Government-Owned Inventions; Availability for Licensing, 66104-66106 [2010-27179]
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66104
Federal Register / Vol. 75, No. 207 / Wednesday, October 27, 2010 / Notices
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
Food and Drug Administration
Food and Drug Administration
[Docket No. FDA–2010–N–0121]
[Docket No. FDA–2009–N–0163]
Agency Information Collection
Activities; Announcement of Office of
Management and Budget Approval;
Draft Guidance, Emergency Use
Authorization of Medical Products
AGENCY:
Food and Drug Administration,
HHS.
ACTION:
AGENCY:
Food and Drug Administration,
HHS.
ACTION:
Notice.
The Food and Drug
Administration (FDA) is announcing
that a collection of information entitled
‘‘The Mammography Quality Standards
Act Requirements’’ has been approved
by the Office of Management and
Budget (OMB) under the Paperwork
Reduction Act of 1995.
FOR FURTHER INFORMATION CONTACT:
Daniel Gittleson, Office of Information
Management, Food and Drug
Administration, 1350 Piccard Dr., PI50–
400B, Rockville, MD 20850, 301–796–
5156, e-mail:
Daniel.Gittleson@fda.hhs.gov.
SUPPLEMENTARY INFORMATION: In the
Federal Register of June 15, 2010 (75 FR
33811), the Agency announced that the
proposed information collection had
been submitted to OMB for review and
clearance under 44 U.S.C. 3507. An
Agency may not conduct or sponsor,
and a person is not required to respond
to, a collection of information unless it
displays a currently valid OMB control
number. OMB has now approved the
information collection and has assigned
OMB control number 0910–0309. The
approval expires on October 31, 2013. A
copy of the supporting statement for this
information collection is available on
the Internet at https://www.reginfo.gov/
public/do/PRAMain.
SUMMARY:
Notice.
The Food and Drug
Administration (FDA) is announcing
that a collection of information entitled
‘‘Draft Guidance, Emergency Use
Authorization of Medical Products’’ has
been approved by the Office of
Management and Budget (OMB) under
the Paperwork Reduction Act of 1995.
SUMMARY:
FOR FURTHER INFORMATION CONTACT:
Jonna Capezzuto, Office of Information
Management, Food and Drug
Administration, 1350 Piccard Dr., PI50–
400B, Rockville, MD 20850, 301–796–
3794, e-mail:
Jonnalynn.capezzuto@fda.hhs.gov.
In the
Federal Register of October 6, 2009 (74
FR 51285), the Agency announced that
the proposed information collection had
been submitted to OMB for review and
clearance under 44 U.S.C. 3507. An
Agency may not conduct or sponsor,
and a person is not required to respond
to, a collection of information unless it
displays a currently valid OMB control
number. OMB has now approved the
information collection and has assigned
OMB control number 0910–0595. The
approval expires on January 31, 2013. A
copy of the supporting statement for this
information collection is available on
the Internet at https://www.reginfo.gov/
public/do/PRAMain.
SUPPLEMENTARY INFORMATION:
Dated: October 21, 2010.
Leslie Kux,
Acting Assistant Commissioner for Policy.
[FR Doc. 2010–27160 Filed 10–26–10; 8:45 am]
BILLING CODE 4160–01–P
srobinson on DSKHWCL6B1PROD with NOTICES
Agency Information Collection
Activities; Announcement of Office of
Management and Budget Approval;
The Mammography Quality Standards
Act Requirements
Dated: October 21, 2010.
Leslie Kux,
Acting Assistant Commissioner for Policy.
[FR Doc. 2010–27159 Filed 10–26–10; 8:45 am]
BILLING CODE 4160–01–P
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:
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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.
SUMMARY:
Immunotoxin for the Treatment of
Neuroblastoma Relapse
Description of Technology:
Immunotoxins are proteins which have
two distinct domains: (1) An antibody
or antibody binding fragment which is
capable of recognizing a single specific
cell surface protein and (2) a toxin
domain which is capable of inducing
cell death. Immunotoxins are currently
being pursued as therapeutics because
they specifically kill diseased cells
while leaving essential, healthy cells
alone. This increases the effectiveness of
the therapy while reducing the
appearance of side-effects. A particular
immunotoxin that is being studied in
clinical trials consists of an anti-CD22
antibody binding fragment and a
mutated Pseudomonas exotoxin A.
Although this immunotoxin is being
explored primarily as a treatment for
hematological malignancies, it can be
used to treat any condition where CD22
is overexpressed on the cell membrane
of diseased cells.
Neuroblastomas are malignant cancers
that start in nerve tissue and primarily
affect infants and children. Although
frontline treatments for neuroblastoma
are often effective, relapse frequently
occurs in high risk cases. The most
common form of relapse in
neuroblastoma patients is caused by
Neuroblastoma tumor initiating cells
(NB–TIC). Therefore, if NB–TIC could
be eliminated, high risk neuroblastoma
patients could have a therapeutic option
for preventing a relapse.
This invention concerns the discovery
that NB–TIC expresses CD22. As a
result, NB–TIC are susceptible to
treatment with an anti-CD22
immunotoxin. By combining frontline
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srobinson on DSKHWCL6B1PROD with NOTICES
Federal Register / Vol. 75, No. 207 / Wednesday, October 27, 2010 / Notices
neuroblastoma treatments with antiCD22 immunotoxins, both the primary
neuroblastoma and cells capable of
initiating a relapse can be eliminated.
As a result, even high risk
neuroblastoma patients should have an
increased chance of surviving
neuroblastoma.
Application: Treatment and
prevention of neuroblastoma relapse.
Advantages:
• Increased therapeutic effectiveness
with decreased non-specific killing of
essential, healthy cells.
• Neuroblastoma relapse commonly
begins in the bone marrow, an
environment which is accessible to
immunotoxins.
• Combined treatment addresses both
the tumor and the cause of relapse,
leading to more efficient treatments than
frontline therapeutics alone.
Development Status: Preclinical stage
of development for treatment of
neuroblastoma relapse; immunotoxins
have clinical data associated with
treatment of hematological
malignancies.
Inventors: Thiele (NCI) et al.
Patent Status: U.S. provisional
application 61/356,202 (E–204–2010/0–
US–01).
For more information, see:
• U.S. Patent 7,355,012—‘‘Mutated
Anti-CD22 Antibodies with Increased
Affinity to CD22—Expressing Leukemia
Cells’’.
• PCT Patent Application WO 2007/
016150—‘‘Mutated Pseudomonas
Exotoxins with Reduced Antigenicity’’.
• PCT Patent Application WO 2009/
032954—‘‘Deletions in Domain II of
Pseudomonas Exotoxin A That Reduce
Non-Specific Toxicity’’.
Licensing Status: Available for
licensing.
Licensing Contact: David A.
Lambertson, PhD; 301–435–4632;
lambertsond@mail.nih.gov.
Collaborative Research Opportunity:
The Center for Cancer Research,
Pediatric Oncology Branch and
Laboratory of Molecular Biology, is
seeking statements of capability or
interest from parties interested in
collaborative research to further
develop, evaluate, or commercialize
recombinant anti-CD22 immunotoxins
for the treatment of neuroblastoma.
Please contact John Hewes, Ph.D. at
301–435–3121 or hewesj@mail.nih.gov
for more information.
Mouse Model of Thyroid Cancer
Description of Technology: This
technology describes a mouse model of
thyroid cancer where the phosphatidylinositol 3-kinase (PI3K)–AKT/protein
kinase B-signaling pathway is
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overactivated. These mice have a knockin dominantly negative mutant thyroid
hormone receptor b gene (TRbPV
mutant) that spontaneously develops
thyroid cancer and distant metastasis
similar to human follicular thyroid
cancer. The thyroids of TRbPV mice
exhibit extensive hyperplasia, which
progresses to capsular invasion,
vascular invasion, anaplasia, and
ultimately, metastasis to distant organs.
Consequently, this mouse model could
be used as a preclinical model to
understand genetic changes during
cancer development and to identify
potential molecular targets for the
diagnosis, prevention, and treatment of
cancer. For example, the inventors have
used the TRbPV mice to show that the
peroxisome proliferator-activated
receptor g (PPARg) could function as a
tumor suppressor in vivo and that the
activation of the PI3K–AKT signaling
contributes to thyroid carcinogenesis
and could be a potential therapeutic
target in follicular thyroid carcinoma.
Applications:
• Identifying potential molecular
targets for cancer diagnosis, prevention,
and treatment.
• Testing kinase inhibitors and other
novel drugs being discovered for the
treatment of thyroid cancer.
• Tools to understand the genetic
changes during cancer development.
Advantages: This model provides the
opportunity to study the alterations in
gene regulation that occur during the
progression and metastasis of thyroid
carcinogenesis, not just the genes that
control initial carcinogenesis.
Development Status: The technology
is currently in the pre-clinical stage of
development.
Inventors: Sheue-yann Cheng (NCI).
Patent Status: HHS Reference No. E–
208–2009/0—Research Tool. Patent
protection is not being pursued for this
technology.
Publications:
1. Furuya F, Lu C, Willingham MC,
Cheng SY. Inhibition of
phosphatidylinositol 3-kinase delays
tumor progression and blocks metastatic
spread in a mouse model of thyroid
cancer. Carcinogenesis. 2007
Dec;28(12):2451–2458. [PubMed:
17660507]
2. Kato Y, Ying H, Zhao L, Furuya F,
Araki O, Willingham MC, Cheng SY.
PPARgamma insufficiency promotes
follicular thyroid carcinogenesis via
activation of the nuclear factor-kappaB
signaling pathway. Oncogene. 2006 May
4;25(19):2736–2747. [PubMed:
16314832]
3. Suzuki H, Willingham MC, Cheng
SY. Mice with a mutation in the thyroid
hormone receptor beta gene
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spontaneously develop thyroid
carcinoma: a mouse model of thyroid
carcinogenesis. Thyroid. 2002
Nov;12(11):963–969. [PubMed:
12490073]
4. Kaneshige M, Kaneshige K, Zhu X,
Dace A, Garrett L, Carter TA,
Kazlauskaite R, Pankratz DG, WynshawBoris A, Refetoff S, Weintraub B,
Willingham MC, Barlow C, Cheng S.
Mice with a targeted mutation in the
thyroid hormone beta receptor gene
exhibit impaired growth and resistance
to thyroid hormone. Proc Natl Acad Sci
U S A. 2000 Nov 21;97(24):13209–
13214. [PubMed: 11069286]
Licensing Status: Available for
licensing.
Licensing Contact: Whitney A.
Hastings; 301–451–7337;
hastingw@mail.nih.gov.
Chemokine-Tumor Antigen Fusion
Proteins as Cancer Vaccines
Description of Technology: Available
for licensing is a tumor vaccine
construct comprising a chemoattractant
(such as human chemokines CCL7 and
CCL20) fused to a tumor antigen
(including human mucin-1, a
transmembrane protein that is
aberrantly expressed in cancer; or single
chain antibody expressed by B cell
malignancy, or melanoma antigen gp100
expressed in human melanomas). The
majority of tumor antigens are believed
to be poorly immunogenic because they
represent oncogene gene products or
other cellular genes which are normally
present in the host. As a result, poor
immunogenicity has been a major
obstacle to successful immunotherapy
with tumor vaccines. Administration of
this fusion chemokine and tumor
antigen protein, or a nucleic acid
encoding this fusion protein, elicits a
tumor specific cellular and humoral
immune response thereby providing a
potent cancer vaccine.
Applications: Cancer immunotherapy.
Development Status: Proof of the
concept and pre-clinical development
have been successfully completed.
Market: The global cancer market is
forecasted to reach US$40 billion by
2012. Cancer vaccine research is coming
to fruition, with a number of products
now in Phase III trials and 15
therapeutic cancer vaccines realistically
expected to launch by 2013. The
therapeutic vaccine market has the
potential to mirror the growth seen in
the monoclonal antibody market, and
reach sales in excess of US$5 billion by
2012.
Inventors: Larry Kwak (NCI) and Arya
Biragyn (NIA) (both NCI at time of
invention).
Related Publications:
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66106
Federal Register / Vol. 75, No. 207 / Wednesday, October 27, 2010 / Notices
1. Coscia M, Biragyn A. Cancer
immunotherapy with chemoattractant
peptides. Semin Cancer Biol. 2004
Jun;14(3):209–218. [PubMed: 15246057].
2. Biragyn A, Belyakov IM, Chow YH,
Dimitrov DS, Berzofsky JA, Kwak LW.
DNA vaccines encoding human
immunodeficiency virus-1 glycoprotein
120 fusions with proinflammatory
chemoattractants induce systemic and
mucosal immune responses. Blood.
2002 Aug 15;100(4):1153–1159.
[PubMed: 12149191].
3. Schiavo R, Baatar D, Olkhanud P,
Indig FE, Restifo N, Taub D, Biragyn A.
Chemokine receptor targeting efficiently
directs antigens to MHC class I
pathways and elicits antigen-specific
CD8+ T-cell responses. Blood. 2006 Jun
15;107(12):4597–4605. [PubMed:
16514063].
4. Biragyn A, Ruffini PA, Coscia M,
Harvey LK, Neelapu SS, Baskar S, Wang
JM, Kwak LW. Chemokine receptormediated delivery directs self-tumor
antigen efficiently into the class II
processing pathway in vitro and induces
protective immunity in vivo. Blood.
2004 Oct 1;104(7):1961–1969. [PubMed:
15191951].
5. Qin H, Nehete PN, He H, Nehete B,
Buchl S, Cha SC, Sastry JK, Kwak LW.
Prime-boost vaccination using
chemokine-fused gp120 DNA and HIV
envelope peptides activates both
immediate and long-term memory
cellular responses in rhesus macaques.
J Biomed Biotechnol. 2010;2010:860160.
[PubMed: 20454526].
6. Qin H, Cha SC, Neelapu SS, Lou Y,
Wei J, Liu YJ, Kwak LW. Vaccine site
inflammation potentiates idiotype DNA
vaccine-induced therapeutic T cell-, and
not B cell-, dependent antilymphoma
immunity. Blood. 2009 Nov
5;114(19):4142–4149. [PubMed:
19749091].
7. Singh A, Nie H, Ghosn B, Qin H,
Kwak LW, Roy K. Efficient modulation
of T-cell response by dual-mode, singlecarrier delivery of cytokine-targeted
siRNA and DNA vaccine to antigenpresenting cells. Mol Ther. 2008
Dec;16(12):2011–2021. [PubMed:
18813280].
Patent Status: U.S. Patent No.
6,562,347 issued 13 May 2003 (HHS
Reference No. E–107–1998/0–US–03).
Licensing Contact: Patrick McCue,
PhD; 301–435–5560;
mccuepat@mail.nih.gov.
Collaborative Research Opportunity:
The National Institute on Aging,
Laboratory of Immunology, is seeking
statements of capability or interest from
parties interested in collaborative
research to further develop, evaluate, or
commercialize cancer vaccines that
target skin antigen-resenting cells.
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Please contact Nicole Guyton at 301–
435–3101 or guytonn@mail.nih.gov for
more information.
Dated: October 21, 2010.
Richard U. Rodriguez,
Director, Division of Technology Development
and Transfer, Office of Technology Transfer,
National Institutes of Health.
[FR Doc. 2010–27179 Filed 10–26–10; 8:45 am]
BILLING CODE 4140–01–P
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:
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.
SUMMARY:
IL–10 and IFNg Peptide Inhibitors
Description of Invention: Available for
licensing are several potent and
selective inhibitors of IL–10 and IFN-g
signaling. Although cytokines play
important roles in cancer and
inflammation, there are no specific
inhibitors of any cytokines to date. IL–
10 and IFN-g cytokine signaling play
crucial roles in inflammation, cancer
growth, and autoimmune diseases. The
investigators have developed short
peptides that potently and selectively
interfere with dimerization of the
cytokines and their binding to the
corresponding receptor. Included in the
patent application are also metabolically
stable lipopeptides mimicking
conserved regions of IL–10 and IFN-g
receptors that interfere with STAT3 and
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STAT1 phosphorylation and subsequent
signaling. Lipopeptides potently inhibit
STAT3 and STAT1-dependent growth
of cancer cells. These compounds are
promising drug candidates for the
treatment of cancer and many infectious
and inflammatory diseases.
Application: Cancer, viral infections
and anti-inflammatory treatments.
Advantages:
• Potent, stable peptide inhibitors.
• Selective IL–10 and IFN-g
inhibitors.
Development Status: The technology
is currently in the pre-clinical stage of
development.
Market: The annual growth rate for
the therapeutic peptide market is
estimated at about 7.5%.
Inventors: Nadya Tarasova et al.
(NCI).
Patent Status: U.S. Provisional
Application No. 61/333,512 filed 11
May 2010 (HHS Reference No. E–167–
2010/0–US–01).
Licensing Status: Available for
licensing.
Licensing Contact: Jennifer Wong;
301–435–4633; wongje@mail.nih.gov.
Collaborative Research Opportunity:
The Center for Cancer Research, Cancer
and Inflammation Program, is seeking
statements of capability or interest from
parties interested in collaborative
research to further develop, evaluate, or
commercialize inhibitors of IL10, IFNg
and STAT3 signaling. Please contact
John Hewes, Ph.D. at 301–435–3121 or
hewesj@mail.nih.gov for more
information.
Diagnostic and Prognostic HCC-Related
Metabolites
Description of Invention: Metabolite
profiling identifies and measures
changes in cellular metabolites as a
means to determine a direct correlation
between gene expression and changes in
biological function. Investigators at the
National Cancer Institute have
identified a unique set of metabolite
biomarkers associated with
hepatocellular carcinoma (HCC), early
stage HCC, HCC patient outcome and
HCC stem-cell subtype. Subsets of this
metabolite/gene signature can
distinguish HCC tumors from normal
tissues with 88–97% accuracy, identify
early stage HCC patients with 62–78%
accuracy, wherein early stage is defined
as TNM stage I, prognose negative
patient outcome, and identify a HCC
stem cell subtype with 70–77%
accuracy. These metabolites and gene
surrogates are elements of the PI3K and
Myc signaling networks which can
potentially be targeted for therapeutic
purposes.
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]]>Agencies
[Federal Register Volume 75, Number 207 (Wednesday, October 27, 2010)]
[Notices]
[Pages 66104-66106]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: 2010-27179]
-----------------------------------------------------------------------
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.
Immunotoxin for the Treatment of Neuroblastoma Relapse
Description of Technology: Immunotoxins are proteins which have two
distinct domains: (1) An antibody or antibody binding fragment which is
capable of recognizing a single specific cell surface protein and (2) a
toxin domain which is capable of inducing cell death. Immunotoxins are
currently being pursued as therapeutics because they specifically kill
diseased cells while leaving essential, healthy cells alone. This
increases the effectiveness of the therapy while reducing the
appearance of side-effects. A particular immunotoxin that is being
studied in clinical trials consists of an anti-CD22 antibody binding
fragment and a mutated Pseudomonas exotoxin A. Although this
immunotoxin is being explored primarily as a treatment for
hematological malignancies, it can be used to treat any condition where
CD22 is overexpressed on the cell membrane of diseased cells.
Neuroblastomas are malignant cancers that start in nerve tissue and
primarily affect infants and children. Although frontline treatments
for neuroblastoma are often effective, relapse frequently occurs in
high risk cases. The most common form of relapse in neuroblastoma
patients is caused by Neuroblastoma tumor initiating cells (NB-TIC).
Therefore, if NB-TIC could be eliminated, high risk neuroblastoma
patients could have a therapeutic option for preventing a relapse.
This invention concerns the discovery that NB-TIC expresses CD22.
As a result, NB-TIC are susceptible to treatment with an anti-CD22
immunotoxin. By combining frontline
[[Page 66105]]
neuroblastoma treatments with anti-CD22 immunotoxins, both the primary
neuroblastoma and cells capable of initiating a relapse can be
eliminated. As a result, even high risk neuroblastoma patients should
have an increased chance of surviving neuroblastoma.
Application: Treatment and prevention of neuroblastoma relapse.
Advantages:
Increased therapeutic effectiveness with decreased non-
specific killing of essential, healthy cells.
Neuroblastoma relapse commonly begins in the bone marrow,
an environment which is accessible to immunotoxins.
Combined treatment addresses both the tumor and the cause
of relapse, leading to more efficient treatments than frontline
therapeutics alone.
Development Status: Preclinical stage of development for treatment
of neuroblastoma relapse; immunotoxins have clinical data associated
with treatment of hematological malignancies.
Inventors: Thiele (NCI) et al.
Patent Status: U.S. provisional application 61/356,202 (E-204-2010/
0-US-01).
For more information, see:
U.S. Patent 7,355,012--``Mutated Anti-CD22 Antibodies with
Increased Affinity to CD22--Expressing Leukemia Cells''.
PCT Patent Application WO 2007/016150--``Mutated
Pseudomonas Exotoxins with Reduced Antigenicity''.
PCT Patent Application WO 2009/032954--``Deletions in
Domain II of Pseudomonas Exotoxin A That Reduce Non-Specific
Toxicity''.
Licensing Status: Available for licensing.
Licensing Contact: David A. Lambertson, PhD; 301-435-4632;
lambertsond@mail.nih.gov.
Collaborative Research Opportunity: The Center for Cancer Research,
Pediatric Oncology Branch and Laboratory of Molecular Biology, is
seeking statements of capability or interest from parties interested in
collaborative research to further develop, evaluate, or commercialize
recombinant anti-CD22 immunotoxins for the treatment of neuroblastoma.
Please contact John Hewes, Ph.D. at 301-435-3121 or hewesj@mail.nih.gov
for more information.
Mouse Model of Thyroid Cancer
Description of Technology: This technology describes a mouse model
of thyroid cancer where the phosphatidy-linositol 3-kinase (PI3K)-AKT/
protein kinase B-signaling pathway is overactivated. These mice have a
knock-in dominantly negative mutant thyroid hormone receptor [beta]
gene (TR[beta]PV mutant) that spontaneously develops thyroid cancer and
distant metastasis similar to human follicular thyroid cancer. The
thyroids of TR[beta]PV mice exhibit extensive hyperplasia, which
progresses to capsular invasion, vascular invasion, anaplasia, and
ultimately, metastasis to distant organs. Consequently, this mouse
model could be used as a preclinical model to understand genetic
changes during cancer development and to identify potential molecular
targets for the diagnosis, prevention, and treatment of cancer. For
example, the inventors have used the TR[beta]PV mice to show that the
peroxisome proliferator-activated receptor [gamma] (PPAR[gamma]) could
function as a tumor suppressor in vivo and that the activation of the
PI3K-AKT signaling contributes to thyroid carcinogenesis and could be a
potential therapeutic target in follicular thyroid carcinoma.
Applications:
Identifying potential molecular targets for cancer
diagnosis, prevention, and treatment.
Testing kinase inhibitors and other novel drugs being
discovered for the treatment of thyroid cancer.
Tools to understand the genetic changes during cancer
development.
Advantages: This model provides the opportunity to study the
alterations in gene regulation that occur during the progression and
metastasis of thyroid carcinogenesis, not just the genes that control
initial carcinogenesis.
Development Status: The technology is currently in the pre-clinical
stage of development.
Inventors: Sheue-yann Cheng (NCI).
Patent Status: HHS Reference No. E-208-2009/0--Research Tool.
Patent protection is not being pursued for this technology.
Publications:
1. Furuya F, Lu C, Willingham MC, Cheng SY. Inhibition of
phosphatidylinositol 3-kinase delays tumor progression and blocks
metastatic spread in a mouse model of thyroid cancer. Carcinogenesis.
2007 Dec;28(12):2451-2458. [PubMed: 17660507]
2. Kato Y, Ying H, Zhao L, Furuya F, Araki O, Willingham MC, Cheng
SY. PPARgamma insufficiency promotes follicular thyroid carcinogenesis
via activation of the nuclear factor-kappaB signaling pathway.
Oncogene. 2006 May 4;25(19):2736-2747. [PubMed: 16314832]
3. Suzuki H, Willingham MC, Cheng SY. Mice with a mutation in the
thyroid hormone receptor beta gene spontaneously develop thyroid
carcinoma: a mouse model of thyroid carcinogenesis. Thyroid. 2002
Nov;12(11):963-969. [PubMed: 12490073]
4. Kaneshige M, Kaneshige K, Zhu X, Dace A, Garrett L, Carter TA,
Kazlauskaite R, Pankratz DG, Wynshaw-Boris A, Refetoff S, Weintraub B,
Willingham MC, Barlow C, Cheng S. Mice with a targeted mutation in the
thyroid hormone beta receptor gene exhibit impaired growth and
resistance to thyroid hormone. Proc Natl Acad Sci U S A. 2000 Nov
21;97(24):13209-13214. [PubMed: 11069286]
Licensing Status: Available for licensing.
Licensing Contact: Whitney A. Hastings; 301-451-7337;
hastingw@mail.nih.gov.
Chemokine-Tumor Antigen Fusion Proteins as Cancer Vaccines
Description of Technology: Available for licensing is a tumor
vaccine construct comprising a chemoattractant (such as human
chemokines CCL7 and CCL20) fused to a tumor antigen (including human
mucin-1, a transmembrane protein that is aberrantly expressed in
cancer; or single chain antibody expressed by B cell malignancy, or
melanoma antigen gp100 expressed in human melanomas). The majority of
tumor antigens are believed to be poorly immunogenic because they
represent oncogene gene products or other cellular genes which are
normally present in the host. As a result, poor immunogenicity has been
a major obstacle to successful immunotherapy with tumor vaccines.
Administration of this fusion chemokine and tumor antigen protein, or a
nucleic acid encoding this fusion protein, elicits a tumor specific
cellular and humoral immune response thereby providing a potent cancer
vaccine.
Applications: Cancer immunotherapy.
Development Status: Proof of the concept and pre-clinical
development have been successfully completed.
Market: The global cancer market is forecasted to reach US$40
billion by 2012. Cancer vaccine research is coming to fruition, with a
number of products now in Phase III trials and 15 therapeutic cancer
vaccines realistically expected to launch by 2013. The therapeutic
vaccine market has the potential to mirror the growth seen in the
monoclonal antibody market, and reach sales in excess of US$5 billion
by 2012.
Inventors: Larry Kwak (NCI) and Arya Biragyn (NIA) (both NCI at
time of invention).
Related Publications:
[[Page 66106]]
1. Coscia M, Biragyn A. Cancer immunotherapy with chemoattractant
peptides. Semin Cancer Biol. 2004 Jun;14(3):209-218. [PubMed:
15246057].
2. Biragyn A, Belyakov IM, Chow YH, Dimitrov DS, Berzofsky JA, Kwak
LW. DNA vaccines encoding human immunodeficiency virus-1 glycoprotein
120 fusions with proinflammatory chemoattractants induce systemic and
mucosal immune responses. Blood. 2002 Aug 15;100(4):1153-1159. [PubMed:
12149191].
3. Schiavo R, Baatar D, Olkhanud P, Indig FE, Restifo N, Taub D,
Biragyn A. Chemokine receptor targeting efficiently directs antigens to
MHC class I pathways and elicits antigen-specific CD8+ T-cell
responses. Blood. 2006 Jun 15;107(12):4597-4605. [PubMed: 16514063].
4. Biragyn A, Ruffini PA, Coscia M, Harvey LK, Neelapu SS, Baskar
S, Wang JM, Kwak LW. Chemokine receptor-mediated delivery directs self-
tumor antigen efficiently into the class II processing pathway in vitro
and induces protective immunity in vivo. Blood. 2004 Oct 1;104(7):1961-
1969. [PubMed: 15191951].
5. Qin H, Nehete PN, He H, Nehete B, Buchl S, Cha SC, Sastry JK,
Kwak LW. Prime-boost vaccination using chemokine-fused gp120 DNA and
HIV envelope peptides activates both immediate and long-term memory
cellular responses in rhesus macaques. J Biomed Biotechnol.
2010;2010:860160. [PubMed: 20454526].
6. Qin H, Cha SC, Neelapu SS, Lou Y, Wei J, Liu YJ, Kwak LW.
Vaccine site inflammation potentiates idiotype DNA vaccine-induced
therapeutic T cell-, and not B cell-, dependent antilymphoma immunity.
Blood. 2009 Nov 5;114(19):4142-4149. [PubMed: 19749091].
7. Singh A, Nie H, Ghosn B, Qin H, Kwak LW, Roy K. Efficient
modulation of T-cell response by dual-mode, single-carrier delivery of
cytokine-targeted siRNA and DNA vaccine to antigen-presenting cells.
Mol Ther. 2008 Dec;16(12):2011-2021. [PubMed: 18813280].
Patent Status: U.S. Patent No. 6,562,347 issued 13 May 2003 (HHS
Reference No. E-107-1998/0-US-03).
Licensing Contact: Patrick McCue, PhD; 301-435-5560;
mccuepat@mail.nih.gov.
Collaborative Research Opportunity: The National Institute on
Aging, Laboratory of Immunology, is seeking statements of capability or
interest from parties interested in collaborative research to further
develop, evaluate, or commercialize cancer vaccines that target skin
antigen-resenting cells. Please contact Nicole Guyton at 301-435-3101
or guytonn@mail.nih.gov for more information.
Dated: October 21, 2010.
Richard U. Rodriguez,
Director, Division of Technology Development and Transfer, Office of
Technology Transfer, National Institutes of Health.
[FR Doc. 2010-27179 Filed 10-26-10; 8:45 am]
BILLING CODE 4140-01-P
