Government-Owned Inventions; Availability for Licensing, 39319-39321 [E8-15562]
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Federal Register / Vol. 73, No. 132 / Wednesday, July 9, 2008 / Notices
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
National Institutes of Health
Government-Owned Inventions;
Availability for Licensing
National Institutes of Health,
Public Health Service, HHS.
ACTION: Notice.
AGENCY:
jlentini on PROD1PC65 with NOTICES
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.
Method for Detection and
Quantification of PLK1 Expression and
Activity
Description of Technology: Polo-like
kinase 1 (Plk1) plays a role in the
regulation of the cell cycle and control
of cellular proliferation. Because Plk1 is
associated with neoplastic
transformation of human cells,
expression of this protein has been
proposed as a prognostic marker for
many types of malignancies. In
mammalian cells, four Plks exist, but
their expression patterns and functions
appear to be distinct from each other.
Available for licensing is a Plk1 ELISA
assay using peptide substrates that are
specific for Plk1, in that they are
phosphorylated and bound by Plk1, but
not by the related polo kinases Plk2,
Plk3 and Plk4.
By exploiting a unique Plk1dependent phosphorylation and binding
property, an easy and reliable ELISA
assay has been developed to quantify
Plk1 expression levels and kinase
activity. With this highly sensitive
assay, Plk1 activity can be measured
with 2–20 microgram of total lysates
without immunoprecipitation or
purification steps. Since deregulated
Plk1 expression has been suggested as a
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prognostic marker for a wide range of
human malignancies, this assay may
provide an innovative tool for assessing
the predisposition for cancer
development, monitoring cancer
progression, and estimating the
prognosis of various types of cancer
patients.
Applications: Optimized PBIP1
polypeptides, a natural substrate of
Plk1, with enhanced specificity and
sensitivity over the native PBIP1
sequence.
ELISA assay to quantify Plk1
expression and kinase activity.
Advantages: Rapid, highly sensitive
assay that requires lower amounts of
starting material than conventional
immunoprecipitation assays.
Assay that is selective for Plk1.
Development Status: The technology
is currently in the pre-clinical stage of
development.
Market: An estimated 1,444,920 new
cancer diagnoses in the U.S. in 2007.
Cancer is the second leading cause of
death in United States. It is estimated
that the cancer therapeutic market
would double to $50 billion a year in
2010 from $25 billion in 2006.
Inventors: Kyung Lee and Jung-Eun
Park (NCI).
Publications: 1. J-E Park, L Li, K
Strebhardt, SH Yuspa, and KS. Lee.
Direct quantification of polo-like kinase
1 activity in cells and tissues using a
highly sensitive and specific ELISA
assay (about to be submitted).
2. KS Lee et al. Mechanisms of
mammalian polo-like kinase 1 (Plk1)
localization: self-versus non-selfpriming. Cell Cycle 2008 Jan;7(2): 141–
145.
3. KS Lee et al. Self-regulated
mechanism of Plk1 localization to
kinetochores: lessons from the Plk1–
PBIP1 interaction. Cell Div. 2008 Jan
23;3:4.
4. YH Kang et al. Self-regulated Plk1
recruitment to kinetochores by the
Plk1–PBIP1 interaction is critical for
proper chromosome segregation. Mol
Cell. 2006 Nov 3;24(3): 409–422.
Patent Status: U.S. Provisional
Application No. 61/054,032 filed 16
May 2008 (HHS Reference No. E–091–
008/0–US–01).
Licensing Status: Available for
exclusive or non-exclusive licensing.
Licensing Contact: Jennifer Wong;
301–435–4633.; wongje@mail.nih.gov.
Collaborative Research Opportunity:
The National Cancer Institute,
Laboratory of Metabolism is seeking
statements of capability or interest from
parties interested in collaborative
research to further develop, evaluate, or
commercialize the PLK1 ELISA assay
described above. Please contact John D.
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39319
Hewes, Ph.D. at 301–435–3121 or
hewesj@mail.nih.gov for more
information.
Cripto-1 Represents a Biomarker for
Chronic Inflammatory Diseases
Description of Technology: Chronic
inflammatory bowel disease (IBD) (e.g.
Crohn’s disease and ulcerative colitis)
and chronic inflammatory arthropathy
such as rheumatoid arthritis represent
an enormous socio-economic burden
due to the cost for long term medication
and rehabilitation and the decreased
productivity due to periods of acute
recurrences. A major characteristic of
these diseases is the tissue infiltration of
specific CD4+ T cells that sustain
inflammation by secreting cytokines.
One of these cytokines, TNF-alpha, is a
current therapeutic target for the
treatment of these chronic inflammatory
diseases.
This technology describes Cripto-1 as
a biomarker for chronic inflammatory
diseases. Cripto-1, an epidermal growth
factor (EGF)-related protein, shows
higher expression levels in tissue
sections of Crohn’s disease, ulcerative
colitis, and rheumatoid arthritis as
compared to adjacent unaffected areas.
Moreover, the inventors show that the
response to Cripto-1 is not due to a
generic immune response, and Cripto-1
expression increases the expression of
TNF-alpha in CD4+ T cells in tissues
affected by chronic inflammatory
disease. As a result, this technology
could be used as a diagnostic biomarker
for chronic inflammatory diseases as
well as a novel therapeutic target to help
control TNF-alpha in chronic
inflammatory diseases.
Applications: Diagnostic tool for the
detection of a chronic inflammatory
disease.
Method to inhibit cytokine
production in a tissue affected with a
chronic inflammatory disease.
Development Status: The technology
is currently in the pre-clinical stage of
development.
Inventors: Luigi Strizzi, David S.
Salomon, Monica I. Gonzales (NCI).
Patent Status: U.S. Provisional
Application No. 61/045,746 filed 17 Apr
2008 (HHS Reference No. E–075–2008/
0–US–01).
Licensing Status: Available for
licensing.
Licensing Contact: Whitney A.
Hastings; 301–451–7337;
hastingw@mail.nih.gov.
Collaborative Research Opportunity:
The National Cancer Institute Mammary
Biology and Tumorigenesis Laboratory
is seeking statements of capability or
interest from parties interested in
collaborative research to further
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Federal Register / Vol. 73, No. 132 / Wednesday, July 9, 2008 / Notices
jlentini on PROD1PC65 with NOTICES
develop, evaluate, or commercialize
Cripto-1 as a biomarker for chronic
inflammatory diseases. Please contact
John D. Hewes, Ph.D. at 301–435–3121
or hewesj@mail.nih.gov for more
information.
Cripto-1 as a Biomarker for Cardiac
Ischemia
Description of Technology: Ischemic
heart disease is a major cause of human
cardiac morbidity and mortality,
affecting over 14 million people in the
United States alone. Current detection
of cardiac ischemia relies upon
identification of electrocardiographic
anomalies and the release of cardiac
markers from the damaged myocardial
tissue. Unfortunately, patients with
acute myocardial infarction are often
insensitive to these tests during the
early phases of intervention and as a
result more markers for cardiac
ischemic disease are needed.
This technology describes Cripto-1 as
a biomarker for infarcted cardiac tissues.
Cripto-1 is a member of the epidermal
growth factor (EGF)-related proteins and
is currently thought to play an
important role in several cancers. The
present invention shows that Cripto-1 is
overexpressed in infarcted myocardial
tissue, and not expressed or weakly
expressed in non-infarct related heart
disease tissues and normal tissues.
Furthermore, the overexpression of
Cripto-1 correlates with the hypoxiainducible factor-1-alpha indicating
specificity to ischemic heart tissue. The
expression of Cripto-1 has also been
shown to be highly expressed in stem
cells, which may have an important role
in the repair of damaged myocardial
tissue. Thus, this technology could
represent a new biomarker for the
diagnosis of myocardial infarction as
well as a surrogate biomarker to monitor
the healing process including
regenerative stem cell activity of the
infarcted myocardial tissue.
Applications:
Diagnostic tool for the detection of
myocardial infarction.
Method to monitor stem cell activity
in damaged myocardial tissue.
Development Status: The technology
is currently in the pre-clinical stage of
development.
Inventors: Luigi Strizzi, Caterina
Bianco, David S. Salomon (NCI).
Patent Status: U.S. Provisional
Application No. 61/046,181 filed 18 Apr
2008 (HHS Reference No. E–049–2008/
0-US–01).
Licensing Status: Available for
licensing.
Licensing Contact: Whitney A.
Hastings; 301–451–7337;
hastingw@mail.nih.gov.
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Collaborative Research Opportunity:
The National Cancer Institute Mammary
Biology and Tumorigenesis Laboratory
is seeking statements of capability or
interest from parties interested in
collaborative research to further
develop, evaluate, or commercialize
Cripto-1 as a biomarker for cardiac
ischemia. Please contact John D. Hewes,
Ph.D. at 301–435–3121 or
hewesj@mail.nih.gov for more
information.
Identification of Persons Likely To
Benefit From Statin Mediated Cancer
Prevention by Pharmacogenetics
Description of Technology: Inhibitors
of 3-hydroxy-3-methylglutaryl (HMG)
coenzyme A reductase (statins) are a
class of well-tolerated compounds that
are the most widely used cholesterollowering drugs in the United States.
Reduced cancer risk among statin users
has also been observed as a secondary
outcome in randomized controlled
clinical trials evaluating effects of
statins on cardiovascular outcomes.
However the observed cancer risk
reduction varied with different clinical
studies. Thus there is a need to identify
individuals who would benefit from
treatment with statins.
The current invention describes a
pharmacogenetic method to identify
candidates who are most likely to
benefit from treatment with statins to
reduce cancer risk, and consequently
minimizing any unnecessary cost and
side effects in individuals who do not
benefit. Specifically, we discovered that
an HMGCR genetic variant rs12654264
is associated with significantly lower
colorectal cancer risk, with most of the
benefit seen in HMGCoA reductase
inhibitor (statin) users. We also
discovered that this same HMGCR
genetic variant is associated with
significantly higher serum cholesterol
levels in Israeli colorectal cancer
patients. The same HMGCR genetic
variant has also been associated with
significantly higher serum cholesterol
levels in two independent groups of
individuals of mixed European descent
[https://www.broad.mit.edu/diabetes/
scandinavs/ and N Engl J
Med. 2008 March 20;358(12):1240–1249
(https://www.ncbi.nlm.nih.gov/pubmed/
18354102?dopt)]. These data suggest
that the same genetic variant modifies
cholesterol metabolism in a manner that
affects both colorectal cancer risk and
cardiovascular risk.
Applications and Market: Statins
account for approximately 80% of the
cholesterol-lowering drugs prescribed in
the United States, and six statins are
currently available on the U.S. market.
Reduced cancer risk is also associated
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with statin use. This invention provides
a method to indentify individuals who
are most likely to benefit from cancer
chemopreventive treatment with statins.
Pharmacogenetic markers can be
developed to identify patient population
that can benefit from statins, therefore
expanding the markets of stains.
Development Status: The inventors
have discovered several novel genetic
variants of HMG coenzyme A reductase
gene, and are further investigating the
functional significance of the variants in
vitro.
Inventors: Dr. Levy Kopelovich (NCI)
et al.
Patent Status: U.S. Provisional
Application No. 60/985,587 filed 05
Nov 2007 (HHS Reference No. E–328–
2007/0–US–01).
Licensing Status: Available for
exclusive or non-exclusive licensing.
Licensing Contact: Betty Tong, PhD;
301–594–6565; tongb@mail.nih.gov.
TGF-beta Gene Expression Signature in
Cancer Prognosis
Description of Technology:
Hepatocellular carcinoma (HCC) is the
third leading cause of cancer death
worldwide, and it is very heterogeneous
in terms of its clinical presentation as
well as genomic and transcriptomic
patterns. This heterogeneity and the
lack of appropriate biomarkers have
hampered patient prognosis and
treatment stratification.
Available for licensing is a novel
temporal TGF-beta gene expression
signature that predicts HCC patient
clinical outcomes. Patients with tumors
expressing late TGF-beta responsive
genes had a malignant prognosis and an
invasive tumor phenotype as evaluated
by decreased survival time, increased
tumor recurrence, and vascular invasion
rate. Additionally, this signature may
also be able to prognose other cancers,
including lung cancer.
Applications: Method to diagnose
cancer.
Method to monitor cancer progression
and aid clinicians to choose appropriate
therapies.
Commercial kits to prognose cancer.
Advantages: Early diagnostic tool to
stratify HCC patients to chose more
effective treatment.
Development Status: The technology
is currently in the pre-clinical stage of
development.
Market: An estimated 1,444,920 new
cancer diagnosed in the U.S. in 2007.
Cancer is the second leading cause of
death in United States.
It is estimated that the cancer
therapeutic market would double to $50
billion a year in 2010 from $25 billion
in 2006.
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Federal Register / Vol. 73, No. 132 / Wednesday, July 9, 2008 / Notices
jlentini on PROD1PC65 with NOTICES
Inventors: Snorri Thorgeirsson (NCI)
and Cedric Coulouaran (NCI)
Relevant Publication: Coulouaran C,
Factor VM, Thorgeirsson SS.
Transforming growth factor-beta gene
expression signature in mouse
hepatocytes predicts clinical outcome in
human cancer. Hepatology 2008
Jun;47(6):2059–2067.
Patent Status: U.S. Provisional
Application No. 60/981,661 filed 22 Oct
2007 (HHS Reference No. E–282–2007/
0-US–01)
Licensing Status: Available for
exclusive or non-exclusive licensing.
Licensing Contact: Jennifer Wong;
301–435–4633; wongje@mail.nih.gov.
Collaborative Research Opportunity:
The National Cancer Institute, Center for
Cancer Research, Laboratory of
Experimental Carcinogenesis is seeking
statements of capability or interest from
parties interested in collaborative
research to further develop, evaluate, or
commercialize a novel temporal TGFbeta gene expression signature that
predicts HCC patient clinical outcomes.
Please contact John D. Hewes, PhD at
301–435–3121 or hewesj@mail.nih.gov
for more information.
A New Pot1 Variant Gene as a
Diagnostic Biomarker for Hereditary
Non-polyposis Colorectal Cancer
Description of Technology: The
diagnosis of Hereditary Nonpolyposis
Colorectal Cancer (HNPCC) is difficult
because the disease lacks phenotypic
signs that might facilitate its
presymptomatic diagnosis. This
invention is based on the identification
of a new splice variant of a gene that
appears to exist specifically in HNPCC,
namely ‘‘Pot1’’ or ‘‘Protection of
Telomeres.’’ Pot1 has a critical role in
ensuring chromosome stability by
binding to telomeres. The invention
presents a variant of Pot1 that is present
in mismatch repair-deficient, but not
proficient, cancer cell lines and
primary, non-tumor tissue samples. The
presence of this variant may be useful
both as a diagnostic marker for HNPCC,
and as a new therapeutic target for the
treatment of HNPCC.
Applications and Modality:
Identification of new ‘‘Pot1’’ variant
gene associated with HNPCC
New gene can be used as a potential
diagnostic biomarker for the diagnosis
of HNPCC.
Pot1 as a new therapeutic target for
the treatment of HNPCC.
Development Status: The technology
is currently in the pre-clinical stage of
development.
Inventors: Qin Yang and Curtis C.
Harris (NCI).
Related Publications:
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1. P Baumann et al. Human Pot1
(protection of telomeres) protein:
cytolocalization, gene structure, and
alternative splicing. Mol Cell Biol. 2002
Nov;22(22):8079–8087.
2. A Umar et al. Revised Bethesda
Guidelines for hereditary nonpolyposis
colorectal cancer (Lynch syndrome) and
microsatellite instability. J Natl Cancer
Inst. 2004 Feb 18;96(4):261–268.
3. HT Lynch et al. Hereditary
nonpolyposis colorectal carcinoma
(HNPCC) and HNPCC-like families:
Problems in diagnosis, surveillance, and
management. Cancer. 2004 Jan
1;100(1):53–64.
4. Q Yang et al. Functional diversity
of human protection of telomeres 1
isoforms in telomere protection and
cellular senescence. Cancer Res. 2007
Dec 15;67(24):11677–11686.
Patent Status: U.S. Provisional
Application No. 60/620,754 filed 20 Oct
2004 (HHS Reference No. E–263–2004/
0–US–01), entitled ‘‘POT1 Alternating
Splice Variants’’
International Patent Application No.
PCT/US2005/037957 filed 19 Oct 2005,
which published as WO 2006/045062
on 27 Apr 2006 (HHS Reference No. E–
263–2004/0–PCT–02)
U.S. Patent Application No. 11/
665,944 filed 20 Apr 2007 (HHS
Reference No. E–263–2004/0-US–03).
Licensing Status: Available for
exclusive and non-exclusive licensing.
Licensing Contact: Surekha Vathyam,
PhD; 301–435–4076;
vathyams@mail.nih.gov.
Collaborative Research Opportunity:
The National Cancer Institute
Laboratory of Human Carcinogenesis is
seeking statements of capability or
interest from parties interested in
collaborative research to further
develop, evaluate, or commercialize
biomarkers of colon cancer. Please
contact John D. Hewes, PhD at 301–435–
3121 or hewesj@mail.nih.gov for more
information.
Dated: June 30, 2008.
Richard U. Rodriguez,
Director, Division of Technology Development
and Transfer, Office of Technology Transfer,
National Institutes of Health.
[FR Doc. E8–15562 Filed 7–8–08; 8:45 am]
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DEPARTMENT OF HEALTH AND
HUMAN SERVICES
National Institutes of Health
Center for Scientific Review; Notice of
Closed Meetings
Pursuant to section 10(d) of the
Federal Advisory Committee Act, as
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39321
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(cX6), 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.
Name of Committee: Center for Scientific
Review Special Emphasis Panel, Gene
Therapy and Inborn Errors-2.
Date: July 14, 2008.
Time: 1 p.m. to 5 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: Richard Panniers, PhD,
Scientific Review Officer, Center for
Scientific Review, National Institutes of
Health, 6701 Rockledge Drive, Room 2212,
MSC 7890, Bethesda, MD 20892, (301) 435–
1741, pannierr@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
Member Conflict Applications from BSPH
and ACE.
Date: July 28, 2008.
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.
(Telephone Conference Call)
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.
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.
(Catalogue of Federal Domestic Assistance
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93.333, Clinical 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: July 1, 2008.
Jennifer Spaeth,
Director, Office of Federal Advisory
Committee Policy.
[FR Doc. E8–15469 Filed 7–8–08; 8:45 am]
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Agencies
[Federal Register Volume 73, Number 132 (Wednesday, July 9, 2008)]
[Notices]
[Pages 39319-39321]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: E8-15562]
[[Page 39319]]
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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.
Method for Detection and Quantification of PLK1 Expression and Activity
Description of Technology: Polo-like kinase 1 (Plk1) plays a role
in the regulation of the cell cycle and control of cellular
proliferation. Because Plk1 is associated with neoplastic
transformation of human cells, expression of this protein has been
proposed as a prognostic marker for many types of malignancies. In
mammalian cells, four Plks exist, but their expression patterns and
functions appear to be distinct from each other. Available for
licensing is a Plk1 ELISA assay using peptide substrates that are
specific for Plk1, in that they are phosphorylated and bound by Plk1,
but not by the related polo kinases Plk2, Plk3 and Plk4.
By exploiting a unique Plk1-dependent phosphorylation and binding
property, an easy and reliable ELISA assay has been developed to
quantify Plk1 expression levels and kinase activity. With this highly
sensitive assay, Plk1 activity can be measured with 2-20 microgram of
total lysates without immunoprecipitation or purification steps. Since
deregulated Plk1 expression has been suggested as a prognostic marker
for a wide range of human malignancies, this assay may provide an
innovative tool for assessing the predisposition for cancer
development, monitoring cancer progression, and estimating the
prognosis of various types of cancer patients.
Applications: Optimized PBIP1 polypeptides, a natural substrate of
Plk1, with enhanced specificity and sensitivity over the native PBIP1
sequence.
ELISA assay to quantify Plk1 expression and kinase activity.
Advantages: Rapid, highly sensitive assay that requires lower
amounts of starting material than conventional immunoprecipitation
assays.
Assay that is selective for Plk1.
Development Status: The technology is currently in the pre-clinical
stage of development.
Market: An estimated 1,444,920 new cancer diagnoses in the U.S. in
2007. Cancer is the second leading cause of death in United States. It
is estimated that the cancer therapeutic market would double to $50
billion a year in 2010 from $25 billion in 2006.
Inventors: Kyung Lee and Jung-Eun Park (NCI).
Publications: 1. J-E Park, L Li, K Strebhardt, SH Yuspa, and KS.
Lee. Direct quantification of polo-like kinase 1 activity in cells and
tissues using a highly sensitive and specific ELISA assay (about to be
submitted).
2. KS Lee et al. Mechanisms of mammalian polo-like kinase 1 (Plk1)
localization: self-versus non-self-priming. Cell Cycle 2008 Jan;7(2):
141-145.
3. KS Lee et al. Self-regulated mechanism of Plk1 localization to
kinetochores: lessons from the Plk1-PBIP1 interaction. Cell Div. 2008
Jan 23;3:4.
4. YH Kang et al. Self-regulated Plk1 recruitment to kinetochores
by the Plk1-PBIP1 interaction is critical for proper chromosome
segregation. Mol Cell. 2006 Nov 3;24(3): 409-422.
Patent Status: U.S. Provisional Application No. 61/054,032 filed 16
May 2008 (HHS Reference No. E-091-008/0-US-01).
Licensing Status: Available for exclusive or non-exclusive
licensing.
Licensing Contact: Jennifer Wong; 301-435-4633.;
wongje@mail.nih.gov.
Collaborative Research Opportunity: The National Cancer Institute,
Laboratory of Metabolism is seeking statements of capability or
interest from parties interested in collaborative research to further
develop, evaluate, or commercialize the PLK1 ELISA assay described
above. Please contact John D. Hewes, Ph.D. at 301-435-3121 or
hewesj@mail.nih.gov for more information.
Cripto-1 Represents a Biomarker for Chronic Inflammatory Diseases
Description of Technology: Chronic inflammatory bowel disease (IBD)
(e.g. Crohn's disease and ulcerative colitis) and chronic inflammatory
arthropathy such as rheumatoid arthritis represent an enormous socio-
economic burden due to the cost for long term medication and
rehabilitation and the decreased productivity due to periods of acute
recurrences. A major characteristic of these diseases is the tissue
infiltration of specific CD4+ T cells that sustain inflammation by
secreting cytokines. One of these cytokines, TNF-alpha, is a current
therapeutic target for the treatment of these chronic inflammatory
diseases.
This technology describes Cripto-1 as a biomarker for chronic
inflammatory diseases. Cripto-1, an epidermal growth factor (EGF)-
related protein, shows higher expression levels in tissue sections of
Crohn's disease, ulcerative colitis, and rheumatoid arthritis as
compared to adjacent unaffected areas. Moreover, the inventors show
that the response to Cripto-1 is not due to a generic immune response,
and Cripto-1 expression increases the expression of TNF-alpha in CD4+ T
cells in tissues affected by chronic inflammatory disease. As a result,
this technology could be used as a diagnostic biomarker for chronic
inflammatory diseases as well as a novel therapeutic target to help
control TNF-alpha in chronic inflammatory diseases.
Applications: Diagnostic tool for the detection of a chronic
inflammatory disease.
Method to inhibit cytokine production in a tissue affected with a
chronic inflammatory disease.
Development Status: The technology is currently in the pre-clinical
stage of development.
Inventors: Luigi Strizzi, David S. Salomon, Monica I. Gonzales
(NCI).
Patent Status: U.S. Provisional Application No. 61/045,746 filed 17
Apr 2008 (HHS Reference No. E-075-2008/0-US-01).
Licensing Status: Available for licensing.
Licensing Contact: Whitney A. Hastings; 301-451-7337;
hastingw@mail.nih.gov.
Collaborative Research Opportunity: The National Cancer Institute
Mammary Biology and Tumorigenesis Laboratory is seeking statements of
capability or interest from parties interested in collaborative
research to further
[[Page 39320]]
develop, evaluate, or commercialize Cripto-1 as a biomarker for chronic
inflammatory diseases. Please contact John D. Hewes, Ph.D. at 301-435-
3121 or hewesj@mail.nih.gov for more information.
Cripto-1 as a Biomarker for Cardiac Ischemia
Description of Technology: Ischemic heart disease is a major cause
of human cardiac morbidity and mortality, affecting over 14 million
people in the United States alone. Current detection of cardiac
ischemia relies upon identification of electrocardiographic anomalies
and the release of cardiac markers from the damaged myocardial tissue.
Unfortunately, patients with acute myocardial infarction are often
insensitive to these tests during the early phases of intervention and
as a result more markers for cardiac ischemic disease are needed.
This technology describes Cripto-1 as a biomarker for infarcted
cardiac tissues. Cripto-1 is a member of the epidermal growth factor
(EGF)-related proteins and is currently thought to play an important
role in several cancers. The present invention shows that Cripto-1 is
overexpressed in infarcted myocardial tissue, and not expressed or
weakly expressed in non-infarct related heart disease tissues and
normal tissues. Furthermore, the overexpression of Cripto-1 correlates
with the hypoxia-inducible factor-1-alpha indicating specificity to
ischemic heart tissue. The expression of Cripto-1 has also been shown
to be highly expressed in stem cells, which may have an important role
in the repair of damaged myocardial tissue. Thus, this technology could
represent a new biomarker for the diagnosis of myocardial infarction as
well as a surrogate biomarker to monitor the healing process including
regenerative stem cell activity of the infarcted myocardial tissue.
Applications:
Diagnostic tool for the detection of myocardial infarction.
Method to monitor stem cell activity in damaged myocardial tissue.
Development Status: The technology is currently in the pre-clinical
stage of development.
Inventors: Luigi Strizzi, Caterina Bianco, David S. Salomon (NCI).
Patent Status: U.S. Provisional Application No. 61/046,181 filed 18
Apr 2008 (HHS Reference No. E-049-2008/0-US-01).
Licensing Status: Available for licensing.
Licensing Contact: Whitney A. Hastings; 301-451-7337;
hastingw@mail.nih.gov.
Collaborative Research Opportunity: The National Cancer Institute
Mammary Biology and Tumorigenesis Laboratory is seeking statements of
capability or interest from parties interested in collaborative
research to further develop, evaluate, or commercialize Cripto-1 as a
biomarker for cardiac ischemia. Please contact John D. Hewes, Ph.D. at
301-435-3121 or hewesj@mail.nih.gov for more information.
Identification of Persons Likely To Benefit From Statin Mediated Cancer
Prevention by Pharmacogenetics
Description of Technology: Inhibitors of 3-hydroxy-3-methylglutaryl
(HMG) coenzyme A reductase (statins) are a class of well-tolerated
compounds that are the most widely used cholesterol-lowering drugs in
the United States. Reduced cancer risk among statin users has also been
observed as a secondary outcome in randomized controlled clinical
trials evaluating effects of statins on cardiovascular outcomes.
However the observed cancer risk reduction varied with different
clinical studies. Thus there is a need to identify individuals who
would benefit from treatment with statins.
The current invention describes a pharmacogenetic method to
identify candidates who are most likely to benefit from treatment with
statins to reduce cancer risk, and consequently minimizing any
unnecessary cost and side effects in individuals who do not benefit.
Specifically, we discovered that an HMGCR genetic variant rs12654264 is
associated with significantly lower colorectal cancer risk, with most
of the benefit seen in HMGCoA reductase inhibitor (statin) users. We
also discovered that this same HMGCR genetic variant is associated with
significantly higher serum cholesterol levels in Israeli colorectal
cancer patients. The same HMGCR genetic variant has also been
associated with significantly higher serum cholesterol levels in two
independent groups of individuals of mixed European descent [https://
www.broad.mit.edu/diabetes/scandinavs/ and N Engl J Med. 2008
March 20;358(12):1240-1249 (https://www.ncbi.nlm.nih.gov/pubmed/
18354102?dopt)]. These data suggest that the same genetic variant
modifies cholesterol metabolism in a manner that affects both
colorectal cancer risk and cardiovascular risk.
Applications and Market: Statins account for approximately 80% of
the cholesterol-lowering drugs prescribed in the United States, and six
statins are currently available on the U.S. market. Reduced cancer risk
is also associated with statin use. This invention provides a method to
indentify individuals who are most likely to benefit from cancer
chemopreventive treatment with statins.
Pharmacogenetic markers can be developed to identify patient
population that can benefit from statins, therefore expanding the
markets of stains.
Development Status: The inventors have discovered several novel
genetic variants of HMG coenzyme A reductase gene, and are further
investigating the functional significance of the variants in vitro.
Inventors: Dr. Levy Kopelovich (NCI) et al.
Patent Status: U.S. Provisional Application No. 60/985,587 filed 05
Nov 2007 (HHS Reference No. E-328-2007/0-US-01).
Licensing Status: Available for exclusive or non-exclusive
licensing.
Licensing Contact: Betty Tong, PhD; 301-594-6565;
tongb@mail.nih.gov.
TGF-beta Gene Expression Signature in Cancer Prognosis
Description of Technology: Hepatocellular carcinoma (HCC) is the
third leading cause of cancer death worldwide, and it is very
heterogeneous in terms of its clinical presentation as well as genomic
and transcriptomic patterns. This heterogeneity and the lack of
appropriate biomarkers have hampered patient prognosis and treatment
stratification.
Available for licensing is a novel temporal TGF-beta gene
expression signature that predicts HCC patient clinical outcomes.
Patients with tumors expressing late TGF-beta responsive genes had a
malignant prognosis and an invasive tumor phenotype as evaluated by
decreased survival time, increased tumor recurrence, and vascular
invasion rate. Additionally, this signature may also be able to
prognose other cancers, including lung cancer.
Applications: Method to diagnose cancer.
Method to monitor cancer progression and aid clinicians to choose
appropriate therapies.
Commercial kits to prognose cancer.
Advantages: Early diagnostic tool to stratify HCC patients to chose
more effective treatment.
Development Status: The technology is currently in the pre-clinical
stage of development.
Market: An estimated 1,444,920 new cancer diagnosed in the U.S. in
2007.
Cancer is the second leading cause of death in United States.
It is estimated that the cancer therapeutic market would double to
$50 billion a year in 2010 from $25 billion in 2006.
[[Page 39321]]
Inventors: Snorri Thorgeirsson (NCI) and Cedric Coulouaran (NCI)
Relevant Publication: Coulouaran C, Factor VM, Thorgeirsson SS.
Transforming growth factor-beta gene expression signature in mouse
hepatocytes predicts clinical outcome in human cancer. Hepatology 2008
Jun;47(6):2059-2067.
Patent Status: U.S. Provisional Application No. 60/981,661 filed 22
Oct 2007 (HHS Reference No. E-282-2007/0-US-01)
Licensing Status: Available for exclusive or non-exclusive
licensing.
Licensing Contact: Jennifer Wong; 301-435-4633;
wongje@mail.nih.gov.
Collaborative Research Opportunity: The National Cancer Institute,
Center for Cancer Research, Laboratory of Experimental Carcinogenesis
is seeking statements of capability or interest from parties interested
in collaborative research to further develop, evaluate, or
commercialize a novel temporal TGF-beta gene expression signature that
predicts HCC patient clinical outcomes. Please contact John D. Hewes,
PhD at 301-435-3121 or hewesj@mail.nih.gov for more information.
A New Pot1 Variant Gene as a Diagnostic Biomarker for Hereditary Non-
polyposis Colorectal Cancer
Description of Technology: The diagnosis of Hereditary Nonpolyposis
Colorectal Cancer (HNPCC) is difficult because the disease lacks
phenotypic signs that might facilitate its presymptomatic diagnosis.
This invention is based on the identification of a new splice variant
of a gene that appears to exist specifically in HNPCC, namely ``Pot1''
or ``Protection of Telomeres.'' Pot1 has a critical role in ensuring
chromosome stability by binding to telomeres. The invention presents a
variant of Pot1 that is present in mismatch repair-deficient, but not
proficient, cancer cell lines and primary, non-tumor tissue samples.
The presence of this variant may be useful both as a diagnostic marker
for HNPCC, and as a new therapeutic target for the treatment of HNPCC.
Applications and Modality: Identification of new ``Pot1'' variant
gene associated with HNPCC
New gene can be used as a potential diagnostic biomarker for the
diagnosis of HNPCC.
Pot1 as a new therapeutic target for the treatment of HNPCC.
Development Status: The technology is currently in the pre-clinical
stage of development.
Inventors: Qin Yang and Curtis C. Harris (NCI).
Related Publications:
1. P Baumann et al. Human Pot1 (protection of telomeres) protein:
cytolocalization, gene structure, and alternative splicing. Mol Cell
Biol. 2002 Nov;22(22):8079-8087.
2. A Umar et al. Revised Bethesda Guidelines for hereditary
nonpolyposis colorectal cancer (Lynch syndrome) and microsatellite
instability. J Natl Cancer Inst. 2004 Feb 18;96(4):261-268.
3. HT Lynch et al. Hereditary nonpolyposis colorectal carcinoma
(HNPCC) and HNPCC-like families: Problems in diagnosis, surveillance,
and management. Cancer. 2004 Jan 1;100(1):53-64.
4. Q Yang et al. Functional diversity of human protection of
telomeres 1 isoforms in telomere protection and cellular senescence.
Cancer Res. 2007 Dec 15;67(24):11677-11686.
Patent Status: U.S. Provisional Application No. 60/620,754 filed 20
Oct 2004 (HHS Reference No. E-263-2004/0-US-01), entitled ``POT1
Alternating Splice Variants''
International Patent Application No. PCT/US2005/037957 filed 19 Oct
2005, which published as WO 2006/045062 on 27 Apr 2006 (HHS Reference
No. E-263-2004/0-PCT-02)
U.S. Patent Application No. 11/665,944 filed 20 Apr 2007 (HHS
Reference No. E-263-2004/0-US-03).
Licensing Status: Available for exclusive and non-exclusive
licensing.
Licensing Contact: Surekha Vathyam, PhD; 301-435-4076;
vathyams@mail.nih.gov.
Collaborative Research Opportunity: The National Cancer Institute
Laboratory of Human Carcinogenesis is seeking statements of capability
or interest from parties interested in collaborative research to
further develop, evaluate, or commercialize biomarkers of colon cancer.
Please contact John D. Hewes, PhD at 301-435-3121 or
hewesj@mail.nih.gov for more information.
Dated: June 30, 2008.
Richard U. Rodriguez,
Director, Division of Technology Development and Transfer, Office of
Technology Transfer, National Institutes of Health.
[FR Doc. E8-15562 Filed 7-8-08; 8:45 am]
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