Federal Register / Vol. 75, No. 177 / Tuesday, September 14, 2010 / Notices 55799 

Dated: September 8, 2010. 

Bernadette Dunham, 

Director, Center for Veterinary Medicine. 

[FR Doc. 2010–22811 Filed 9–13–10; 8:45 am] 

BILLING CODE 4160–01–S 

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. 

Assay for Arf GTP-Binding Proteins 

Description of Invention: The 

worldwide laboratory research reagents 

market is expected to surpass $13 

billion in 2010, and the field of 

biotechnology appears key to 

maintaining the market’s growth. 

Antibodies are becoming increasingly 

significant, especially for targeting the 

diseased cells and cell compounds. 

Researchers at the National Cancer 

Institute (NCI), NIH, have developed an 

antibody-based assay that measures 

levels of Arf GTP-binding proteins, 

some of which have been linked to the 

invasive behavior of cancer cells. The 

assay is robust, can be performed both 

on cell lysates and fixed cells, and can 

distinguish among specific endogenous 

Arf-GTP isoforms. 

Applications: 

• Research on Arf function in 

physiology and cancer. 

• Research on cancer invasion. 

• Research on membrane traffic and 

actin reorganization. 

Advantages: 

• Ability to distinguish between the 

specific isoforms (i.e., Arf1, Arf3, Arf4, 

Arf5, and Arf6). 

• Antibodies bind preferentially to 

the GTP-bound form of Arf. 

Inventor: Paul A. Randazzo (NCI). 

Relevant Publications: 

1. Spang A et al. Arf GAPs: 

gatekeepers of vesicle generation. FEBS 

Lett. 2010 Jun 18;584(12):2646–2651. 

[PubMed: 20394747]. 

2. Campa F and Randazzo PA. Arf 

GTPase-activating proteins and their 

potential role in cell migration and 

invasion. Cell Adh Migr. 2008 Oct; 

2(4):258–262. [PubMed: 19262159]. 

Patent Status: HHS Reference No. E– 

198–2010/0—Research Material. Patent 

protection is not being pursued for this 

technology. 

Licensing Status: Available for 

licensing. 

Licensing Contact: Patrick P. McCue, 

PhD, (301) 435–5560; 

mccuepat@mail.nih.gov. 

Collaborative Research Opportunity: 

The Center for Cancer Research, 

Laboratory of Cellular and Molecular 

Biology, is seeking statements of 

capability or interest from parties 

interested in collaborative research to 

further develop, evaluate, or 

commercialize this technology. Please 

contact John D. Hewes, PhD at 301–435– 

3121 or hewesj@mail.nih.gov for more 

information. 

Sequences Encoding Two Novel Human 

Polyomaviruses 

Description of Invention: Researchers 

at the National Cancer Institute, NIH, 

have discovered two species of a 

previously unknown polyomavirus 

genus. 

Polyomaviruses are a diverse group of 

DNA-based viruses that infect humans 

and various animals. At least one 

human polyomavirus, the Merkel cell 

polyomavirus (MCV), plays a causal role 

in the development of an unusual form 

of skin cancer called Merkel cell 

carcinoma. The coat proteins of 

polyomaviruses can spontaneously 

assemble into virus-like particles (VLPs) 

similar to those that have been used in 

the recent vaccines against human 

papillomaviruses (HPVs). 

Applications: 

• Development of clinical diagnostic 

assays to detect linkages between the 

new polyomaviruses and human 

cancers. 

• Development of a VLP-based 

prophylactic vaccine similar to the HPV 

vaccine. 

Advantages: DNA sequences have 

broad applications in the studies of 

polyomavirus infection mechanisms 

and carcinogenesis. Notably, they are: 

• Identification and purification of 

the normal and mutated polyomaviral 

proteins. 

• Studies of antisense 

oligonucleotides in polyomavirus 

biology. 

• Development of polyclonal and 

monoclonal antibodies against 

polyomaviruses. 

Development Status: Pre-clinical. 

Inventors: Christopher B. Buck and 

Diana V. Pastrana (NCI). 

Relevant Publication: Schowalter RM 

et al. Merkel cell polyomavirus and two 

previously unknown polyomaviruses 

are chronically shed from human skin. 

Cell Host Microbe Jun 25;7(6):509–515. 

[PubMed: 20542254]. 

Patent Status: U.S. Provisional 

Application No. 61/318,080 filed 26 Mar 

2010 (HHS Reference No. E–051–2010/ 

0–US–01). 

Licensing Status: Available for 

licensing. 

Licensing Contact: Patrick P. McCue, 

PhD; 301–435–5560; 

mccuepat@mail.nih.gov. 

Fenoterol and Fenoterol Analogues for 

Treatment of Glioma, Glioblastoma, 

and Astrocytoma 

Description of Invention: To date 

there is no effective treatment for the 

brain tumors or brain cancers 

indentified as gliomas, glioblastomas, or 

astrocytomas. 

This technology relates to the 

discovery that fenoterol and related 

analogues block astrocytoma and 

glioblastoma cell division at low doses. 

In a xenograft model utilizing the 

1321N1 astrocytoma tumor implanted in 

the flank of SKID mice, the (R,R)-4- 

methoxyfenoterol analogue significantly 

decreased tumor growth relative to a 

control group receiving vehicle and 

studies utilizing [3H]-(R,R)-4- 

methoxyfenoterol have shown that the 

compound readily passes the bloodbrain barrier. The anti-tumor effect is 

associated with the ability of fenoterol 

and related analogues to induce 

production of cyclic adenosine 

monophosphate (cAMP), which is 

normally decreased in glioblastomas 

and astrocytomas. Induced cAMP 

production inhibits brain tumor growth 

in vivo. Fenoterol and related analogues 

are beta-2 adrenergic receptor (b2 AR) 

agonists and the anti-tumor effect is 

associated with the expression of this 

receptor. Since there is a heterogeneous 

expression of b2 AR in human brain 

tumors, patients who will respond to 

fenoterol therapy can be predetermined 

leading to individualized treatment. In 

addition to use in the initial treatment 

of brain tumors, the systemic and CNS 

bioavailability of the drug after oral 


jlentini on DSKJ8SOYB1PROD with NOTICES
55800 Federal Register / Vol. 75, No. 177 / Tuesday, September 14, 2010 / Notices 

administration and the minimal 

systemic toxicity suggest that fenoterol 

and it analogs can be used in the 

adjuvant treatment of patients with b2 

AR-positive gliomas, glioblastomas or 

astrocytomas. Studies with a number of 

fenoterol analogs and CNS-implanted 

tumors are in progress. 

The fenoterol analogues discussed in 

this technology are subject to HHS Ref. 

No. E–205–2006/3 (U.S. Patent 

Application No. 12/376,945 and PCT 

Publication No. WO/2008/022038). 

Applications: Therapeutic in the front 

line and adjuvant treatment of glioma, 

glioblastoma and astrocytoma. 

Advantages: Potential first-in-class 

therapeutic for multiple types of brain 

tumors. 

Development Status: In vivo: tumor 

models in SKID mice. In vitro: cellbased assays using human glioblastoma 

and astrocytoma cell lines. Further in 

vivo studies in animal models are 

underway. 

Market: Approximately 17,000 

Americans are diagnosed with gliomas 

annually (http://www.mayoclinic.org/ 

glioma/). 

Inventors: Irving W. Wainer (NIA), 

et al. 

Publication: Submitted. 

Patent Status: U.S. Provisional 

Application No. 61/312,642 filed 10 Mar 

2010 (HHS Reference No. E–013– 

2010/0). 

Licensing Status: Available for 

licensing. 

Licensing Contact: Fatima Sayyid, 

M.H.P.M.; 301–435–4521; 

Fatima.Sayyid@nih.hhs.gov. 

Collaborative Research Opportunity: 

The National Institute on Aging, 

Laboratory of Clinical Investigation, is 

seeking statements of capability or 

interest from parties interested in 

collaborative research to further 

develop, evaluate, or commercialize the 

use of fenoterol and fenoterol analogs in 

the front line and adjuvant treatment of 

CNS tumors and other b2 AR expressing 

tumors. Please contact Nicole Darack, 

PhD at 301–435–3101 or 

darackn@mail.nih.gov for more 

information. 

Chemical Attraction: Cell Lines 

Expressing the CXCR1 or CXCR2 

Chemokine Receptors 

Description of Invention: 

Chemoattractant receptors have been 

identified as important factors in 

regulating many innate and adaptive 

immune responses. Modulation of these 

receptors have implications for shifting 

immune responses to create either a 

dampening effect in fighting 

inflammatory diseases, such as 

autoimmune diseases or cardiovascular 

diseases, or a boosting effect to generate 

more effective responses to infectious 

agents, tumors, and promote wound 

healing. Chemokine receptors are 

expressed on a variety of tumor cells 

and play a role in helping cancer cells 

sense new microenvironments for 

metastatic growth. 

Scientists at the National Institutes of 

Health (NIH) have developed human 

embryonic kidney (HEK) 293 cell lines 

that express the CXCR1 chemokine 

receptor or the CXCR2 chemokine 

receptor. These two receptors are also 

known as the IL-8 receptor-alpha and 

IL-8 receptor-beta, respectively. They 

both effectively bind IL-8, a potent 

neutrophil chemoattractant, as well as 

other chemokines with varying 

affinities. The collection of cell lines 

produced by these scientists includes 

HEK 293 cells that express the wild-type 

CXCR1, wild-type CXCR2, or mutant 

variants of each receptor. The cell lines 

were created by stably transfecting 

vectors containing the cDNA for each 

receptor into HEK 293 cells. HEK 293 

cells transfected with the wild-type 

CXCR1 or CXCR2 display strong 

chemoattractant properties when placed 

in the presence of their corresponding 

CXC family chemokines, such as IL-8. 

Application: 

• Research tools for testing the 

activity of potential drugs and 

chemokine analogs in their ability to 

block cellular responses triggered by 

CXC chemokines, such as inflammatory 

responses induced by IL-8 

• Cell lines expressing the wild-type 

CXCR1 or CXCR2 can serve as positive 

controls in chemokine receptor studies 

designed to identify novel 

chemoattractants or agents that inhibit 

chemokinetic functions. 

• Research tool for screening 

compounds that block these receptors as 

a possible anti-cancer agent to inhibit 

angiogenesis and metastasis 

Advantages: 

• Both wild-type and mutant cell 

lines available: Wild-type CXCR1/ 

CXCR2 receptors or mutant receptors 

with point and deletion mutations have 

been cloned into HEK 293 cells. These 

cell lines will have varying degrees of 

potency for their chemoattractant 

responses to provide a range of 

functional comparisons in chemokine 

studies. 

• Experimental verification of 

response to CXC family chemokines: 

The scientists have compiled years of 

data over various publications 

indicating that these receptors respond 

appropriately to a profile of 

chemokines. 

Inventors: Joost Oppenheim, Adit 

Ben-Baruch, Ji Ming Wang, David 

Kelvin (all NCI). 

Publications: 

1. E Cohen-Hillel, et al. Cell migration 

to the chemokine CXCL8: paxillin is 

activated and regulates adhesion and 

cell motility. Cell Mol Life Sci. 2009 

Mar;66(5):884–899. [PubMed: 

19151925]. 

2. H Attal, et al. Intracellular crosstalk between the GPCR CXCR1 and 

CXCR2: role of carboxyl terminus 

phosphorylation sites. Exp Cell Res. 

2008 Jan 15;314(2):352–365. [PubMed: 

17996233]. 

3. A Ben-Baruch, et al. The 

differential ability of IL–8 and 

neutrophil-activating peptide-2 to 

induce attenuation of chemotaxis is 

mediated by their divergent capabilities 

to phosphorylate CXCR2 (IL–8 receptor 

B). J Immunol. 1997 Jun 

15;158(12):5927–5933. [PubMed: 

9190946]. 

4. A Ben-Baruch, et al. IL–8 and NAP– 

2 differ in their capacities to bind and 

chemoattract 293 cells transfected with 

either IL–8 receptor type A or type B. 

Cytokine 1997 Jan;9(1):37–45. [PubMed: 

9067094]. 

5. A Ben-Baruch, et al. Interleukin-8 

receptor beta. The role of the carboxyl 

terminus in signal transduction. J Biol 

Chem. 1995 Apr 21;270(16):9121–9128. 

[PubMed: 7721826]. 

Patent Status: HHS Reference No. E– 

221–2009/0—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. 

DLC–1 Gene Deleted in Cancers 

Description of Invention: 

Chromosomal regions that are 

frequently deleted in cancer cells are 

thought to be the loci of tumor 

suppressor genes, which restrict cell 

proliferation. Recurrent deletions on the 

short arm of human chromosome 8 in 

liver, breast, lung and prostate cancers 

have raised the possibility of the 

presence of tumor suppressor genes in 

this location. 

The inventors have discovered the 

deletion of human DLC–1 gene in 

hepatocellular cancer (HCC) cells. They 

have performed in vitro experiments 

demonstrating the deletion in over 40% 

of human primary HCC and in 90% of 

HCC cell lines. The DLC–1 gene is 

located on human chromosome 8p21.3– 

22, a region frequently deleted in many 

types of human cancer. DLC–1 mRNA is 


jlentini on DSKJ8SOYB1PROD with NOTICES
Federal Register / Vol. 75, No. 177 / Tuesday, September 14, 2010 / Notices 55801 

expressed in all normal tissues tested, 

but it has either no or low expression in 

a high percentage of several types of 

human cancer, such as liver, breast, 

lung, and prostate cancers. Through in 

vitro and in vivo tumor suppression 

experiments, the inventors further 

demonstrated that DLC–1 acts as a new 

tumor suppressor gene for different 

types of human cancer. 

Applications: 

• Method to diagnose HCC. 

• Method to treat HCC patients with 

DLC–1 compositions. 

• Transgenic model to study HCC and 

other types of human cancer. 

• DLC–1 compositions. 

Market: 

• Primary liver cancer accounts for 

about 2% of cancers in the U.S., but up 

to half of all cancers in some 

undeveloped countries. 

• 251,000 new cases are reported 

annually. 

• Post-operative five year survival 

rate of HCC patients is 30–40%. 

Development Status: The technology 

is currently in the pre-clinical stage of 

development. 

Inventors: Bao-Zhu Yuan, Snorri S. 

Thorgeirsson, Nicholas Popescu (NCI). 

Publications: 

1. BZ Yuan et al. DLC–1 operates as 

a tumor suppressor gene in human nonsmall cell lung carcinomas. Oncogene. 

2004 Feb 19;23(7):1405–1411. [PubMed: 

14661059]. 

2. BZ Yuan et al. DLC–1 gene inhibits 

human breast cancer cell growth and in 

vitro tumorigenicity. Oncogene. 2003 

Jan 23;22(3):445–450. [PubMed: 

12545165]. 

3. BZ Yuan et al. Promoter 

hypermethylation of DLC–1, a candidate 

tumor suppressor gene, in several 

common human cancers. Cancer Genet 

Cytogenet. 2003 Jan 15;140(2):113–117. 

[PubMed: 12645648]. 

4. BZ Yuan et al. Cloning, 

characterization, and chromosomal 

localization of a gene frequently deleted 

in human liver cancer (DLC–1) 

homologous to rat RhoGAP. Cancer Res. 

1998 May 15;58(10):2196–2199. 

[PubMed: 9605766]. 

Patent Status: 

• U.S. Patent No. 6,897,018 issued 24 

May 2005 (HHS Reference No. E–042– 

1998/0–US–03). 

• U.S. Patent No. 7,534,565 issued 19 

May 2009 (HHS Reference No. E–042– 

1998/0–US–05). 

Licensing Status: Available for 

licensing. 

Licensing Contact: Jennifer Wong; 

301–435–4633; wongje@mail.nih.gov. 

Collaborative Research Opportunity: 

The National Cancer Institute, 

Laboratory of Experimental 

Carcinogenesis, is seeking statements of 

capability or interest from parties 

interested in collaborative research to 

further develop, evaluate, or 

commercialize diagnostics based on 

tumor suppressor genes. Please contact 

John D. Hewes, PhD, at 301–435–3121 

or hewesj@mail.nih.gov for more 

information. 

Dated: September 7, 2010. 

Richard U. Rodriguez, 

Director, Division of Technology Development 

and Transfer, Office of Technology Transfer, 

National Institutes of Health. 

[FR Doc. 2010–22834 Filed 9–13–10; 8:45 am] 

BILLING CODE 4140–01–P 

DEPARTMENT OF HEALTH AND 

HUMAN SERVICES 

Centers for Medicare & Medicaid 

Services 

[CMS–1338–CN] 

RIN 0938–AP87 

Medicare Program; Prospective 

Payment System and Consolidated 

Billing for Skilled Nursing Facilities for 

FY 2011; Correction 

AGENCY: Centers for Medicare & 

Medicaid Services (CMS), HHS. 

ACTION: Correction notice. 

SUMMARY: This document corrects 

technical errors that appeared in the 

notice with comment period published 

in the Federal Register on July 22, 2010 

entitled, ‘‘Medicare Program; 

Prospective Payment System and 

Consolidated Billing for Skilled Nursing 

Facilities for FY 2011.’’ 

DATES: Effective Date: This correction is 

effective October 1, 2010. 

FOR FURTHER INFORMATION CONTACT: Bill 

Ullman, (410) 786–5667. 

SUPPLEMENTARY INFORMATION: 

I. Background 

In FR Doc. 2010–17628 of July 22, 

2010 (75 FR 42886), there were several 

technical errors that are identified and 

corrected in the ‘‘Correction of Errors’’ 

section below. The corrections 

described below are effective as if they 

had been included in the document 

published on July 22, 2010. 

Accordingly, the corrections are 

effective October 1, 2010. 

II. Summary of Errors 

We are correcting the titles and wage 

index columns (along with the resulting 

values) of Tables 8A and 8B, which 

appeared on page 42911 of the July 22, 

2010 notice with comment period. 

These two tables illustrate the skilled 

nursing facility (SNF) prospective 

payment system (PPS) payment rate 

computations for a hypothetical ‘‘XYZ’’ 

SNF located in Cedar Rapids, IA (Urban 

CBSA 16300) under the RUG–IV and 

Hybrid RUG–III (HR–III) systems, 

respectively. In the title of the tables as 

well as in the third column (‘‘Wage 

Index’’), the wage index value for Cedar 

Rapids, IA is incorrectly displayed as 

0.8858. Accordingly, in section III of 

this document (‘‘Correction of Errors’’), 

we are revising the entries in Tables 8A 

and 8B to reflect the correct wage index 

value of 0.8844. We are similarly 

revising the immediately preceding 

portion of the preamble text, which 

references the total PPS payment 

amounts displayed in these two tables. 

However, we note that the 

corresponding entry for CBSA 16300, as 

it appears in an addendum to the July 

22, 2010 notice with comment period 

(Table A, ‘‘FY 2011 Wage Index for 

Urban Areas Based on CBSA Labor 

Market Areas’’), already reflects the 

correct wage index value of 0.8844 (75 

FR 42923). We are also revising the 

footnote that appears in Tables 8A and 

8B to clarify that in these examples, all 

10 of the Medicare days listed under the 

‘‘CC2’’ RUG group would involve a 

resident with AIDS and, thus, would 

qualify for the special 128 percent 

adjustment under section 511 of the 

Medicare Prescription Drug, 

Improvement, and Modernization Act of 

2003 (MMA) (Pub. L. 108–173, enacted 

on December 8, 2003). 

III. Correction of Errors 

In FR Doc. 2010–17628 (75 FR 42886), 

make the following corrections: 

1. On page 42910, third column, in 

line five from the bottom of the page, 

the phrase ‘‘$41,979 for RUG–IV and 

$36,517 for HR–III, respectively’’ is 

revised to read ‘‘$41,935 for RUG–IV and 

$36,479 for HR–III, respectively’’. 

2. On page 42911, Tables 8A and 8B 

are revised to read as follows: 

3. On page 42911, underneath Table 

8A and Table 8B, we removed the 

asterisk statement ‘‘*Reflects a 128 

percent adjustment from section 511 of 

the MMA’’ and replaced it with 

‘‘*Reflects a 128 percent adjustment 

from section 511 of the MMA. All CC2 

days should be considered to be for a 

resident with AIDS.’’ 


jlentini on DSKJ8SOYB1PROD with NOTICES