Government-Owned Inventions; Availability for Licensing, 26707-26710 [E9-12874]

Agencies

• DEPARTMENT OF HEALTH AND HUMAN SERVICES
• National Institutes of Health

[Federal Register Volume 74, Number 105 (Wednesday, June 3, 2009)]
[Notices]
[Pages 26707-26710]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: E9-12874]


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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.

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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.

Diagnostic Markers for Melanoma

    Description of Technology: This invention relates to diagnostic and 
prognostic markers for melanoma. It discloses the identification of 
somatic mutations in genes of the microphthalmia-associated 
transcription factor (MITF) pathway in patients with melanoma.
    Melanoma is an aggressive and often fatal cancer with increasing 
incidence worldwide. Previous studies have linked the MITF pathway to 
the progression of melanoma. However, little is known about somatic 
mutations in genes of the MITF pathway that contribute to the 
development and progression of melanoma. To assess the role of the MITF 
pathway in melanoma, NIH investigators evaluated primary and metastatic 
melanoma samples for the presence of somatic mutations in two genes of 
the MITF pathway, MITF and SRY (sex determining region Y)--box 10 
(SOX10). They identified 16 previously unidentified somatic mutations 
in these genes. These studies suggest that MITF and SOX10 genes be used 
as diagnostic markers in human metastatic melanoma.

Applications

     Diagnosis and prognosis of patients with melanoma by 
detecting any mutations in the MITF or SOX10 gene.
     Selection of therapy for melanoma patient; an MITF 
inhibitor can be selected for therapy if the patient has any of the 
disclosed mutations in MITF.
    Market: Cancer is the second leading cause of death in the U.S. 
There is an acute need for cancer biomarkers that can be detected from 
clinically relevant samples and used for early diagnosis, therapeutic 
follow-up and prognosis of malignant diseases. Melanoma is the most 
serious type of cancer of the skin. The percentage of people who 
develop melanoma has more than doubled in the past 30 years. There are 
68,720 estimated new cases and 8,650 estimated deaths from melanoma in 
the United States in 2009, according to the National Cancer Institute.
    Inventors: Yardena R. Samuels et al. (NHGRI).
    Publication: Cronin JC WJ, Loftus SK, Prickett TD, Wei X, Ridd, 
Vemula S, Burrell AS, Agrawal NS, Lin JC, Banister CE, Buckhaults P, 
Rosenberg SA, Bastian BC, Pavan WJ, Samuels Y: Frequent mutations in 
the MITF pathway in melanoma. Pigment Cell and Melanoma Research 2009, 
(In Press).
    Patent Status: U.S. Provisional Application No. 61/214,415 filed 22 
Apr 2009 (HHS Reference No. E-053-2009/0-US-01).
    Licensing Status: Available for licensing.
    Licensing Contact: Betty B. Tong, Ph.D; 301-594-6565; 
tongb@mail.nih.gov.
    Collaborative Research Opportunity: The National Human Genome 
Research Institute's Cancer Genetics Branch is seeking statements of 
capability or interest from parties interested in collaborative 
research to further develop, evaluate, or commercialize these newly 
identified candidate melanoma diagnostic and prognostic markers. Please 
contact NHGRI's Technology Development Coordinator (TDC) Claire T. 
Driscoll at cdriscol@mail.nih.gov for more information.

T Cells Attacking Cancer: T Cell Receptors That Recognize the 
Tyrosinase Tumor Antigen

    Description of Technology: A problem with current chemotherapy-
based cancer treatments is the harsh side-effects associated with many 
cancer drugs. Thus, there is an urgent need to develop new therapeutic 
strategies combining fewer side-effects and more specific anti-tumor 
activity. Adoptive cell transfer (ACT) is a promising new 
immunotherapeutic approach to treat cancer and other diseases by 
directing an individual's innate and adaptive immune system to 
recognize specific disease-associated antigens.
    T cell receptors (TCRs) are proteins that recognize antigens in the 
context of infected or transformed cells and activate T cells to 
mediate an immune response and destroy abnormal cells. TCRs consist of 
two domains, one variable domain that recognizes the antigen and one 
constant region that helps the TCR anchor to the membrane and transmit 
recognition signals by interacting with other proteins.
    Scientists at the National Institutes of Health (NIH) have isolated 
T cells that recognize the human tyrosinase tumor-associated antigen 
(TAA) from the tumor infiltrating lymphocytes (TIL) of a melanoma 
cancer patient. The human tyrosinase antigen is a tumor antigen 
expressed in a variety of cancers, including skin cancer (melanoma) and 
brain cancer (glioblastoma). Utilizing the tyrosinase specific T cells, 
these scientists developed human/mouse hybrid TCRs with enhanced 
affinity for the tyrosinase TAA. The TCR sequences were modified by 
making specific amino acid substitutions and replacing certain TCR 
regions with mouse homologues. These TCRs also showed CD8-independency 
and, thus, can be expressed in both CD8 and CD4 T cells. T cells 
expressing these engineered TCRs recognize skin and brain tumor cells 
in culture. These T cells also exhibit enhanced cytokine induction and 
better tumor reactivity compared to unmodified TCRs. Previous versions 
of gene-modified T cells developed by NIH researchers demonstrated 
objective clinical responses in some cancer patients, which have 
validated gene-modified T cell immunotherapy as a promising cancer 
treatment strategy. TCRs directed against the tyrosinase TAA could 
serve as valuable new immunotherapeutic tools for attacking tumors, 
especially in patients whose tumors do not express other common TAAs.

Applications

     Immunotherapeutics to treat and/or prevent the recurrence 
of a variety of human cancers, including melanomas and glioblastomas, 
that express tyrosinase by transferring T cells engineered with 
tyrosinase-specific TCRs into cancer patients.

[[Page 26708]]

     A drug component of a combination immunotherapy regimen 
aimed at targeting the specific tumor-associated antigens expressed by 
the cancer cells of individual patients.
     Immunotherapeutic to treat and/or prevent tumors that do 
not express other common tumor-associated antigens, such as MART-1, 
gp100, and NY-ESO-1.

Advantages

     The parent tyrosinase-specific TCR was isolated from tumor 
infiltrating lymphocytes, so the genetically-modified versions should 
have an elevated affinity for tyrosinase.
     The tyrosinase-specific T cells recognize skin and brain 
cancer cells in culture. These T cells are predicted to have broad 
anti-cancer activity once developed to a clinical level.
     CD8 independency: The tyrosinase-specific TCRs can be 
expressed in both CD8 and CD4 T cells to maximize the cell-mediated 
immune response to the tumor.
     The tyrosinase-specific T cells should not be rejected by 
a patient's immune system since the mouse tyrosinase-recognition 
enhancing TCR sequences are incorporated into a human TCR backbone.
    Market: Cancer continues to be a medical and financial burden on 
U.S. public health. According to U.S. estimates, cancer is the second 
leading cause of death with over 565,000 deaths reported in 2008 and 
almost 1.5 million new cases were reported (excluding some skin 
cancers) in 2008. In 2007, the NIH estimated that the overall cost of 
cancer was $219.2 billion dollars and $89 billion went to direct 
medical costs. Despite our increasing knowledge of oncology and cancer 
treatment methods, the fight against cancer will continue to benefit 
from the development of new therapeutics aimed at treating individual 
patients.
    Inventors: Steven A. Rosenberg et al. (NCI).
    Development Status: This technology is in the pre-clinical stage of 
development. The inventors plan to develop the technology into clinical 
grade reagent for a clinical trial if the pre-clinical data continues 
to show promising results.
    Patent Status: U.S. Provisional Application No. 61/147,846 filed 28 
Jan 2009 (HHS Reference No. E-043-2009/0-US-01).
    Licensing Status: Available for licensing.
    Licensing Contact: Samuel E. Bish, PhD; 301-435-5282; 
bishse@mail.nih.gov.
    Collaborative Research Opportunity: The National Cancer Institute, 
Surgery Branch, Tumor Immunology Section, is seeking statements of 
capability or interest from parties interested in collaborative 
research to further develop, evaluate, or commercialize T Cells 
Attacking Cancer: T Cell Receptors that Recognize the Tyrosinase Tumor 
Antigen. Please contact John D. Hewes, PhD at 301-435-3121 or 
hewesj@mail.nih.gov for more information.

Genomics-Based Diagnostic Assay for Cancer

    Description of Technology: Molecular profiling with high throughput 
assays has gained utility in the management of select cancer patients 
and several gene expression-based assays are now marketed for improved 
prognostic accuracy for patients with cancer.
    This technology describes a genomics based diagnostic assay for the 
diagnosis and prognosis of cancer patients. Using a mouse model of 
breast cancer, the inventors identified a gene expression signature 
that can predict the outcome for human breast cancer patients with as 
few as six genes. The gene signature includes a total of 79 cancer 
survival factor-associated genes and was validated using available 
genomic test sets that were based on previously conducted human 
clinical trials. More recently, the six-gene-model was validated for 
cancers other than breast using multiple, independent, publicly-
available human lung cancer datasets. In addition to predicting the 
outcome of cancer patients, this technology could also be used to 
stratify patients for further therapy and treat patients by 
administering therapeutic agents that alter the activity of one of the 
aforementioned cancer survival factor-associated genes.

Applications

     Methods for cancer diagnosis and prognosis by evaluating 
expression levels of certain cancer survival factor-associated 
molecules in patients.
     Treatment of cancer by administering therapeutic agents 
that alter biological activity of cancer survival factor-associated 
molecule.
    Advantages: Prognostic outcome of breast and lung cancer patients 
can be identified in as few as six genes.
    Development Status: Pre-clinical stage of development.
    Inventors: Steven K. Libutti and Mei He (NCI).
    Patent Status: U.S. Provisional Application No. 61/152,597 filed 13 
Feb 2009 (HHS Reference No. E-023-2009/0-US-01).
    Licensing Status: Available for licensing.
    Licensing Contact: Whitney A. Hastings; 301-451-7337; 
hastingsw@mail.nih.gov.

New Weapons To Attack Cancer: T Cell Receptors Designed To Recognize 
Tumors With Enhanced Affinity

    Description of Technology: Given the unpleasant side-effects 
associated with many cancer drugs, there is an urgent need to develop 
new therapeutic strategies combining fewer side-effects and more 
specific anti-tumor activity. Adoptive immunotherapy is a promising new 
approach to cancer treatment that engineers an individual's innate and 
adaptive immune system to fight against specific diseases, including 
cancer.
    T cell receptors (TCRs) are proteins that recognize antigens in the 
context of infected or transformed cells and activate T cells to 
mediate an immune response and destroy abnormal cells. TCRs consist of 
two domains, one variable domain that recognizes the antigen and one 
constant region that helps the TCR anchor to the membrane and transmit 
recognition signals by interacting with other proteins.
    Scientists at the National Institutes of Health (NIH) have 
developed T cells with an enhanced ability to recognize the tumor 
associated antigens (TAAs) NY-ESO-1 and MART-1. These T cells were 
engineered to increase their ability to recognize these TAAs by making 
small genetic modifications to the TCRs that recognize these TAAs. NY-
ESO-1 is a cancer-testis antigen found in normal testis and various 
tumors. MART-1 is a melanoma antigen found on normal melanocytes and 
overexpressed in malignant melanomas. Previous versions of gene-
modified T cells developed by these researchers to attack tumors 
demonstrated objective clinical responses in some cancer patients, 
which validated gene-modified T cell adoptive immunotherapy as a 
promising cancer treatment strategy. These latest versions of the NY-
ESO-1 and MART-1 specific TCRs, designated 1G4 NY-ESO-1 and DMF5 MART-
1, were rationally engineered to enhance anti-tumor activity. These 
TCRs cause T cells to exhibit enhanced cytokine production and 
increased lysis of tumor cells when stimulated with NY-ESO-1 or MART-1. 
Infusing these T cells into patients via adoptive immunotherapy could 
prove to be powerful new tools for attacking tumors.

Applications

     Immunotherapeutics to treat and/or prevent the recurrence 
of a variety of

[[Page 26709]]

human cancers that overexpress the NY-ESO-1 or MART-1 TAA, including 
melanoma, lung, breast, ovarian, prostate, thyroid, and bladder cancer, 
by adoptively transferring gene-modified T cells into patients.
     A drug component of a combination immunotherapy regimen 
aimed at targeting the specific tumor-associated antigens expressed by 
cancer cells within individual patients.

Advantages

     NY-ESO-1 and MART-1 are overexpressed on a variety of 
cancers. Thus, this gene-modified TCR immunotherapy has wide 
applicability to treat a host of cancer types while reducing the side-
effects of treatment.
     These latest engineered TCRs have improved affinity for 
their corresponding TAA compared to previously developed TCRs with 
modified sequences.
    Development Status: These technologies are in clinical development. 
A clinical protocol (08-C-0121) is being conducted with the enhanced 
1G4 NY-ESO-1 TCR.
    Market: Cancer continues to be a medical and financial burden on 
U.S. public health. According to U.S. estimates, cancer is the second 
leading cause of death with over 565,000 deaths reported in 2008 and 
almost 1.5 million new cases were reported (excluding some skin 
cancers) in 2008. In 2007, the NIH estimated that the overall cost of 
cancer was $219.2 billion dollars and $89 billion went to direct 
medical costs. Despite our increasing knowledge of oncology and cancer 
treatment methods, the fight against cancer will continue to benefit 
from the development of new therapeutics aimed at treating individual 
patients.
    Inventors: Paul F. Robbins et al. (NCI).

Publications

    1. PF Robbins et al. Single and dual amino acid substitutions in 
TCR CDRs can enhance antigen-specific T cell functions. J Immunol. 2008 
May 1;180(9):6116-6131.
    2. Y Zhao et al. High-affinity TCRs generated by phage display 
provide CD4+ T cells with the ability to recognize and kill tumor cell 
lines. J Immunol. 2007 Nov 1;179(9):5845-5854.

Patent Status

     U.S. Provisional Patent Application No. 60/974,872 filed 
25 Sep 2007 (HHS Reference No. E-312-2007/0-US-01).
     PCT Patent Application No. PCT/US2008/77333 filed 23 Sep 
2008 (HHS Reference No. E-312-2007/1-PCT-01).
    Licensing Status: Available for licensing.
    Licensing Contact: Samuel E. Bish, PhD; 301-435-5282; 
bishse@mail.nih.gov.
    Collaborative Research Opportunity: The National Cancer Institute, 
Center for Cancer Research, Surgery Branch, is seeking statements of 
capability or interest from parties interested in collaborative 
research to further develop, evaluate, or commercialize TCRs that 
enhance the function of gene-modified T cells. Please contact John D. 
Hewes, PhD at 301-435-3121 or hewesj@mail.nih.gov for more information.

Steroid Derivatives as Inhibitors of Human Tyrosyl-DNA 
Phosphodiesterase (Tdp1)

    Description of Technology: Tyrosyl-DNA phosphodiesterase (Tdp1) is 
an enzyme that repairs topoisomerase I (Top1)-mediated DNA damage 
induced by chemotherapeutic agents and ubiquitous DNA lesions that 
interfere with transcription. The current technology are steroid 
derivatives that human inhibit Tdp1.
    Currently, there are various types of Top1 inhibitors used in 
chemotherapy, e.g., camptothecin. However, Tdp1 inhibitors are expected 
to be effective in combination therapy with Top1 inhibitors for the 
treatment of cancers. Combining Tdp1 inhibitors with Top1 inhibitors 
would allow Tdp1 to potentiate the antiproliferative activity of Top1 
inhibitors. In addition to Tdp1's effect on Top1, Tdp1 inhibitors can 
also exhibit antitumor activity independently, as tumors are shown to 
have excess free radicals, and Tdp1 repairs DNA damage by oxygen 
radicals.
    Applications: It is anticipated that Tdp1 inhibitors in association 
with Top1 inhibitors can have selective activity toward tumor tissues. 
Tdp1 inhibitors may exhibit antitumor activity by themselves because 
tumors have excess free radicals.
    Development Status: The technology is currently in the pre-clinical 
stage of development.
    Inventors: Yves Pommier et al. (NCI)
    Relevant Publication: A manuscript directly related to the above 
technology will be available as soon as it is accepted for publication.
    Patent Status: PCT Application No. PCT/US2008/004541 filed 5 Apr 
2008, claiming priority to 5 Apr 2007 (HHS Reference No. E-130-2007/2-
PCT-01).
    Licensing Status: Available for licensing.
    Licensing Contact: Betty Tong, Ph.D.; 301-594-6565; 
tongb@mail.nih.gov.
    Collaborative Research Opportunity: The Center for Cancer Research, 
National Cancer Institute, Laboratory of Molecular Pharmacology, is 
seeking statements of capability or interest from parties interested in 
collaborative research to further develop, evaluate, or commercialize 
inhibitors of Tyrosyl-DNA phosphodiesterase (Tdp1). Please contact John 
D. Hewes, Ph.D. at 301-435-3121 or hewesj@mail.nih.gov for more 
information.

Method for Spectroscopic Quantitation of HER2 in Biological Samples

    Description of Technology: An important clinical objective in 
certain cancer patients is the quantitation of HER2. The level of HER2 
expression in some tumors correlates with disease stage and severity. 
For example, HER2 positive breast cancer is a more aggressive disease 
with a greater likelihood of recurrence, a poorer prognosis, and a 
decreased chance of survival compared with HER2-negative breast cancer.
    This invention discloses a mass spectrometry method for 
quantitatively measuring HER2 in a variety of biological samples such 
as tissue, serum, or plasma. This invention is unlike traditional 
assays that use antibodies for detection of a HER2 and is superior to 
the current immunohistochemistry methods to stage tumor development. 
Consequently, a mass spectrometry-based clinical assay could be used to 
allow physicians to more effectively determine patient treatment. 
Furthermore, since this technology can also be used to assay formalin-
fixed prostate tissue (FFPE) tissues, it could be a useful biomarker 
for pathology labs.

Applications

     Diagnostic assay for cancer that measures HER2 levels in 
clinical samples, such as tissues and biological fluids.
     Prognostic assay to determine the stage of cancer and the 
appropriate cancer treatment.
     Research tool that could be used to correlate HER2 
expression with the expression of other proteins.

Market

     This novel in vitro diagnostic test for cancer has use in 
oncology and pathology laboratories of hospitals and commercial 
clinical laboratories.
     In the United States, almost 1.5 million new cancer cases 
are expected to be diagnosed in 2009.
    Development Status: Pre-clinical stage of development.

[[Page 26710]]

    Inventors: Thomas P. Conrads (NCI) et al.

Relevant Publications

    1. BL Hood, MM Darfler, TG Guiel, B Furusato, DA Lucas, BR 
Ringeisen, IA Sesterhenn, TP Conrads, TD Veenstra, DB Krizman. 
Proteomic analysis of formalin-fixed prostate tissue. Mol Cell 
Proteomics 2005 Nov;4(11):1741-1753.
    2. DA Prieto, BL Hood, MM Darfler, TG Guiel, DA Lucas, TP Conrads, 
TD Veenstra, DB Krizman. Liquid tissue\TM\: proteomic profiling of 
formalin fixed tissues. Biotechniques 2005 Jun;38:S32-S35.
    3. DS Kirkpatrick, SA Gerber, SP Gygi. The absolute quantification 
strategy: A general procedure for the quantification of proteins and 
post-translational modifications. Methods 2005 Mar;35(3):265-273.
    4. AM Hawkridge et al. Quantitative mass spectral evidence for the 
absence of circulating brain natriuretic peptide (BNP-32) in severe 
human heart failure. Proc Natl Acad Sci USA 2005 Nov 29;102(48):17442-
17447.
    5. L Anderson and CL Hunter. Quantitative mass spectrometric MRM 
assays for major plasma proteins. Mol Cell Proteomics 2006 
Apr;5(4):573-588.
    Patent Status: PCT Application No. PCT/US2007/003478 filed 4 Sep 
2008 (HHS Reference No. E-204-2006/0-PCT-01).
    Licensing Status: Available for licensing.
    Licensing Contact: Whitney Hastings; 301-451-7337; 
hastingw@mail.nih.gov.

Tools To Identify Candidates for Effective Cancer Therapy: Antibodies 
to Human Asparagine Synthetase

    Description of Technology: Scientists at the National Institutes of 
Health (NIH) have developed peptide-specific polyclonal antibodies 
against human asparagine synthetase (ASNS), the enzyme that forms 
asparagine from aspartate using ATP. ASNS serves as a key biomarker for 
acute lymphoblastic leukemia (ALL) and other malignancies because these 
cancer cells express little or no ASNS compared to normal cells. As a 
result, these leukemia cells must acquire asparagine from the 
bloodstream to survive and proliferate to form tumors. Patients with 
ALL can be treated with L-asparaginase (L-ASP) to break down asparagine 
in the body and starve leukemia cells by preventing them from acquiring 
asparagine. The anti-ASNS antibodies could be used to detect ASNS 
levels in patient samples to help select patients that could benefit 
from L-ASP therapy. Studies at the NIH have shown that L-ASP therapy 
may prove to be a useful treatment for other types of cancer besides 
leukemia.

Applications

     Diagnostic tool to detect levels of asparagine synthetase 
(ASNS) in human samples to identify cancer patients that can benefit 
from L-asparaginase (L-ASP) treatment.
     Screening tool to identify other cancer cell types 
treatable by L-ASP therapy, such as ovarian cancer cells, which show 
diminished ASNS levels.
     Research tool to quantitate levels of ASNS in laboratory 
procedures, including various immunoassays, flow cytometry, and tissue 
sample analysis.
    Advantages: These antibodies have been validated in immunoassays 
that showed that ASNS expression in a strong predictor of L-ASP 
efficacy in NCI-60 ovarian cancer cell lines.
    Inventors: Paul K. Goldsmith et al. (NCI).

Relevant Publications

    1. PL Lorenzi et al. Asparagine synthetase as a causal, predictive 
biomarker for L-asparaginase activity in ovarian cancer cells. Mol 
Cancer Ther. 2006 Nov;5(11):2613-2623.
    2. KJ Bussey et al. Integrating data on DNA copy number with gene 
expression levels and drug sensitivities in the NCI-60 cell line panel. 
Mol Cancer Ther. 2006 Apr;5(4):853-867.
    3. PL Lorenzi et al. Asparagine synthetase as a predictive 
biomarker for L-asparaginase activity in ovarian cancer cells. Mol 
Cancer Ther. 2008 Oct;7(10):3123-3128.
    Patent Status: HHS Reference No. E-101-2006/0--Research Tool. 
Patent protection is not being pursued for this technology.
    Licensing Status: Available for licensing under a Biological 
Materials License Agreement.
    Licensing Contact: Samuel E. Bish, Ph.D.; 301-435-5282; 
bishse@mail.nih.gov.

Mouse Model With Targeted Disruption of the Neurofibromatosis Type-1 
(Nf1) Gene

    Description of Technology: This invention relates to a mouse model 
having a targeted disruption of the neurofibromatosis type-1 (NF1) 
gene.
    The neurofibromatosis (NF1) gene shows significant homology to 
mammalian GAP and is an important regulator of the Ras signal 
transduction pathway. To study the function of NF1 in normal 
development and to develop a mouse model of NF1 disease, the inventors 
have used gene targeting in ES cells to generate mice carrying a null 
mutation at the mouse Nf1 locus. Although heterozygous mutant mice, 
aged up to 10 months, have not exhibited any obvious abnormalities, 
homozygous mutant embryos die in utero. Embryonic death is likely 
attributable to a severe malformation of the heart. Interestingly, 
mutant embryos also display hyperplasia of neural crest-derived 
sympathetic ganglia. These results identify new roles for NF1 in 
development and indicate that some of the abnormal growth phenomena 
observed in NF1 patients can be recapitulated in neurofibromin-
deficient mice. In addition, lethally-irradiated wild type mice 
transplanted with fetal liver cells taken from NF1 null embryos develop 
a form of juvenile chronic myelomonocytic leukemia (JMML) that is very 
similar to what is seen in children with NF1 disease.

Applications

     Research tool in studying some forms of human neuron 
diseases/injuries in addition to juvenile chronic myelomonocytic 
leukemia (JMML).
     Testing various therapeutic treatments for this disease.
    Inventors: Neal G. Copeland et al. (NCI).
    Patent Status: HHS Reference No. E-162-2004/0--Research Tool. 
Patent protection is not being pursued for this technology.
    Licensing Status: Available for licensing under a Biological 
Materials License Agreement.
    Licensing Contact: Betty Tong, Ph.D.; 301-594-6565; 
tongb@mail.nih.gov.

    Dated: May 27, 2009.
Richard U. Rodriguez,
Director, Division of Technology Development and Transfer, Office of 
Technology Transfer, National Institutes of Health.
[FR Doc. E9-12874 Filed 6-2-09; 8:45 am]
BILLING CODE 4140-01-P