Federal Register / Vol. 76, No. 155 / Thursday, August 11, 2011 / Notices 49777 

next-generation smallpox vaccines in 

humans; (3) discuss the most 

appropriate methods to bridge 

immunogenicity of next-generation 

smallpox vaccines to licensed smallpox 

vaccines in clinical trials; and (4) 

discuss viable methods of extrapolating 

clinical efficacy of next-generation 

smallpox vaccines from 

immunogenicity and efficacy data from 

relevant animal models. 

Transcripts: Transcripts of the public 

workshop may be requested in writing 

from the Division of Freedom of 

Information Office (ELEM–1029), Food 

and Drug Administration, 12420 

Parklawn Dr., Element Bldg., Rockville, 

MD 20857, approximately 15 working 

days after the public workshop at a cost 

of 10 cents per page. A transcript of the 

public workshop will be available on 

the Internet at http://www.fda.gov/ 

BiologicsBloodVaccines/NewsEvents/ 

WorkshopsMeetingsConferences/ 

TranscriptsMinutes/default.htm. 

Dated: August 4, 2011. 

Leslie Kux, 

Acting Assistant Commissioner for Policy. 

[FR Doc. 2011–20367 Filed 8–10–11; 8:45 am] 

BILLING CODE 4160–01–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. 

Tumor Markers for Potentially 

Predicting Outcome of Antiangiogenesis Therapy 

Description of Technology: During the 

past decade, anti-angiogenesis therapy 

has evolved as a promising approach to 

the treatment of cancer. However, a 

significant fraction of patients do not 

benefit from anti-angiogenesis therapy, 

either by itself or in combination with 

chemotherapy. A significant need 

remains for a means of predicting 

clinical benefit from anti-angiogenesis 

therapy. 

Researchers at the National Cancer 

Institute, NIH, have identified tumor 

cell apoptosis, p53, and HER2 as having 

potential predictive significance for 

treatment outcome in breast cancer 

patients who received anti-angiogenesis 

therapy in combination with 

chemotherapy. The researchers have 

developed a quantitative antibody-based 

testing method for correlating 

expression of p53 and HER2 and tumor 

apoptosis with clinical outcome. These 

markers can be potentially applied to 

predict which patients should receive 

anti-angiogenesis therapy plus 

chemotherapy. 

Potential Commercial Applications: 

• A diagnostic kit for predicting 

benefit of anti-angiogenesis therapy plus 

chemotherapy in breast cancer patients. 

• A testing service for breast cancer 

patients. 

Competitive Advantages: 

• The clinical predictive markers p53, 

HER2 and tumor apoptosis indicators 

are easily and readily evaluated using 

the new assay. 

• The new assay is potentially useful 

to determine which patients should or 

should not receive anti-angiogenesis 

therapy plus chemotherapy for longer 

survival and progression-free survival in 

patients with breast cancer. 

• A study with a large sample size 

will be planned by the inventors and 

potential collaborators. 

Development Stage: 

• Pilot. 

• In vivo data available (human). 

Inventors: Sherry Yang (NCI), Seth 

Steinberg (NCI), et al. 

Publication: Yang S, et al. p53, HER2 

and tumor cell apoptosis correlate with 

clinical outcome after neoadjuvant 

bevacizumab plus chemotherapy in 

breast cancer. Int J Oncol. 2011 May; 

38(5):1445–1452. [PMID 21399868] 

Intellectual Property: HHS Reference 

No. E–096–2011/0—U.S. Patent 

Application No. 61/448,092 filed 01 

March 2011 

Licensing Contact: Patrick McCue, 

Ph.D.; 301–435–5560; 

mccuepat@mail.nih.gov 

Collaborative Research Opportunity: 

The National Clinical Target Validation 

Laboratory, DCTD, NCI, NIH, is seeking 

statements of capability or interest from 

parties interested in collaborative 

research to further develop, evaluate, or 

commercialize p53, tumor apoptosis, 

and HER2 as markers for antiangiogenesis therapy. For collaboration 

opportunities, please contact John 

Hewes, Ph.D. at hewesj@mail.nih.gov. 

TRRAP and GRIN2A Mutations for the 

Diagnosis and Treatment of Melanoma 

Description of Technology: Using 

whole-exome sequencing of matched 

normal and metastatic tumor DNAs, 

researchers at the NIH have identified 

several novel somatic (e.g., tumorspecific) alterations, many of which 

have not previously been known to be 

genetically altered in tumors or linked 

to melanoma. In particular, the 

researchers identified a recurrent 

‘‘hotspot’’ mutation in the 

transformation/transcription domainassociated protein (TRRAP) gene, found 

the glutamate receptor ionotropic Nmethyl D-aspartate 2A (GRIN2A) gene as 

a highly mutated in melanoma, and 

have shown that the majority of 

melanoma tumors have alterations in 

genes encoding members of the 

glutamate signaling pathway. Therefore, 

this technology not only provides a 

comprehensive map of genetic 

alterations in melanoma, but has 

important diagnostic and therapeutic 

applications. Mutations in the TRRAP 

and GRIN2A genes can be used as 

diagnostic markers for melanoma and 

may serve as therapeutic targets in the 

treatment of melanoma. In addition, 

glutamate antagonists have previously 

been shown to inhibit proliferation of 

human tumor cells, and therefore 

further investigation of the pathway in 

melanoma could allow for the 

identification of new therapeutic 

proteins that target this pathway. 

Potential Commercial Applications: 

• Diagnostic array for the detection of 

TRRAP and GRIN2A mutations. 

• Method of identifying TRRAP and 

GRIN2A inhibitors as therapeutic agents 

to treat malignant melanoma patients. 

• Method of selecting a therapy based 

on the presence of TRRAP and GRIN2A 

mutations. 

Competitive Advantages: 

• Complete analysis of melanoma 

exome alterations. 

• TRRAP, GRIN2A, and the other 

identified mutations are highly frequent 

and/or highly mutated in melanomas. 

• Glutamate antagonists have already 

been shown to inhibit tumor growth. 

Thus, this technology may prove useful 


srobinson on DSK4SPTVN1PROD with NOTICES
49778 Federal Register / Vol. 76, No. 155 / Thursday, August 11, 2011 / Notices 

for the development of novel diagnostic 

tests and therapeutics. 

Development Stage: Pre-clinical. 

Inventors: Yardena Samuels and 

Xiaomu Wei (NHGRI). 

Publication: Wei X, et al. Exome 

sequencing identifies GRIN2A as 

frequently mutated in melanoma. Nat 

Genet. 2011 May;43(5):442–446. [PMID: 

21499247]. 

Intellectual Property: 

• HHS Reference No. E–013–2011/ 

0—U.S. Provisional Application No. 61/ 

462,471 filed 02 February 2011. 

• Research Tool—Patent protection is 

not being pursued for the TRRAP and 

GRIN2A melanoma metastatic cell lines. 

Related Technologies: 

• HHS Reference No. E–272–2008/ 

0—U.S. Patent Application No. 13/ 

128,125 filed 06 May 2011, European 

and Australian applications filed; 

Mutations of the ERBB4 Gene in 

Melanoma. 

• HHS Reference No. E–229–2010/ 

0—Research Tool; ERBB4 Mutations 

Identified in Human Melanoma 

Metastasis Cell Lines (2690, 2379, 2197, 

2183, 2535, 2645, 1770, 2359, 2238, 

2319, 2190). 

• HHS Reference No. E–232–2010/ 

0—Research Tool; Isocitrate 

Dehydrogenase 1 (IDH1) R132 Mutation 

Human Melanoma Metastasis Cell Line. 

Licensing Contact: Whitney Hastings; 

301–451–7337; hastingw@mail.nih.gov. 

Cells and Nanoparticles With Altered 

Protein Expression Patterns Useful for 

the Modulation of T Cell Activity for 

Immunotherapy 

Description of Technology: NIH 

scientists have developed human cells 

and nanoparticles to enhance 

immunotherapy. Specifically, 

researchers have identified that cells or 

nanoparticles expressing a high 

temperature requirement serine 

peptidase 1 (HtrA1) activator and/or a 

cytokine-induced Src homology 2 

protein (CIS) inhibitor are capable of 

increasing T cell activity. These 

compositions can be used primarily in 

T cell immunotherapy against various 

cancers and infectious diseases where 

enhanced T cell activity is beneficial. 

Conversely, cells or nanoparticles that 

express a HtrA1 inhibitor and/or a CIS 

activator can suppress T cell activity. 

These compositions can be utilized to 

treat various auto- or alloimmune 

diseases and can be used to prevent 

transplant rejections. 

HtrA1 (also known as L56, ARMD7, 

ORF480, and PRSS11) is a serine 

protease that is known to inhibit the 

TGF-beta family proteins. CIS (also 

known as G18, SOCS, CIS–1, and CISH) 

is a member of the suppression of 

cytokine signaling (SOCS) family of 

proteins and inhibit the JAK/STAT 

signaling pathways. CIS acts to inhibit 

HtrA1 and repress cell activation 

targets. Immunotherapy, although an 

effective treatment strategy, sometimes 

fails when cells lose activity. T cells 

adoptively transferred into patients 

where CIS is inhibited and/or HtrA1 is 

activated should maintain their activity 

and lead to more successful adoptive T 

cell transfers. 

Potential Commercial Applications: 

• Immunotherapy for cancer or 

infectious diseases using human cells or 

nanoparticles expressing an HtrA1 

activator and/or a CIS inhibitor 

• Therapeutic for treating 

autoimmune diseases using human cells 

and or nanoparticles expressing an 

HtrA1 inhibitor and/or a CIS activator 

• Agents expressing an HtrA1 

inhibitor and/or a CIS activator to 

prevent organ, tissue, or cell transplant 

rejection and treat alloimmune diseases, 

such as graft-versus-host disease 

• Components of a combination 

therapy to increase or suppress T cell 

activity in a patient 

Competitive Advantages: 

• Some patients do not respond to T 

cell immunotherapy due to lack of cell 

persistence, survival, or activity as well 

as for other poorly understood reasons. 

Modifying HtrA1 and CIS in currently 

existing T cell immunotherapies should 

increase the success rate of these 

therapies by increasing the persistence 

and survival of the infused cells. 

• T cells can become ‘‘exhausted’’ as 

they mature following activation by 

target antigen. Cells with altered 

expression of HtrA1 and/or CIS may be 

able to avoid exhaustion after repeated 

activation. 

Development Stage: 

• Pre-clinical. 

• In vitro data available. 

• In vivo data available (animal). 

Inventors: Douglas C. Palmer and 

Nicholas P. Restifo (NCI). 

Publication: Palmer DC and Restifo 

NP. Suppressors of cytokine signaling 

(SOCS) in T cell differentiation, 

maturation, and function. Trends 

Immunol. 2009 Dec;30(12):592–602. 

[PMID 19879803]. 

Intellectual Property: HHS Reference 

No. E–069–2010/0—U.S. Patent 

Application No. 61/420,825 filed 08 

December 2010. 

Licensing Contact: Samuel E. Bish, 

Ph.D.; 301–435–5282; 

bishse@mail.nih.gov 

Dated: August 5, 2011. 

Richard U. Rodriguez, 

Director, Division of Technology Development 

and Transfer, Office of Technology Transfer, 

National Institutes of Health. 

[FR Doc. 2011–20447 Filed 8–10–11; 8:45 am] 

BILLING CODE 4140–01–P 

DEPARTMENT OF HEALTH AND 

HUMAN SERVICES 

National Institutes of Health National 

Institute of Environmental Health 

Sciences; Notice of Meeting 

Pursuant to section 10(a) of the 

Federal Advisory Committee Act, as 

amended (5 U.S.C. App.), notice is 

hereby given of a meeting of the 

Interagency Breast Cancer and 

Environmental Research Coordinating 

Committee. 

The meeting will be open to the 

public, with attendance limited to space 

available. Individuals who plan to 

attend and need special assistance, such 

as sign language interpretation or other 

reasonable accommodations, should 

notify the Contact Person listed below 

in advance of the meeting. 

Name of Committee: Interagency Breast 

Cancer and Environmental Research 

Coordinating Committee. 

Date: September 26–27, 2011. 

Time: 8:30 a.m. to 5 p.m. 

Agenda: The purpose of the meeting is to 

continue the work of the Committee, to share 

and coordinate information on existing 

research activities, & make recommendations 

to NIH & other Federal agencies on how to 

improve existing research programs related to 

breast cancer & the environment. The agenda 

will be posted on the web: http:// 

www.niehs.nih.gov/about/orgstructure/ 

boards/ibcercc/. 

Place: Nat. Inst. of Environmental Health 

Sciences, Building 101, Rodbell Auditorium, 

111 T. W. Alexander Drive, Research 

Triangle Park, NC 27709. 

Contact Person: Gwen W. Collman, PhD, 

Director, Division of Extramural Research 

and Training (DERT), Nat. Inst. of 

Environmental Health Sciences, National 

Institutes of Health, 615 Davis Dr., KEY615/ 

3112, Research Triangle Park, NC 27709, 

(919) 541–4980, collman@niehs.nih.gov. 

Any member of the public interested in 

presenting oral comments to the Committee 

should submit their remarks in writing at 

least 10 days in advance of the meeting. 

Comments in document format (i.e. WORD, 

Rich Text, PDF) may be submitted via e-mail 

to ibcercc@niehs.nih.gov. You do not need to 

attend the meeting in order to submit 

comments. 

Interested individuals and representatives 

of organizations may submit a letter of intent, 

a brief description of the organization 

represented, and a short description of the 

oral comments you wish to present. Only one 

representative per organization may be 

allowed to present oral comments and if 


srobinson on DSK4SPTVN1PROD with NOTICES