Federal Register / Vol. 73, No. 193 / Friday, October 3, 2008 / Notices 57635 

DEPARTMENT OF HEALTH AND 

HUMAN SERVICES 

National Institutes of Health 

Submission for OMB Review; 

Comment Request: The National 

Survey of Physicians Attitudes 

Regarding the Care of Cancer 

Survivors (SPARCCS) (NCI) 

SUMMARY: Under the provisions of 

Section 3507(a)(1)(D) of the Paperwork 

Reduction Act of 1995, the National 

Cancer Institute (NCI), the National 

Institutes of Health (NIH), has submitted 

to the Office of Management and Budget 

(OMB) a request to review and approve 

the information collection listed below. 

This proposed information collection 

was previously published in the Federal 

Register on July 31, 2008 (Vol. 73, No. 

148, p. 44751) and allowed 60-days for 

public comment. There were no public 

comments received. The purpose of this 

notice is to allow an additional 30 days 

for public comment. The National 

Institutes of Health may not conduct or 

sponsor, and the respondent is not 

required to respond to, an information 

collection that has been extended, 

revised, or implemented on or after 

October 1, 1995, unless it displays a 

currently valid OMB control number. 

Proposed Collection: Title: NIH– 

Survey of Physicians Attitudes 

Regarding the Care of Cancer Survivors 

(SPARCCS). Type of Information 

Collection Request: New. Need and Use 

of Information Collection: The purpose 

of this study is to identify the beliefs, 

knowledge, attitudes, and practices of 

primary care physicians and cancer 

specialists regarding the components 

described by the IOM. These data will 

inform the process of standardization of 

survivorship care practices; augment the 

data collected in other cancer 

survivorship studies and monitor the 

progress being made toward achieving 

NCI strategic goals of improving the 

quality of cancer care across the cancer 

control continuum. This questionnaire 

adheres to The Public Health Service 

Act, Section 412 (42 U.S.C. 285a–1) and 

Section 413 (42 U.S.C. 285a–2), which 

authorizes the Division of Cancer 

Control and Population Sciences of the 

National Cancer Institute (NCI) to 

establish and support programs for the 

detection, diagnosis, prevention and 

treatment of cancer; and to collect, 

identify, analyze and disseminate 

information on cancer research, 

diagnosis, prevention and treatment. 

Frequency of Response: Once. Affected 

Public: Individuals and Businesses. 

Type of Respondents: Primary care and 

medical oncology physicians practicing 

in a non-federal facility. The annual 

reporting burden is estimated at 904 

hours as shown in Table 1. The total 

burden hours is estimated at 1808 hours 

over the two year field period of the 

study. There is no capital, operating or 

maintenance costs to report. 

TABLE 1—ESTIMATES OF ANNUAL BURDEN HOURS

Type of 

respondents Survey Number of respondents 

Frequency of 

response 

Average time 

per response 

(minutes/hour) 

Annual burden 

hours 

Receptionists ............................................. Screener .................. 2,033 1 5/60 169 

Family Practice .......................................... PCP Instrument ....... 250 1 20/60 83 

General Internists ...................................... PCP Instrument ....... 250 1 20/60 83 

OB/GYNs ................................................... PCP Instrument ....... 50 1 20/60 17 

Oncologists ................................................ Oncology Instrument 550 1 20/60 183 

Receptionists & Administrators .................. Follow-Up Phone 

Calls.

1,103 4 5/60 368 

Total .................................................... .................................. 4,236 ............................ ............................ 904 

Request for Comments: Written 

comments and/or suggestions from the 

public and affected agencies are invited 

on one or more of the following points: 

(1) Whether the proposed collection of 

information is necessary for the proper 

performance of the function of the 

agency, including whether the 

information will have practical utility; 

(2) The accuracy of the agency’s 

estimate of the burden of the proposed 

collection of information, including the 

validity of the methodology and 

assumptions used; (3) Ways to enhance 

the quality, utility, and clarity of the 

information to be collected; and (4) 

Ways to minimize the burden of the 

collection of information on those who 

are to respond, including the use of 

appropriate automated, electronic, 

mechanical, or other technological 

collection techniques or other forms of 

information technology. 

Direct Comments To OMB: Written 

comments and/or suggestions regarding 

the item(s) contained in this notice, 

especially regarding the estimated 

public burden and associated response 

time, should be directed to the 

Attention: NIH Desk Officer, Office of 

Management and Budget, at 

OIRA_submission@omb.eop.gov or by 

fax to 202–395–6974. To request more 

information on the proposed project or 

to obtain a copy of the data collection 

plans and instruments, contact Arnie 

Potosky, Ph.D., Task Order Monitor, 

Applied Research Branch, Division of 

Cancer Control and Population 

Sciences, National Cancer Institute, 

National Institutes of Health, Bethesda, 

Maryland, 20892–7344, or call non-tollfree number (301)402–3362 or e-mail 

your request, including your address to: 

potoskya@mail.nih.gov. 

Comments Due Date: Comments 

regarding this information collection are 

best assured of having their full effect if 

received within 30 days of the date of 

this publication. 

Dated: August 23, 2008. 

Vivian Horovitch-Kelley, 

NCI Project Clearance Liaison Office, 

National Institutes of Health. 

[FR Doc. E8–23443 Filed 10–2–08; 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 

mstockstill on PROD1PC66 with NOTICES

57636 Federal Register / Vol. 73, No. 193 / Friday, October 3, 2008 / Notices 

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. 

Matriptase Hypomorphic Mouse Model 

of a Human Ichthyosis 

Description of Technology: Available 

for licensing are mice with greatly 

reduced levels of matriptase, a 

membrane protease involved in 

epithelial development, immune 

function, and carcinogenesis. These 

mice were created to study autosomal 

recessive ichthyosis with hypotricosis 

(ARIH), an inherited human disease that 

has been linked to a mutation in the 

ST14 gene that encodes matriptase. 

These mice manifest the same defects 

seen in people afflicted by ARIH, so it 

can be an effective model for studying 

the role of matriptase in disorders that 

affect skin development. 

Applications: 

• Research tool for skin development 

research. 

• Model to develop and test 

therapeutics for treating skin disorders, 

including skin cancer. 

• Model immunity and allergy. 

Advantages: Well characterized 

animal model closely related to a 

human genetic disorder. 

Market: Ichthyosis is a series of 

genetic skin diseases characterized by 

dry, thickened, scaling skin that affects 

more than one million Americans. 

Presently, there is no cure for 

ichthyosis, only treatments to help 

manage symptoms. 

Development Status: Well 

characterized mouse model of human 

ARIH. 

Inventors: Thomas H. Bugge (NIDCR) 

et al. 

Publication: K List et al. Autosomal 

ichthyosis with hypotrichosis syndrome 

displays low matriptase proteolytic 

activity and is phenocopied in ST14 

hypomorphic mice. J Biol Chem. 2007 

Dec 14;282(50):36714–36723. 

Patent Status: HHS Reference No. E– 

323–2008/0—Biological Material. Patent 

protection is not being pursued for this 

technology. 

Licensing Status: Available for nonexclusive licensing under a Biological 

Materials License Agreement. 

Licensing Contact: Adaku 

Nwachukwu, J.D.; 301–435–5560; 

madua@mail.nih.gov. 

Collaborative Research Opportunity: 

The National Institute of Dental and 

Craniofacial Research, Oral and 

Pharyngeal Cancer Branch, is seeking 

statements of capability or interest from 

parties interested in collaborative 

research to further develop, evaluate, or 

commercialize this technology. Please 

contact David W. Bradley, Ph.D. at 301– 

402–0540 or bradleyda@nidcr.nih.gov 

for more information. 

Prostatic Adenocarcinoma Cells 

Expressing or Lacking the Tumor 

Suppressor Gene PTEN 

Description of Technology: PTEN is a 

tumor suppressor gene that is frequently 

deleted or mutated in a variety of 

human cancers, including prostate, 

breast, endometrial, lung, and ovarian 

cancers. In prostate cancer cells, PTEN 

deletion is the most common event 

observed. The loss of PTEN is thought 

to play and important role in tumor cell 

proliferation and metastasis due to a 

lack of control of the signaling pathways 

that mediate cellular processes such as 

apoptosis and migration. Previously 

PTEN had been shown to downregulate 

cyclin D1 expression as well as regulate 

p53 protein levels and transcriptional 

activity, and recently the inventors of 

this technology have shown that PTEN 

decreases surface IGF–IR protein levels 

in prostate cancer cell lines in an Aktindependent manner. 

PC3 cells are prostate cancer cells that 

lack PTEN gene. This technology 

describes PC3 cells that overexpress the 

PTEN gene. These cell lines can be used 

to study the role of the PTEN gene in 

cancer growth and metastasis. 

Market: 

• Prostate cancer is the most common 

type of cancer found in American men, 

and it has been estimated that there 

were more than 230,000 new cases in 

the U.S. in 2007. Prostate cancer is also 

the second leading cause of cancer 

death in men. 

• In the U.S. over 2 million women 

have been treated for breast cancer, with 

more than 200,000 women diagnosed in 

the year 2007 alone. Breast cancer is the 

second leading cause of cancer death in 

women. 

Development Status: The technology 

is currently in the pre-clinical stage of 

development. 

Inventors: Derek LeRoith and Michael 

Quon (NIDDK). 

Publication: H Zhao et al. PTEN 

inhibits cell proliferation and induces 

apoptosis by downregulating cell 

surface IGF–IR expression in prostate 

cancer cells. Oncogene 2004 Jan 

22;23(3):786–794. 

Patent Status: HHS Reference No. E– 

292–2008/0—Research Tool. Patent 

protection is not being pursued for this 

technology. 

Licensing Status: Available for 

licensing. 

Licensing Contact: Whitney A. 

Hastings; 301–451–7337; 

hastingw@mail.nih.gov. 

Fully Human Anti-Human NKG2D 

Monoclonal Antibody 

Description of Technology: Available 

for licensing is a fully human 

monoclonal antibody (KYK–2.0 IgG1) 

with high specificity and affinity to 

human NKG2D, a stimulatory or 

costimulatory receptor located on the 

cell surface of natural killer (NK) cells 

and CD8+ T cells. NKG2D plays a role 

in mediating immune responses in 

autoimmune and infectious diseases 

and cancer and it makes NKG2D an 

attractive target for therapeutic 

intervention. Nonetheless, monoclonal 

antibodies to NKG2D that are suitable 

for clinical investigations have not been 

available. In solution, KYK–2.0 IgG1 

interferes with the cytolytic activity of 

human NK cells. When immobilized, 

KYK–2.0 IgG1 induces human NK cell 

activation. The dual antagonistic and 

agonistic activity promises a broad 

range of therapeutic applications. 

Application: Therapeutic fully human 

monoclonal antibody for a variety of 

indications including autoimmune and 

infectious diseases, cancer, and 

transplantation. 

Advantage: The dual antagonistic and 

agonistic activity in concert with low 

immunogenicity suggests broad and 

potent therapeutic utility of KYK–2.0 

IgG1 and its derivatives. 

Development Status: The technology 

is currently in the pre-clinical stage of 

development. 

Market: 

• Monoclonal antibody market is one 

of the fastest growing and most lucrative 

sectors of the pharmaceutical industry 

with a 48.1% growth between 2003 and 

2004. 

• Monoclonal antibody market is 

estimated to be worth $30.3 billion in 

2010. 

Inventors: Christoph Rader and Ka 

Yin Kwong (NCI) 

Related Publication: KY Kwong, S 

Baskar, H Zhang, CL Mackall, C Rader. 

Generation, affinity maturation, and 

characterization of a human anti-human 

NKG2D monoclonal antibody with dual 

antagonistic and agonistic activity. J Mol 

mstockstill on PROD1PC66 with NOTICES

Federal Register / Vol. 73, No. 193 / Friday, October 3, 2008 / Notices 57637 

Biol., in press (available online 2008 

Sep 16, doi:10.1016/j.jmb.2008.09.008). 

Patent Status: U.S. Provisional 

Application No. 61/086,027 filed 04 

Aug 2008 (HHS Reference No. E–211– 

2008/0–US–01). 

Licensing Status: Available for 

exclusive or non-exclusive licensing. 

Licensing Contact: Jennifer Wong; 

301–435–4633; wongje@mail.nih.gov. 

Collaborative Research Opportunity: 

The Experimental Transplantation and 

Immunology Branch, Center for Cancer 

Research, National Cancer Institute is 

seeking statements of capability or 

interest from parties interested in 

collaborative research to further 

develop, evaluate, or commercialize the 

fully human anti-human NKG2D 

monoclonal antibody KYK–2.0 IgG1. 

Please contact John D. Hewes, Ph.D. at 

301–435–3121 or hewesj@mail.nih.gov 

for more information. 

Methods for the Detection and 

Treatment of Lung Cancer 

Description of Technology: Lung 

cancer is the third most common 

malignant disease and the first leading 

cause of cancer death in the western 

world. Non-small cell lung cancer 

(NSCLC) is one of the leading causes of 

death accounting for nearly 30% of all 

cancer deaths. Despite considerable 

research, lung cancer remains difficult 

to diagnose and treat effectively. Current 

chemotherapeutic regimens provide 

poor survival benefits and the unmet 

clinical need among lung cancer 

patients is very high. The prognosis is 

very bleak since most patients are 

diagnosed with lung cancer at a late 

stage. 

The inventors have discovered that 

approximately 20% of common adult 

NSCLC have an aberrant activation of 

CRTC gene members with marked 

induction of CRTC regulated genes. 

CRTC activation is linked with the loss 

of LKB1/STK11 kinases which results in 

CRTC underphosphorylation and 

enhanced nuclear localization. As the 

LKB1/STK11 signaling pathways has 

been exploited in potential cancer 

therapeutic treatments, this novel 

unrecognized consequence the loss of 

LKB1/STK11 function associated with 

aberrant CRTC activation in cancer 

offers new candidate diagnostic and 

therapeutic targets for NSCLC. 

Applications: 

• Novel cancer diagnostics and 

therapeutic treatments. 

• Method to detect and treat lung 

cancer. 

Development Status: The technology 

is currently in the pre-clinical stage of 

development. 

Market: 

• Lung cancer is the leading cause of 

cancer deaths among both men and 

women in the U.S. 

• The NSCLC market was estimated 

to be worth US$3.7 billion in 2006 and 

will increase by 17% by 2012. 

Inventors: Frederic Kaye and Amy 

Coxon (NCI). 

Patent Status: U.S. Provisional 

Application No.61/036,830 filed 13 Mar 

2008 (HHS Reference No. E–069–2008/ 

0–US–01). 

Licensing Status: Available for 

exclusive or non-exclusive licensing. 

Licensing Contact: Jennifer Wong; 

301–435–4633; wongje@mail.nih.gov. 

Human Perilipin Proteins 

Description of Technology: Perilipins 

are important regulators of lipid storage 

in fat cells. These proteins stabilize fat 

droplets and control their breakdown by 

controlling access of lipid-degrading 

enzymes. Since these proteins are 

central to the storage and breakdown of 

body fat it very likely that they are 

crucial for the regulation of body 

weight. Perilipin expression is elevated 

in obese animals and humans. 

Mutations in the perilipin gene are 

associated with increased risk of obesity 

in women. Importantly, when the 

perilipin gene is inactivated the obesity 

of model mice is reversed. Therefore, 

perilipin could be a good candidate for 

therapeutic targeting to treat obesity in 

humans. 

This NIH invention claims DNA 

sequences of splice variants that code 

for human perilipin protein isoforms 

and methods of expressing the 

recombinant protein in bacteria or 

mammalian cells. It also claims 

substantially purified perilipin proteins 

and methods for detecting their 

presence in a biological sample. 

Applications: 

• Drug development for obesity. 

• Diagnostics for detection of 

perilipins. 

• Antigens for antibody production. 

• Markers for identifying true 

adipocytes. 

Advantages: 

• Cloned DNA sequences ready for 

protein expression. 

• Isoforms allow greater flexibility in 

designing therapeutics. 

Development Status: Pre-clinical. 

Inventors: Constantine Londos, 

Andrew S. Greenberg, Alan R. Kimmel, 

John J. Egan (NIDDK). 

Related Publication: AS Greenberg et 

al. Perilipin, a major hormonally 

regulated adipocyte-specific 

phosphoprotein associated with the 

periphery of lipid storage droplets. J 

Biol Chem. 1991 Jun 15;266(17):11341– 

11346. 

Patent Status: 

• U.S. Patent No. 6,074,842 issued 13 

Jun 2000 (HHS Reference No. E–111– 

1991/0–US–03). 

• U.S. Patent No. 5,585,462 issued 17 

Dec 1996 (HHS Reference No. E–111– 

1991/1–US–01). 

Licensing Status: Available for 

exclusive or non-exclusive licensing. 

Licensing Contact: Surekha Vathyam, 

PhD; 301–435–4076; 

vathyams@mail.nih.gov. 

Dated: September 29, 2008. 

Richard U. Rodriguez, 

Director, Division of Technology Development 

and Transfer, Office of Technology Transfer, 

National Institutes of Health. 

[FR Doc. E8–23436 Filed 10–2–08; 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. 

Murine Monoclonal Antibodies 

Effective To Treat Respiratory 

Syncytial Virus 

Description of Technology: Available 

for licensing through a Biological 

Materials License Agreement are the 

murine MAbs described in Beeler et al, 

‘‘Neutralization epitopes of the F 

glycoprotein of respiratory syncytial 

virus: effect of mutation upon fusion 

function,’’ J Virol. 1989 Jul;63(7):2941– 

mstockstill on PROD1PC66 with NOTICES