Government-Owned Inventions; Availability for Licensing, 12764-12766 [2010-5765]
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12764
Federal Register / Vol. 75, No. 51 / Wednesday, March 17, 2010 / Notices
• Used as single agents or in
combination with other anti-cancer
treatments like chemotherapy,
biological therapy, or radiation.
Advantages: Targeting the PH domain
improves specificity against Akt kinase
in comparison to inhibitors of the ATP
domain which typically are unspecific.
Inventors: Phillip A. Dennis (NCI) et
al.
wwoods2 on DSK1DXX6B1PROD with NOTICES_PART 1
Relevant Publications
1. Memmott RM, Gills JJ,
Hollingshead M, Powers MC, Chen Z,
Kemp B, Kozikowski A, Dennis PA.
Phosphatidylinositol ether lipid
analogues induce AMP-activated
protein kinase-dependent death in
LKB1-mutant non small cell lung cancer
cells. Cancer Res. 2008 Jan
15;68(2):580–588. [PubMed: 18199555.]
2. Gills JJ, Castillo SS, Zhang C,
Petukhov PA, Memmott RM,
Hollingshead M, Warfel N, Han J,
Kozikowski AP, Dennis PA.
Phosphatidylinositol ether lipid
analogues that inhibit AKT also
independently activate the stress kinase,
p38alpha, through MKK3/6independent and -dependent
mechanisms. J Biol Chem. 2007 Sep
14;282(37):27020–27029. [PubMed:
17631503.]
3. Gills JJ, Holbeck S, Hollingshead M,
Hewitt SM, Kozikowski AP, Dennis PA.
Spectrum of activity and molecular
correlates of response to
phosphatidylinositol ether lipid
analogues, novel lipid-based inhibitors
of Akt. Mol Cancer Ther. 2006
Mar;5(3):713–722. [PubMed: 16546986.]
´
4. Caron RW, Yacoub A, Li M, Zhu X,
Mitchell C, Hong Y, Hawkins W,
Sasazuki T, Shirasawa S, Kozikowski
AP, Dennis PA, Hagan MP, Grant S,
Dent P. Activated forms of H–RAS and
K–RAS differentially regulate membrane
association of PI3K, PDK–1, and AKT
and the effect of therapeutic kinase
inhibitors on cell survival. Mol Cancer
Ther. 2005 Feb;4(2):257–270. [PubMed:
15713897.]
5. Castillo SS, Brognard J, Petukhov
PA, Zhang C, Tsurutani J, Granville CA,
Li M, Jung M, West KA, Gills JG,
Kozikowski AP, Dennis PA. Preferential
inhibition of Akt and killing of Aktdependent cancer cells by rationally
designed phosphatidylinositol ether
lipid analogues. Cancer Res. 2004 Apr
15;64(8):2782–2792. [PubMed:
15087394.]
6. Kozikowski AP, Sun H, Brognard J,
Dennis PA. Novel PI analogues
selectively block activation of the prosurvival serine/threonine kinase Akt. J
Am Chem Soc. 2003 Feb 5;125(5):1144–
1145. [PubMed: 12553797.]
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15:08 Mar 16, 2010
Jkt 220001
Patent Status: U.S. Patent No.
7,378,403 issued 27 May 2008 (HHS
Reference No. E–245–2002/0–US–03),
and related international filings.
Licensing Status: Available for
licensing.
Licensing Contact: Surekha Vathyam,
PhD; 301–435–4076;
vathyams@mail.nih.gov.
Dated: March 10, 2010.
Richard U. Rodriguez,
Director, Division of Technology Development
and Transfer, Office of Technology Transfer,
National Institutes of Health.
[FR Doc. 2010–5764 Filed 3–16–10; 8:45 am]
BILLING CODE 4140–01–P
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
National Institutes of Health
Government-Owned Inventions;
Availability for Licensing
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.
Spontaneously Transformed Mouse
Epithelial Cancer Cell Lines Serving as
Mouse Models: A New Model for
Cancer Research
Description of Invention: Investigators
at the NIH have created a collection of
45 mouse epithelial cancer cell lines
derived from six organs: Bladder, cervix,
colon, lung, kidney, and mammary
glands. These cells lines were obtained
from spontaneously transformed
primary cell cultures without genetic,
viral or chemical manipulation so they
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can serve as mouse models for studying
the natural process of oncogenesis.
The cell lines were characterized
cytogenetically during their
transformation from normal to
spontaneously immortalization and
were found to recapitulate many of the
changes observed in human cancer cells
such as the deregulation of oncogenes
(Myc, Mdm2) and tumor suppressor
genes (Cdnk4a/Ink4a/p16, Rb).
Carcinomas that arise from the
epithelial cells lining organs lead to the
most common cancers in humans.
However, research on cellular
transformation has largely relied on
fibroblast cells which are not of
epithelial origin and therefore, may not
reflect the changes that lead to epithelial
oncogenesis. The availability of these
mouse epithelial cancer cell lines
should allow for a more accurate
analysis of this process.
Applications: These cell lines serve as
‘‘ideal’’ murine tumor models as they
show evidence of progression,
permitting analysis of the genetic and
biological changes observed in the
equivalent human carcinomas and
associated with tumor progression.
Their tumor histology is comparable to
human cancers.
The cell lines have unique properties
that make them suitable for study of the
following:
• Unlimited replicative potential.
• Exhibit tumorigenic potential and
EMT (Epithelial Mesencymal
Transition).
• Exhibit high degree of chromosome
instability (chromosome
rearrangements, amplifications) in
regions orthologous to those altered in
human cancers.
• Use in mapping mouse genes
homologous to human cancer genes and
for the study of the effects of
deregulation of cancer associated genes,
through silencing or overexpression.
• For use in gene expression studies
of tumor progression, comparing
profiles to human cancers involving the
same tissue types.
• Use as experimental controls in the
analysis of oncogene signaling
pathways.
• Use in the studying telomerase
pathway regulation (200-fold expression
difference between cell lines).
• Use of mouse as model of epithelial
carcinomas and specifically cancers of
the bladder, cervix, colon, lung,
mammarys and kidney cancers.
• These mouse models serve as
vehicles to test the efficacy of new
therapies, targeting specific targets
associated with the transformation of six
different mouse epithelial tissues.
E:\FR\FM\17MRN1.SGM
17MRN1
Federal Register / Vol. 75, No. 51 / Wednesday, March 17, 2010 / Notices
wwoods2 on DSK1DXX6B1PROD with NOTICES_PART 1
• Use for discovering drugs that alter
the tumorigenic potential, invasiveness,
and the Epithelial-Mesenchymal
Transition state.
Advantages:
• Cytogenetically defined epithelial
cell lines from mouse that model human
carcinomas.
• Spontaneously transformed primary
cell cultures were generated from
isogenic mouse strain that has a low
propensity for epithelial tumors in vivo
therefore, not involving other mouse
strains potentially influencing the
genetic background.
• These cell lines were generated
without viral, chemical or genetic
manipulation and thus can serve as
mouse models for studying the natural
process of oncogenesis and as mouse
models of human cancers.
• Genomically defined colon,
bladder, and kidney cell lines showing
oncogene deregulation (i.e. Mdm2 and
Myc overexpression).
Development Status:
• Ready for use.
• Pre-clinical.
Market: Cancer is the second most
common cause of death in the United
States. More than half a million
Americans are expected to die of cancer.
The cell lines will serve as a valuable
tool for cancer researchers.
Inventors: Hesed AM. Padilla-Nash et
al. (NCI).
Publications: None currently available
for this technology.
Patent Status: HHS Reference No. E–
089–2010/0—Research Material. Patent
protection is not being pursued for this
technology.
Licensing Status: Available for
licensing under a Biological Materials
License Agreement.
Licensing Contact: Sabarni Chatterjee,
PhD; 301–435–5587;
chatterjeesa@mail.nih.gov.
Collaborative Research Opportunity:
The National Cancer Institute, Cancer
Genetics Branch, is seeking statements
of capability or interest from parties
interested in collaborative research to
further develop, evaluate, or
commercialize this technology. Please
contact John Hewes, PhD at 301–435–
3131 or hewesj@mail.nih.gov for more
information.
Tumor Tissues Harboring Mutations in
cAMP-Specific Phosphodiesterases
Useful for the Study of Endocrine
Tumors
Description of Invention: Researchers
at the National Institute of Child Health
and Human Development (NICHD),
NIH, have made available samples of
patient-derived adrenal and heart
tumors that harbor genetic mutations
VerDate Nov<24>2008
15:08 Mar 16, 2010
Jkt 220001
that have been implicated in the
predisposition of endocrine tumors. An
endocrine tumor is a growth that affects
the parts of the body that secrete
hormones. Because an endocrine tumor
arises from cells that produce hormones,
the tumor itself can produce hormones
and cause serious illness.
The tumor samples made available
herein contain deletions in the cyclic
nucleotide phosphodiesterase (PDE)
PDE7A or PDE8B genes that impair PDE
function and are characterized by high
sensitivity to changes in cAMP levels.
Commercially, phosphodiesterase
inhibitors are widely used in the
treatment of various disorders,
including asthma, pulmonary
hypertension, and erectile dysfunction,
suggesting a potential utility for these
tissues in a wide range of investigations.
Applications: Useful in the
investigation of the mechanisms of
phosphodiesterase inhibition.
Inventors: Constantine Stratakis et al.
(NICHD).
Patent Status: HHS Reference No. E–
059–2010/0—Research Tool. Patent
protection is not being pursued for this
technology.
Licensing Status: Available for
licensing under a biological material
license.
Licensing Contact: Patrick P. McCue,
PhD; 301–435–5560;
mccuepat@mail.nih.gov.
Collaborative Research Opportunity:
The National Institute of Child Health
and Human Development, Division of
Intramural Research, is seeking
statements of capability or interest from
parties interested in collaborative
research. Please contact Joseph Conrad,
PhD at 301–435–3107 or
jmconrad@mail.nih.gov for more
information.
Akt-Ser473 Phosphorylation as a
Marker for Predicting Taxane
Chemotherapy Outcome
Description of Invention: Over the
past decades, taxanes such as paclitaxel
and docetaxel have emerged as effective
chemotherapy agents for breast cancer
and other malignancies. Taxanes are
effective in many patients, however, not
all patients benefit from this type of
chemotherapy. A significant need
remains for a means of predicting
clinical outcome from taxane-based
chemotherapy.
Akt, a serine/threonine kinase that
can block apoptosis, has been
implicated in the regulation of
microtubule dynamics and organization.
Akt phosphorylation and its transducing
downstream events play a central role in
cell survival and cell cycle progression
at the G2/M transition. Paclitaxel or
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12765
docetaxel inhibits Akt-Ser473
phosphorylation (pAkt) and induces
mitotic arrest. Therefore, taxanes may
cause more damage to tumor cells that
are dependent on pAkt for survival and
cell cycle progression, significantly
impacting treatment outcome.
Researchers at the National Cancer
Institute, NIH, have identified pAkt as
having predictive significance for
paclitaxel chemotherapy outcome in
patients with early stage breast cancer.
The researchers have developed an
immunohistochemistry method for
determining pAkt status with
appropriate controls for assay
performance and cutoff for pAkt
positivity. They also discovered
methods of correlating pAkt expression
with clinical outcome (disease-free
survival and overall survival). pAkt is a
novel predictive marker of taxane
chemotherapy, and can be applied to
indicate which patients should receive
taxane-based chemotherapy.
Applications: A Kit for identifying
pAkt-positive tumors in surgical tumor
specimens or tumor biopsies prior to
treatment (adjuvant, neoadjuvant
therapy or therapy for metastatic
disease); and methods for predicting
clinical outcome from taxane
chemotherapy.
Advantages: pAkt is a useful clinical
predictive marker to determine which
patients should or should not receive
taxane-based chemotherapy for cancer.
Determining pAkt status would allow
patients with pAkt-positive tumors to
elect taxane therapy for whom are likely
to benefit, and allow patients with pAktnegative tumors for whom are unlikely
to benefit to be spared from taxane
therapy as well as toxicity, and earlier
use of other therapies that could be
more effective. The application of this
invention may potentially reduce the
cost of cancer care.
Inventors: Sherry X. Yang et al. (NCI).
Related Publications:
1. Yang, SX, Costantino JP, Mamounas
EP, Nguyen D, Jeong J–H, Wolmark N,
Kim C, Kidwell K, Paik S, Swain SM.
Correlation of levels of Akt
phosphorylation at Ser473 with benefit
from paclitaxel chemotherapy in
NSABP B–28 patients with nodepositive breast cancer. J Clin Oncol.
2009 (May 20 Supplement);27(15S):537.
2. Yang SX, Costantino JP, Mamounas
EP, Nguyen D, Jeong J–H, Wolmark N,
Kim C, Kidwell K, Paik S, Swain SM.
Akt phosphorylation at Ser473 predicts
benefit to paclitaxel chemotherapy in
node-positive breast cancer. J Clin
Oncol. 2010, In Press.
Patent Status: U.S. Provisional
Application No. 61/180,558 filed 22
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17MRN1
12766
Federal Register / Vol. 75, No. 51 / Wednesday, March 17, 2010 / Notices
May 2009 (HHS Reference No. E–191–
2009/0–US–01).
Licensing Status: Available for
licensing.
Licensing Contact: Patrick P. McCue,
PhD; 301–496–7057;
mccuepat@mail.nih.gov.
Collaborative Research Opportunity:
The National Cancer Institute is seeking
statements of capability or interest from
parties interested in collaborative
research to further develop, evaluate, or
commercialize the pAkt assay for use in
a clinical setting. The National Cancer
Institute would be particularly
interested in discussing collaborations
to provide additional clinical validation
of pAkt as a primary biomarker. Please
contact John Hewes, PhD at 301–435–
3131 or hewesj@mail.nih.gov for more
information.
Dated: March 10, 2010.
Richard U. Rodriguez,
Director, Division of Technology Development
and Transfer, Office of Technology Transfer,
National Institutes of Health.
[FR Doc. 2010–5765 Filed 3–16–10; 8:45 am]
756, 6707 Democracy Boulevard, Bethesda,
MD 20892–5452, (301) 594–7682,
pateldg@niddk.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: National Institute of
Diabetes and Digestive and Kidney Diseases
Special Emphasis Panel; Translational
Research.
Date: May 20, 2010.
Time: 8 a.m. to 5 p.m.
Agenda: To review and evaluate grant
applications.
Place: Bethesda Marriott Suites, 6711
Democracy Boulevard, Bethesda, MD 20817.
Contact Person: Michele L. Barnard, PhD,
Scientific Review Officer, Review Branch,
DEA, NIDDK, National Institutes of Health,
Room 753, 6707 Democracy Boulevard,
Bethesda, MD 20892–2542, (301) 594–8898,
barnardm@extra.niddk.nih.gov.
(Catalogue of Federal Domestic Assistance
Program Nos. 93.847, Diabetes,
Endocrinology and Metabolic Research;
93.848, Digestive Diseases and Nutrition
Research; 93.849, Kidney Diseases, Urology
and Hematology Research, National Institutes
of Health, HHS)
Dated: March 10, 2010.
Jennifer Spaeth,
Director, Office of Federal Advisory
Committee Policy.
BILLING CODE 4140–01–P
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
[FR Doc. 2010–5768 Filed 3–16–10; 8:45 am]
BILLING CODE 4140–01–P
National Institutes of Health
Contact Person: Kenneth A. Roebuck, PhD,
Scientific Review Officer, Center for
Scientific Review, National Institutes of
Health, 6701 Rockledge Drive, Room 5106,
MSC 7852, Bethesda, MD 20892, (301) 435–
1166, roebuckk@csr.nih.gov.
Name of Committee: Center for Scientific
Review Special Emphasis Panel; Ethical,
Legal and Societal Implications of Genetic
Information.
Date: April 19, 2010.
Time: 12 p.m. to 1 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: Cheryl M. Corsaro, PhD,
Scientific Review Officer, Center for
Scientific Review, National Institutes of
Health, 6701 Rockledge Drive, Room 2204,
MSC 7890, Bethesda, MD 20892, (301) 435–
1045, corsaroc@csr.nih.gov.
(Catalogue of Federal Domestic Assistance
Program Nos. 93.306, Comparative Medicine;
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: March 10, 2010.
Jennifer Spaeth,
Director, Office of Federal Advisory
Committee Policy.
[FR Doc. 2010–5770 Filed 3–16–10; 8:45 am]
BILLING CODE 4140–01–P
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
Pursuant to section 10(d) of the
Federal Advisory Committee Act, as
amended (5 U.S.C. App.), 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.
wwoods2 on DSK1DXX6B1PROD with NOTICES_PART 1
National Institute of Diabetes and
Digestive and Kidney Diseases; Notice
of Closed Meetings
National Institutes of Health
National Institutes of Health
Center for Scientific Review; Notice of
Closed Meetings
National Center on Minority Health and
Health Disparities; Notice of Closed
Meetings
Name of Committee: National Institute of
Diabetes and Digestive and Kidney Diseases
Special Emphasis Panel; RO1 Review.
Date: April 6, 2010.
Time: 2 p.m. to 4 p.m.
Agenda: To review and evaluate grant
applications.
Place: National Institutes of Health, Two
Democracy Plaza, 6707 Democracy
Boulevard, Bethesda, MD 20892. (Telephone
Conference Call)
Contact Person: D.G. Patel, PhD, Scientific
Review Officer, Review Branch, DEA,
NIDDK, National Institutes of Health, Room
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Jkt 220001
Pursuant to section 10(d) of the
Federal Advisory Committee Act, as
amended (5 U.S.C. App.), 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.
Name of Committee: Center for Scientific
Review Special Emphasis Panel; Member
Conflict: AOIC & VACC.
Date: April 7–8, 2010.
Time: 8 a.m. to 5 p.m.
Agenda: To review and evaluate grant
applications.
Place: National Institutes of Health, 6701
Rockledge Drive, Bethesda, MD 20892.
(Virtual Meeting)
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Pursuant to section 10(d) of the
Federal Advisory Committee Act, as
amended (5 U.S.C. App.), 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.
Name of Committee: National Center on
Minority Health and Health Disparities
Special Emphasis Panel Loan Repayment
Program for Health Disparities Research—
Panel 2.
Date: April 5, 2010.
Time: 8 a.m. to 5 p.m.
Agenda: To review and evaluate grant
applications.
E:\FR\FM\17MRN1.SGM
17MRN1
]]>Agencies
[Federal Register Volume 75, Number 51 (Wednesday, March 17, 2010)]
[Notices]
[Pages 12764-12766]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: 2010-5765]
-----------------------------------------------------------------------
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.
Spontaneously Transformed Mouse Epithelial Cancer Cell Lines Serving as
Mouse Models: A New Model for Cancer Research
Description of Invention: Investigators at the NIH have created a
collection of 45 mouse epithelial cancer cell lines derived from six
organs: Bladder, cervix, colon, lung, kidney, and mammary glands. These
cells lines were obtained from spontaneously transformed primary cell
cultures without genetic, viral or chemical manipulation so they can
serve as mouse models for studying the natural process of oncogenesis.
The cell lines were characterized cytogenetically during their
transformation from normal to spontaneously immortalization and were
found to recapitulate many of the changes observed in human cancer
cells such as the deregulation of oncogenes (Myc, Mdm2) and tumor
suppressor genes (Cdnk4a/Ink4a/p16, Rb).
Carcinomas that arise from the epithelial cells lining organs lead
to the most common cancers in humans. However, research on cellular
transformation has largely relied on fibroblast cells which are not of
epithelial origin and therefore, may not reflect the changes that lead
to epithelial oncogenesis. The availability of these mouse epithelial
cancer cell lines should allow for a more accurate analysis of this
process.
Applications: These cell lines serve as ``ideal'' murine tumor
models as they show evidence of progression, permitting analysis of the
genetic and biological changes observed in the equivalent human
carcinomas and associated with tumor progression. Their tumor histology
is comparable to human cancers.
The cell lines have unique properties that make them suitable for
study of the following:
Unlimited replicative potential.
Exhibit tumorigenic potential and EMT (Epithelial
Mesencymal Transition).
Exhibit high degree of chromosome instability (chromosome
rearrangements, amplifications) in regions orthologous to those altered
in human cancers.
Use in mapping mouse genes homologous to human cancer
genes and for the study of the effects of deregulation of cancer
associated genes, through silencing or overexpression.
For use in gene expression studies of tumor progression,
comparing profiles to human cancers involving the same tissue types.
Use as experimental controls in the analysis of oncogene
signaling pathways.
Use in the studying telomerase pathway regulation (200-
fold expression difference between cell lines).
Use of mouse as model of epithelial carcinomas and
specifically cancers of the bladder, cervix, colon, lung, mammarys and
kidney cancers.
These mouse models serve as vehicles to test the efficacy
of new therapies, targeting specific targets associated with the
transformation of six different mouse epithelial tissues.
[[Page 12765]]
Use for discovering drugs that alter the tumorigenic
potential, invasiveness, and the Epithelial-Mesenchymal Transition
state.
Advantages:
Cytogenetically defined epithelial cell lines from mouse
that model human carcinomas.
Spontaneously transformed primary cell cultures were
generated from isogenic mouse strain that has a low propensity for
epithelial tumors in vivo therefore, not involving other mouse strains
potentially influencing the genetic background.
These cell lines were generated without viral, chemical or
genetic manipulation and thus can serve as mouse models for studying
the natural process of oncogenesis and as mouse models of human
cancers.
Genomically defined colon, bladder, and kidney cell lines
showing oncogene deregulation (i.e. Mdm2 and Myc overexpression).
Development Status:
Ready for use.
Pre-clinical.
Market: Cancer is the second most common cause of death in the
United States. More than half a million Americans are expected to die
of cancer. The cell lines will serve as a valuable tool for cancer
researchers.
Inventors: Hesed AM. Padilla-Nash et al. (NCI).
Publications: None currently available for this technology.
Patent Status: HHS Reference No. E-089-2010/0--Research Material.
Patent protection is not being pursued for this technology.
Licensing Status: Available for licensing under a Biological
Materials License Agreement.
Licensing Contact: Sabarni Chatterjee, PhD; 301-435-5587;
chatterjeesa@mail.nih.gov.
Collaborative Research Opportunity: The National Cancer Institute,
Cancer Genetics Branch, is seeking statements of capability or interest
from parties interested in collaborative research to further develop,
evaluate, or commercialize this technology. Please contact John Hewes,
PhD at 301-435-3131 or hewesj@mail.nih.gov for more information.
Tumor Tissues Harboring Mutations in cAMP-Specific Phosphodiesterases
Useful for the Study of Endocrine Tumors
Description of Invention: Researchers at the National Institute of
Child Health and Human Development (NICHD), NIH, have made available
samples of patient-derived adrenal and heart tumors that harbor genetic
mutations that have been implicated in the predisposition of endocrine
tumors. An endocrine tumor is a growth that affects the parts of the
body that secrete hormones. Because an endocrine tumor arises from
cells that produce hormones, the tumor itself can produce hormones and
cause serious illness.
The tumor samples made available herein contain deletions in the
cyclic nucleotide phosphodiesterase (PDE) PDE7A or PDE8B genes that
impair PDE function and are characterized by high sensitivity to
changes in cAMP levels. Commercially, phosphodiesterase inhibitors are
widely used in the treatment of various disorders, including asthma,
pulmonary hypertension, and erectile dysfunction, suggesting a
potential utility for these tissues in a wide range of investigations.
Applications: Useful in the investigation of the mechanisms of
phosphodiesterase inhibition.
Inventors: Constantine Stratakis et al. (NICHD).
Patent Status: HHS Reference No. E-059-2010/0--Research Tool.
Patent protection is not being pursued for this technology.
Licensing Status: Available for licensing under a biological
material license.
Licensing Contact: Patrick P. McCue, PhD; 301-435-5560;
mccuepat@mail.nih.gov.
Collaborative Research Opportunity: The National Institute of Child
Health and Human Development, Division of Intramural Research, is
seeking statements of capability or interest from parties interested in
collaborative research. Please contact Joseph Conrad, PhD at 301-435-
3107 or jmconrad@mail.nih.gov for more information.
Akt-Ser473 Phosphorylation as a Marker for Predicting Taxane
Chemotherapy Outcome
Description of Invention: Over the past decades, taxanes such as
paclitaxel and docetaxel have emerged as effective chemotherapy agents
for breast cancer and other malignancies. Taxanes are effective in many
patients, however, not all patients benefit from this type of
chemotherapy. A significant need remains for a means of predicting
clinical outcome from taxane-based chemotherapy.
Akt, a serine/threonine kinase that can block apoptosis, has been
implicated in the regulation of microtubule dynamics and organization.
Akt phosphorylation and its transducing downstream events play a
central role in cell survival and cell cycle progression at the
G2/M transition. Paclitaxel or docetaxel inhibits Akt-Ser473
phosphorylation (pAkt) and induces mitotic arrest. Therefore, taxanes
may cause more damage to tumor cells that are dependent on pAkt for
survival and cell cycle progression, significantly impacting treatment
outcome.
Researchers at the National Cancer Institute, NIH, have identified
pAkt as having predictive significance for paclitaxel chemotherapy
outcome in patients with early stage breast cancer. The researchers
have developed an immunohistochemistry method for determining pAkt
status with appropriate controls for assay performance and cutoff for
pAkt positivity. They also discovered methods of correlating pAkt
expression with clinical outcome (disease-free survival and overall
survival). pAkt is a novel predictive marker of taxane chemotherapy,
and can be applied to indicate which patients should receive taxane-
based chemotherapy.
Applications: A Kit for identifying pAkt-positive tumors in
surgical tumor specimens or tumor biopsies prior to treatment
(adjuvant, neoadjuvant therapy or therapy for metastatic disease); and
methods for predicting clinical outcome from taxane chemotherapy.
Advantages: pAkt is a useful clinical predictive marker to
determine which patients should or should not receive taxane-based
chemotherapy for cancer. Determining pAkt status would allow patients
with pAkt-positive tumors to elect taxane therapy for whom are likely
to benefit, and allow patients with pAkt-negative tumors for whom are
unlikely to benefit to be spared from taxane therapy as well as
toxicity, and earlier use of other therapies that could be more
effective. The application of this invention may potentially reduce the
cost of cancer care.
Inventors: Sherry X. Yang et al. (NCI).
Related Publications:
1. Yang, SX, Costantino JP, Mamounas EP, Nguyen D, Jeong J-H,
Wolmark N, Kim C, Kidwell K, Paik S, Swain SM. Correlation of levels of
Akt phosphorylation at Ser473 with benefit from paclitaxel chemotherapy
in NSABP B-28 patients with node-positive breast cancer. J Clin Oncol.
2009 (May 20 Supplement);27(15S):537.
2. Yang SX, Costantino JP, Mamounas EP, Nguyen D, Jeong J-H,
Wolmark N, Kim C, Kidwell K, Paik S, Swain SM. Akt phosphorylation at
Ser473 predicts benefit to paclitaxel chemotherapy in node-positive
breast cancer. J Clin Oncol. 2010, In Press.
Patent Status: U.S. Provisional Application No. 61/180,558 filed 22
[[Page 12766]]
May 2009 (HHS Reference No. E-191-2009/0-US-01).
Licensing Status: Available for licensing.
Licensing Contact: Patrick P. McCue, PhD; 301-496-7057;
mccuepat@mail.nih.gov.
Collaborative Research Opportunity: The National Cancer Institute
is seeking statements of capability or interest from parties interested
in collaborative research to further develop, evaluate, or
commercialize the pAkt assay for use in a clinical setting. The
National Cancer Institute would be particularly interested in
discussing collaborations to provide additional clinical validation of
pAkt as a primary biomarker. Please contact John Hewes, PhD at 301-435-
3131 or hewesj@mail.nih.gov for more information.
Dated: March 10, 2010.
Richard U. Rodriguez,
Director, Division of Technology Development and Transfer, Office of
Technology Transfer, National Institutes of Health.
[FR Doc. 2010-5765 Filed 3-16-10; 8:45 am]
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