16406 Federal Register / Vol. 74, No. 68 / Friday, April 10, 2009 / Notices 

inflammation and cancer. Using a 

thioglycollate challenge as a measure of 

the impact of the deletion of MCP–1, 

MCP–1 deficient mice exhibit a 60% 

reduction in the number of monocytes/ 

macrophages at 96 hours compared to 

wild type mice. Unlike previously 

generated MCP–1 deficient mice in 

which the expression of the neighboring 

gene for MCP–3 is down-regulated (our 

own data), the expression of MCP–3 is 

up-regulated in this mouse model. 

Applications: This mouse may be 

useful as an in vivo model for 

evaluating the role of MCP–1 and MCP– 

3 in cancer or other diseases associated 

with inflammation due to the 

accumulation of monocytes. 

Inventor: Teizo Yoshimura (NCI) 

Patent Status: HHS Reference No. E– 

241–2005/0—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, PhD; 

301–594–6565; tongb@mail.nih.gov. 

Collaborative Research Opportunity: 

The National Cancer Institute, Center for 

Cancer Research, Laboratory of 

Molecular Immunoregulation, Cancer 

and Inflammation Program, is seeking 

statements of capability or interest from 

parties interested in collaborative 

research to further develop, evaluate, or 

commercialize agents useful to treat 

patients with inflammation or cancer. 

Please contact John D. Hewes, PhD at 

301–435–3121 or hewesj@mail.nih.gov 

for more information. 

DU145 Camptothecin (CPT)-Resistant 

Cell Line 

Description of Technology: Drug 

resistance is a major limitation of 

chemotherapy. Understanding how drug 

resistance develops may lead to more 

effective treatments. This invention 

describes the DU145 Camptothecin 

(CPT)-resistant prostate cancer cell line 

that can be used to study mechanisms 

of drug resistance. 

Inventor: Yves G. Pommier (NCI) 

Related Publication: Y Urasaki et al. 

Characterization of a novel 

topoisomerase I mutation from a 

camptothecin-resistant human prostate 

cancer cell line. Cancer Res. 2001 Mar 

1;61(5):1964–1969. 

Patent Status: HHS Reference No. E– 

159–2005/0—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, PhD; 

301–594–6565; tongb@mail.nih.gov. 

Creation and Characterization of 

Carcinogen-Altered Mouse Epidermal 

Cell Lines 

Description of Technology: The 

invention relates to the creation of three 

(3) cell lines that may be used as models 

of putative initiated cancer cells. The 

cell lines can be used in basic research 

assays and low/high throughput 

screening assays. 

Cell line 308 evolved from a calciumresistant focus from adult mouse 

epidermis that was exposed to the 

carcinogen, 7,12- 

dimethylbenz[a]anthracene (DMBA). 

Cell lines F and D were derived by 

treating primary newborn mouse 

epidermal cells in culture with Nmethyl-Nı ́-nitro-N-nitrosoguanidine 

(MNNG) and DMBA, respectively. These 

three (3) noncancerous cell lines 

derived from differentiation-resistant, 

carcinogen-induced foci may be 

considered to be putative initiated cells. 

Inventor: Stuart H. Yuspa (NCI) 

Related Publications: 

1. SH Yuspa and DL Morgan. Mouse 

skin cells resistant to terminal 

differentiation associated with initiation 

of carcinogenesis. Nature 1981 Sep 

3;293(5287):72–74. 

2. H Hennings et al. Response of 

carcinogen-altered mouse epidermal 

cells to phorbol ester tumor promoters 

and calcium. J Invest Dermatol. 1987 

Jan;88(1):60–65. 

Patent Status: HHS Reference No. E– 

154–2004/0—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, PhD; 

301–594–6565; tongb@mail.nih.gov. 

A Mouse Model for Conditional Gene 

Deletion of c-Met Receptor 

Description of Technology: c-Met 

oncogene has been implicated in a 

variety of human cancers as well as 

degenerative diseases. Signaling via the 

c-Met receptor is essential for survival 

as evidenced by the embryonal death of 

mice in which the c-Met has been 

deleted. Further analysis of the role of 

the signaling pathway supported by cMet receptor in the adult organism is 

hindered by its embryonic lethality. The 

establishment of a mouse model for the 

conditional c-Met gene deletion will 

provide a unique opportunity to explore 

the function of c-Met in the adult mouse 

by selectively deleting the receptor gene 

in various tissues. Such a mouse model 

is established at the National Institutes 

of Health and available for licensing. 

Applications: 

• Animal model to study the 

physiological role of the c-Met receptor. 

• Animal model for testing potential 

drug targeted to the c-Met signal 

transduction pathway. 

Inventor: Snorri S. Thorgeirsson (NCI) 

Patent Status: HHS Reference No. E– 

048–2003/0—Research Tool. Patent 

protection is not being pursued for this 

technology. 

Licensing Status: c-Met receptor 

conditional KO mice are available for 

licensing. 

Licensing Contact: Betty Tong, PhD; 

301–594–6565; tongb@mail.nih.gov. 

Dated: April 6, 2009. 

Richard U. Rodriguez, 

Director, Division of Technology Development 

and Transfer, Office of Technology Transfer, 

National Institutes of Health. 

[FR Doc. E9–8212 Filed 4–9–09; 8:45 am] 

BILLING CODE 4140–01–P 

DEPARTMENT OF HEALTH AND 

HUMAN SERVICES 

National Institutes of Health 

Center for Scientific Review; Amended 

Notice of Meeting 

Notice is hereby given of a change in 

the meeting of the Center for Scientific 

Review Special Emphasis Panel, March 

26, 2009, 12 p.m. to March 27, 2009, 3 

p.m., National Institutes of Health, 6701 

Rockledge Drive, Bethesda, MD 20892 

which was published in the Federal 

Register on March 12, 2009, 74 FR 

10748. 

The meeting will be held April 16, 

2009, 3 p.m. to April 17, 2009, 6 p.m. 

The meeting location remains the same. 

The meeting is closed to the public. 

Dated: April 2, 2009. 

Jennifer Spaeth, 

Director, Office of Federal Advisory 

Committee Policy. 

[FR Doc. E9–8018 Filed 4–9–09; 8:45 am] 

BILLING CODE 4140–01–M 

DEPARTMENT OF HEALTH AND 

HUMAN SERVICES 

National Institutes of Health 

Center for Scientific Review; Amended 

Notice of Meeting 

Notice is hereby given of a change in 

the meeting of the Center for Scientific 

Review Special Emphasis Panel, April 

20, 2009, 9 a.m. to April 21, 2009, 3 

p.m., National Institutes of Health, 6701 

Rockledge Drive, Bethesda, MD 20892 

which was published in the Federal 

Register on March 31, 2009, 74 FR 

14570–14571.