National Institutes of Health, DHHS.
The inventions listed below are owned by agencies 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.
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.
XAGE-1, A Gene Expressed in Multiple Cancers and Uses Thereof
Drs. Ira H. Pastan (NCI), Xiu F. Liu (NCI), Byungkook Lee (NCI) and Lee J. Helman (NCI)
DHHS Ref. No. E-161-00/0 (Provisional Application) filed September 1, 2000 and E-161-00/1 (PCT Application) filed August 31, 2001
Licensing Contact: Richard Rodriguez; 301/496-7056 ext. 287; e-mail: email@example.com.
The XAGE-1 gene is a human X-linked gene that is strongly expressed in breast cancer, lung cancer and several other cancers as well as normal testes. The largest open reading frame of the XAGE-1 transcript encodes a putative protein of 16.3 kD (p16) with a potential transmembrane domain at the amino terminus. In addition, the XAGE-1 transcript contains a second ATG in the reading frame corresponding to residue 66, which would encode a 9 kD protein (p9). In vitro transfection experiments using 293 T cells have revealed a 9 kD protein. However, the size of the endogenously expressed protein is not yet known. XAGE-1 shares homology with GAGE/PAGE proteins in the C-terminal end. Start Printed Page 336
The invention relates to the fact that the XAGE-1 gene is expressed in a number of human cancers, specifically: breast, lung, prostate, pancreatic, and ovarian cancers. The proteins p9 and p16, immunogenic fragments thereof, analogs of these proteins, and nucleic acids encoding these proteins, fragments, or analogs, can be administered to persons with XAGE-1 expressing cancers to raise or augment an immune response to the cancer. The invention further provides nucleic acid sequences encoding the protein, as well as expression vectors, host cells, and antibodies to the proteins. Further, the invention provides immunoconjugates that comprise an antibody to p16 or to p9, and an effector molecule, such as a label, a radioisotope, or a toxin. The invention also provides methods of inhibiting the growth of XAGE-1 expressing cells by contacting them with immunoconjugates of an anti-p9 or p16 antibody and a toxic moiety. The invention also provides kits for the detection of p9 or p16 proteins in a sample. The XAGE-1 gene and encoded protein could be of value in the development of a cancer diagnostic and/or a cancer immunotherapy.
The above mentioned invention is available for licensing on an exclusive or non-exclusive basis.
Histone Deacetylase Inhibitors in Diagnosis and Treatment of Thyroid Neoplasms
Tito A. Fojo and Susan Bates (NCI)
DHHS Reference No. E-286-00/0 filed 10 Jan 2001
Licensing Contact: Matthew Kiser; 301/496-7056 ext. 224; e-mail: firstname.lastname@example.org.
The invention disclosed are novel approaches to thyroid cancer therapy. These approaches include methods to enhance thyroid specific gene expression, for example methods to enhance expression of thyroglobulin and/or the Na/I symporter in thyroid cancer cells. Enhanced expression of thyroid-specific genes promotes cellular differentiation and reduces biologically aggressive behavior such as invasion and metastasis. In addition, enhanced expression of thyroglobulin and/or the Na/I symporter increases the ability of thyroid cancer cells to concentrate iodine, thereby making the cells more susceptible to radioactive iodine therapy. Also disclosed are methods for detecting thyroid neoplasms in a subject, by administering a therapeutically effective amount of a histone deacetylase inhibitor, administering a detectable agent whose uptake or concentration in thyroid cells is increased by administration of the histone deacetylase inhibitor, and detecting the detectable agent.Start Signature
Dated: December 20, 2001.
Director, Division of Technology, Development and Transfer, Office of Technology Transfer, National Institutes of Health.
[FR Doc. 02-11 Filed 1-2-02; 8:45 am]
BILLING CODE 4140-01-P