.S. Patent 6,485,925 issued 26 Nov
2002 (HHS Reference No. E–068–1998/
0–US–06).
U.S. Patent 6,893,835 issued 17 May
2005 (HHS Reference No. E–068–1998/
0–US–07).
U.S. Patent 6,911,203 issued 28 Jun
2005 (HHS Reference No. E–068–1998/
0–US–08).
U.S. Patent 7,056,693 issued 06 Jun
2006 (HHS Reference No. E–068–1998/
0–US–10).
U.S. Patent 7,183,071 issued 27 Feb
2007 (HHS Reference No. E–068–1998/
0–US–11).
International rights available.
Licensing Status: Available for
licensing.
Licensing Contact: Surekha Vathyam,
Ph.D.; 301–435–4076;
vathyams@mail.nih.gov.
Dated: March 5, 2009.
Richard U. Rodriguez,
Director, Division of Technology Development
and Transfer, Office of Technology Transfer,
National Institutes of Health.
[FR Doc. E9–5418 Filed 3–12–09; 8:45 am]
BILLING CODE 4140–01–P
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
National Institutes of Health
sroberts on PROD1PC70 with NOTICES
Center for Scientific Review; Notice of
Closed Meetings
Pursuant to section 10(d) of the
Federal Advisory Committee Act, as
amended (5 U.S.C. Appendix 2), notice
is hereby given of the following
meetings.
The meetings 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
the discussions could disclose
confidential trade secrets or commercial
property such as patentable material,
and personal information concerning
individuals associated with the grant
applications, the disclosure of which
would constitute a clearly unwarranted
invasion of personal privacy.
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Name of Committee: Center for Scientific
Review Special Emphasis Panel, Small
Business: Orthopaedics and Skeletal Biology.
Date: March 20, 2009.
Time: 8 a.m. to 5 p.m.
Agenda: To review and evaluate grant
applications.
Place: Beacon Hotel and Corporate
Quarters, 1615 Rhode Island Avenue, NW.,
Washington, DC 20036.
Contact Person: Daniel F. McDonald, PhD,
Scientific Review Officer, Center for
Scientific Review, National Institutes of
Health, 6701 Rockledge Drive, Room 4110,
MSC 7814, Bethesda, MD 20892, (301) 435–
1215, mcdonald@csr.nih.gov.
This notice is being published less than 15
days prior to the meeting due to the timing
limitations imposed by the review and
funding cycle.
Name of Committee: Center for Scientific
Review Special Emphasis Panel, Ligament/
Tendon Repair and Replacement.
Date: March 26, 2009.
Time: 10 a.m. to 12:30 p.m.
Agenda: To review and evaluate grant
applications.
Place: National Institutes of Health, 6701
Rockledge Drive, Bethesda, MD 20892,
(Telephone Conference Call).
Contact Person: John P. Holden, PhD,
Scientific Review Officer, Center for
Scientific Review, National Institutes of
Health, 6701 Rockledge Drive, Room 4211,
MSC 7814, Bethesda, MD 20892, 301–496–
8551, holdenjo@csr.nih.gov.
This notice is being published less than 15
days prior to the meeting due to the timing
limitations imposed by the review and
funding cycle.
Name of Committee: Center for Scientific
Review Special Emphasis Panel, Review of
HIV/AIDS Related SBIR/STTR Applications.
Date: April 1, 2009.
Time: 10 a.m. to 2 p.m.
Agenda: To review and evaluate grant
applications.
Place: National Institutes of Health, 6701
Rockledge Drive, Bethesda, MD 20892
(Virtual Meeting).
Contact Person: Mark P. Rubert, PhD,
Scientific Review Officer, Center for
Scientific Review, National Institutes of
Health, 6701 Rockledge Drive, Room 5218,
MSC 7852, Bethesda, MD 20892, 301–435–
1775, rubertm@csr.nih.gov.
Name of Committee: Center for Scientific
Review Special Emphasis Panel, BMIT/MEDI
Member Conflict—Imaging.
Date: April 2, 2009.
Time: 11 a.m. to 3 p.m.
Agenda: To review and evaluate grant
applications.
Place: National Institutes of Health, 6701
Rockledge Drive, Bethesda, MD 20892
(Virtual Meeting).
Contact Person: Dharam S. Dhindsa, DVM,
PhD, Scientific Review Officer, Center for
Scientific Review, National Institutes of
Health, 6701 Rockledge Drive, Room 5110,
MSC 7854, Bethesda, MD 20892, (301) 435–
1174, dhindsad@csr.nih.gov.
(Catalogue of Federal Domestic
Assistance Program Nos. 93.306,
Comparative Medicine; 93.333, Clinical
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Research, 93.306, 93.333, 93.337,
93.393–93.396, 93.837–93.844, 93.846–
93.878, 93.892, 93.893, National
Institutes of Health, HHS)
Dated: March 4, 2009.
Jennifer Spaeth,
Director, Office of Federal Advisory
Committee Policy.
[FR Doc. E9–5139 Filed 3–12–09; 8:45 am]
BILLING CODE 4140–01–M
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
National Institutes of Health
Center for Scientific Review; Amended
Notice of Meeting
Notice is hereby given of a change in
the meeting of the Center for Scientific
Review Special Emphasis Panel,
February 26, 2009, 8 a.m. to February
28, 2009, 5 p.m., National Institutes of
Health, 6701 Rockledge Drive, Bethesda,
MD, 20892 which was published in the
Federal Register on February 6, 2009,
74 FR 6292–6294.
The meeting will be held March 25,
2009 to March 27, 2009. The meeting
time and location remain the same. The
meeting is closed to the public.
Dated: March 5, 2009.
Jennifer Spaeth,
Director, Office of Federal Advisory
Committee Policy.
[FR Doc. E9–5344 Filed 3–12–09; 8:45 am]
BILLING CODE 4140–01–M
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
National Institutes of Health
Eunice Kennedy Shriver National
Institute of Child Health & Human
Development; Notice of Closed
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 the following
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
the discussions could disclose
confidential trade secrets or commercial
property such as patentable material,
and personal information concerning
individuals associated with the grant
applications, the disclosure of which
would constitute a clearly unwarranted
invasion of personal privacy.
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]]>Agencies
[Federal Register Volume 74, Number 48 (Friday, March 13, 2009)]
[Notices]
[Pages 10945-10948]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: E9-5418]
-----------------------------------------------------------------------
DEPARTMENT OF HEALTH AND HUMAN SERVICES
National Institutes of Health
Government-Owned Inventions; Availability for Licensing
AGENCY: National Institutes of Health, Public Health Service, HHS.
ACTION: Notice.
-----------------------------------------------------------------------
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 10946]]
Gene Signature for Predicting Hepatocellular Carcinoma Patient
Prognosis
Description of Technology: A progressive sequence of somatic
mutations and epigenetic changes of oncogenes or tumor suppressor genes
are believed to cause tumor development. However, high genomic
instability in tumors causes the accumulation of genomic aberrations
that do not contribute to tumor progression. Therefore it is important
to distinguish between ``driver'' mutations which are functionally
important and ``passenger'' mutations which do not provide a selective
advantage to the tumor cells.
The current invention describes a driver gene signature for
predicting survival in patients with hepatocellular carcinoma (HCC).
The gene signature includes ten HCC-associated genes, and the NIH
researchers further discovered that a decrease in DNA copy number or
mRNA expression of some genes is associated with a poor prognosis in
HCC tumors, while a decrease in DNA copy number or mRNA expression of a
few other genes is associated with a good prognosis.
Available for licensing is a method of predicting the prognosis of
a patient diagnosed with HCC by detecting expression of one of more
HCC-associated genes, and a method of identifying an agent for use in
treating HCC.
Applications: Prognosis for hepatocellular carcinoma (HCC) patient
survival; Potential new method to identify therapeutic treatment for
HCC patients.
Market: Hepatocellular carcinoma (HCC) is the most frequent
malignant tumor in the liver and the third leading cause of cancer
death worldwide. Systemic chemotherapy has been shown to be ineffective
and tumor recurrence rate after surgical resection is high due to
relapse and metastasis. Therefore, the development of new drugs will be
crucial to prevent relapse and to prolong patient survival.
Development Status: Early-stage development.
Inventors: Xin Wei Wang and Stephanie Roessler (NCI).
Patent Status: U.S. Provisional Application No. 61/198,813 filed 10
Nov 2008 (HHS Reference No. E-024-2009/0-US-01).
Licensing Status: Available for licensing.
Licensing Contact: Betty Tong, Ph.D.; 301-594-6565;
tongb@mail.nih.gov.
Collaborative Research Opportunity: The National Cancer Institute,
Center for Cancer Research, Laboratory of Human Carcinogenesis, is
seeking statements of capability or interest from parties interested in
collaborative research to further develop, evaluate, or commercialize
Gene Signature for Predicting Hepatocellular Carcinoma Patient
Prognosis. Please contact John D. Hewes, Ph.D. at 301-435-3121 or
hewesj@mail.nih.gov for more information.
Lasonolide Compounds as Reagents for Inducing Premature Chromosome
Condensation and Methods of Treating Cancer
Description of Technology: Lasonolide A is a natural product
initially isolated from an extract of the shallow water Caribbean
marine sponge. The chemical structure of lasonolide A was identified in
2002, and it was chemically synthesized in 2007. The current invention
discloses the discovery that lasonolide A may be used as a new reagent
for inducing premature chromosome condensation in non-dividing cells;
and a novel anti-proliferative and anti-metastatic agent for cancer
treatment. Currently, it is difficult to analyze the cytogenetic
composition of the genome of non-dividing cells because the chromosomes
are loosely distributed in the nucleus, lasonolide A may be useful for
performing cytogenetic studies in cells by inducing premature
chromosome condensation without inducing mitosis. In addition, the
invention also reveals that lasonolide A inhibits cancer cell motility.
As such, lasonolide A may be used as an anti-cancer agent by itself or
in combination with other anti-cancer agents such as inhibitors of
topoisomerases.
Applications: A new reagent for inducing premature chromosome
condensation in non-dividing cells; a novel anti-cancer agent.
Market: Cancer continues to be a burden to the public health of
Americans. After heart disease, cancer is the most common cause of
death in the United States. For 2008, it was estimated that about
565,650 Americans were expected to die of cancer. The incidence of
cancer has been dropping over the years but it is estimated that over
1.4 million Americans would be diagnosed with cancer in 2008.
Therefore, there is a continued need for the development of new
therapies to effectively treat this disease.
Development Status: Early-stage development.
Inventors: Yves G. Pommier (NCI) et al.
Patent Status: U.S. Provisional Application No. 61/137,193 filed 28
Jul 2008 (HHS Reference No. E-247-2008/ 0-US-01).
Licensing Status: Available for licensing.
Licensing Contact: Betty Tong, Ph.D.; 301-594-6565;
tongb@mail.nih.gov.
Collaborative Research Opportunity: The National Cancer Institute,
Center for Cancer Research, Laboratory of Molecular Pharmacology, is
seeking statements of capability or interest from parties interested in
collaborative research to further develop, evaluate, or commercialize
Lasonolide Compounds as Reagents for Inducing Premature Chromosome
Condensation and Methods of Treating Cancer. Please contact John D.
Hewes, Ph.D. at 301-435-3121 or hewesj@mail.nih.gov for more
information.
Increased Image Quality for Early Colon Polyp Detection
Description of Technology: The invention relates to a method for
improving the specificity and sensitivity of computer tomographic
colonoscopy (CTC) computer aided detection (CAD). Currently CTC CAD
programs are capable of delivering high sensitivity and low false
positive results when used to detect large polyps of 1 cm or greater in
diameter. However, CTC CAD is not as effective at detecting medium-
sized polyps (6-9 mm in diameter) as it demonstrates lower
sensitivities and higher false positives in this range. Since early
polyp detection is critical to the survival of patients with colon
cancer, the ability to accurately detect medium size polyps could be
advantageous to the outcome of colon cancer treatment.
The invention uses a wavelet-based analysis to distinguish true
polyps from false positives in CTC images. The steps involved include
generating a 2D projection image, computing features of the 2D images
from their Haar wavelet coefficients, applying the feature selection
algorithm, and training a classifier using the selected features to
classify CTC CAD.
Using this technology, it will be possible to create high quality
images for viewing the colon surface in 3D with reduced false positives
in the medium-sized range for colon polyps. The technology can also be
used to locate anomalies in both medical and non-medically related
image applications such as endoscopy, microscopy, and photography.
Applications: High quality images for early colon polyp detection;
Sensitive and efficient colon cancer diagnosis; Locating anomalies in
several different image applications.
Development Status: Early stage.
[[Page 10947]]
Inventors: Ronald M. Summers et al. (CC)
Publications:
1. J Li, R Van Uitert, J Yao, N Petrick, M Franaszek, A Huang, RM
Summers. Wavelet method for CT colonography computer-aided polyp
detection. Med Phys. 2008 Aug;35(8):3527-3538.
2. S Greenblum, J Li, A Huang, RM Summers. Wavelet analysis in
virtual colonoscopy. Proc. SPIE, Vol. 6143, 614336 (March 13, 2006);
doi:10.1117/12.655680.
Patent Status: U.S. Patent Application No. 11/685,127 filed 12 Mar
2007 (HHS Reference No. E-314-2006/0-US-02); No foreign rights
available.
Licensing Status: Available for licensing.
Licensing Contact: Jeffrey A. James, Ph.D.; 301-435-5474;
jeffreyja@mail.nih.gov.
Microdissection and High-Throughput Analysis of Biological Samples
Description of Technology: A variety of techniques have been used
to microdissect specific cells or cell populations from a histological
sample under direct microscopic visualization. Original microdissection
techniques involved painstaking (and sometimes clumsy) manual
dissection using needles or other micro-manipulation devices to isolate
individual cells based on visible, histological characteristics.
The subject technology is a method of performing specific target
activated transfer from a biological sample (i.e., tissue) for analysis
using a device system that can be automated for high throughput
analysis. The method employs a localized reagent, such as an
absorbative stain, that specifically determines the microadhesion of
desired cellular material in a tissue sample to a transfer surface such
as a thermoplastic polymer film. The energy from a light or heat source
causes the microadhesion of the target cells or cell populations to the
thermoplastic transfer surface. Subsequent separation of the film from
the tissue section selectively removes the adhered target from the
tissue section. The transfer surface is activated from within the
target to adhere the target to the transfer surface, for example by
heating the target to adhere or to a thermoplastic transfer surface.
Such in situ activation can be achieved by exposing the biological
sample to an immunoreagent that specifically binds to the target (or a
component of the target). The immunoreagent can alter the transfer
surface directly (for example with a heat generating enzyme carried by
the immunoreagent), or indirectly (for example by changing a
characteristic of the target). In some embodiments, the immunoreagent
deposits a precipitate in the target that increases its light
absorption relative to surrounding tissue, such that the biological
specimen can be exposed to light to selectively heat the target.
Alternatively, the immunoreagent is an immunofluorescent agent that
carries a fluorophore that absorbs light and emits heat.
Applications: Microdissection of specific cells or cell populations
from a histological sample; High throughput analysis of biological
samples.
Advantages: Automated system for high throughput microdissection
and analysis; Does not require a visual detection step.
Development Status: In vitro data can be provided upon request.
Inventors: Michael R. Emmert-Buck (NCI), Robert F. Bonner (NICHD),
Michael A. Tangrea (NCI), Thomas J. Pohida (CIT), Rodrigo F. Chuaqui
(NCI).
Patent Status:
International Patent Application No. PCT/US03/23317 filed 23 July
2003, which published as WO 2004/068104 on 12 Aug 2004 (HHS Reference
No. E-113-2003/0-PCT-02),
U.S. Patent Application No. 10/543,218 filed 22 Jul 2005 (HHS
Reference No. E-113-2003/0-US-03),
Canadian Patent Application No. 2513646 filed 23 Jul 2003 (HHS
Reference No. E-113-2003/0-CA-05),
Australian Patent Application No. 2003256803 filed 23 Jul 2003 (HHS
Reference No. E-113-2003/0-AU-04),
U.S. Patent Application No. 11/202,848 filed 12 Aug 2005 (HHS
Reference No. E-113-2003/1-US-01).
Licensing Status: Available for licensing,
Licensing Contact: Kevin W. Chang, Ph.D.; 301-435-5018,
changke@mail.nih.gov,
Collaborative Research Opportunity: The National Cancer Institute,
Center for Cancer Research, Laboratory of Pathology, is seeking
statements of capability or interest from parties interested in
collaborative research to further develop, evaluate, or commercialize
Target Activated Microtransfer--Expression Microdissection (xMD).
Please contact John D. Hewes, Ph.D. at 301-435-3121 or
hewesj@mail.nih.gov for more information.
Use of Anthrax Lethal Factor To Treat Cancer and Screening Methods for
MAPK Kinase Protease Activity
Description of Technology: Anthrax toxin, produced by Bacillus
anthracis, is composed of three proteins: Protective antigen (PA),
edema factor (EF), and lethal factor (LF). PA by itself has little or
no toxic effect upon cells, but serves to bind cell surface receptors
and mediate the entry of EF and LF into the cell. EF has been
identified as an adenylate cyclase and together with PA forms a toxin
(edema toxin; EdTx) which can induce edema formation when injected
subcutaneously. LF and PA together form a toxin (lethal toxin; LeTx)
which can cause rapid lysis of certain macrophage-derived cell lines in
vitro as well as death when injected intravenously.
Indirect evidence had suggested that LF was a metalloprotease.
However, the intracellular target of LF remained unknown until recently
when NIH scientists discovered that LF proteolytically inactivates
mitogen activated protein kinase kinase 1 and 2 (MAPKK1, 2). Using
oocytes of the frog Xenopus laevis as well as tumor derived NIH3T3
(490) cells expressing an effector domain mutant form of the human
V12HaRas oncogene these scientists demonstrated that LF induced
proteolysis of MAPKK 1 and 2, resulting in their irreversible
inactivation. MAPKK 1 and 2 are components of the mitogen activated
protein kinase (MAPK) signal transduction pathway, an evolutionarily
conserved pathway that controls cell proliferation and differentiation
in response to extracellular signals and also plays a crucial role in
regulating oocyte meiotic maturation. Further, the MAPK pathway has
been shown to be constitutively activated in many primary human as well
as in tumor-derived cell lines. Consistent with this, treatment of
V12Ha-Ras transformed NIH 3T3 cells with LeTx inhibits cell
proliferation and causes their reversion to a non-transformed
phenotype.
This invention specifically relates to in vitro and ex vivo methods
of screening for modulators, homologues, and mimetics of LF mitogen
activated protein kinase kinase (MAPKK) protease activity. Applications
for this technology could be:
A novel tool (LF) for the study of the cellular role of
the MAPK pathway in normal or tumor cells.
Investigation of LF for developing inhibitors for cancer
therapy. By analyzing structural-functional relationships, additional
compounds with improved specificity, increased potency, and reduced
toxicity can be generated. Mimetics which block MAPKK activity or the
determination of mechanisms of regulation of proteases that target
MAPKK at or near the same site targeted by LF could be developed.
A protease-based assay for LF by using a peptide to test
for LF cleavage.
[[Page 10948]]
There is no commercial test for anthrax. This assay could be used for
testing soldiers for anthrax exposure. Characterization of the
interaction between LF and MAPKK at the amino acid level may lead to
the generation of inhibitors which may prove useful in treating
anthrax.
Inventors: Nicholas S. Duesbery (NCI), Craig Webb (NCI), Stephen H.
Leppla (NIDCR), George F. Vande Woude (NCI).
Patent Status:
U.S. Patent 6,485,925 issued 26 Nov 2002 (HHS Reference No. E-068-
1998/0-US-06).
U.S. Patent 6,893,835 issued 17 May 2005 (HHS Reference No. E-068-
1998/0-US-07).
U.S. Patent 6,911,203 issued 28 Jun 2005 (HHS Reference No. E-068-
1998/0-US-08).
U.S. Patent 7,056,693 issued 06 Jun 2006 (HHS Reference No. E-068-
1998/0-US-10).
U.S. Patent 7,183,071 issued 27 Feb 2007 (HHS Reference No. E-068-
1998/0-US-11).
International rights available.
Licensing Status: Available for licensing.
Licensing Contact: Surekha Vathyam, Ph.D.; 301-435-4076;
vathyams@mail.nih.gov.
Dated: March 5, 2009.
Richard U. Rodriguez,
Director, Division of Technology Development and Transfer, Office of
Technology Transfer, National Institutes of Health.
[FR Doc. E9-5418 Filed 3-12-09; 8:45 am]
BILLING CODE 4140-01-P
