Organic compounds -- part of the class 532-570 series – Organic compounds – Carbohydrates or derivatives
Reexamination Certificate
2011-07-12
2011-07-12
Joike, Michele K (Department: 1636)
Organic compounds -- part of the class 532-570 series
Organic compounds
Carbohydrates or derivatives
C536S024100, C435S320100
Reexamination Certificate
active
07977468
ABSTRACT:
Tumor suppressor genes play a major role in the pathogenesis of human lung cancer and other cancers. Cytogenetic and allelotyping studies of fresh tumor and tumor-derived cell lines showed that cytogenetic changes and allele loss on the short arm of chromosome 3 (3p) are most frequently involved in about 90% of small cell lung cancers and greater than 50% of non-small cell lung cancers. A group of recessive oncogenes, Fus1, 101F6, Gene 21 (NPRL2), Gene 26 (CACNA2D2), Luca 1 (HYAL1), Luca 2 (HYAL2), PL6, 123F2 (RaSSFI), SEM A3 and Beta* (BLU), as defined by homozygous deletions in lung cancers, have been located and isolated at 3p21.3.
REFERENCES:
patent: 7144711 (2006-12-01), Cismowski et al.
patent: 2342470 (2002-09-01), None
patent: WO 98/16655 (1998-04-01), None
patent: WO 00/61626 (2000-10-01), None
patent: WO 02/076454 (2002-10-01), None
Clark et al. Polycations and cationic lipids enhance adenovirus transduction and transgene expression in tumor cells. Cancer Gene Ther. Sep.-Oct. 1999;6(5):437-46.
Dow et al. Lipid-DNA complexes induce potent activation of innate immune responses and antitumor activity when administered intravenously. J Immunol. Aug. 1, 1999;163(3):1552-61.
Brand et al. Targeted gene expression as a means of altering cell fates and generating dominant phenotypes. Development 118: 401-415, 1993.
Office communication issued in Australian Application No. 200127337, dated Jan. 27, 2006.
Bernues et al., “Analysis of 3p allelic losses in renal cell carcinomas: Comparison with cytogenetic results,”Cancer Genet Cytogenet; 107:121-124, 1998.
Buchhagen et al., “Two regions of homozygosity on chromosome 3p in squamous cell carcinoma of the head and neck: comparison with cytogenetic analysis,”Head&Neck, 18:529-537, 1996.
Burbee et al., “Epigenetic inactivation of RASSFIA in lung and breast cancers and malignant phenotype suppression,”J. Natl Cancer Inst., 93:691-699, 2001.
Daigo et al., “Molecular cloning of a candidate tumor suppressor gene, DLCI, from chromosome 3p21.31,”Canc. Research, 59:1966-1972, 1999.
Daly et al., “A homozygous deletion on chromosome 3 in small cell lung cancer cell line correlates with a region of tumor suppressive activity”,Oncogene8:1721-1729, 1993.
Dammann et al., “Epigenetic inactivation of a RAS association domain family protein from the lung tumour suppressor locus 3p21.3,”Nat Genet, 25:315-319, 2000.
Deng et al., “Synergistic tumor suppression by coexpression of FUS1 and p53 is associated with down-regulation of murine double minute-2 and activation of the apoptotic protease-activating factor 1-dependent apoptotic pathway in human non-small cell lung cancer cells,”Cancer Res., 67:709-717, 2007.
Dermer “Another anniversary for the war on cancer,” Bio/Technol., 12:320, 1994.
Duh et al., “A novel gene (Blu) that resides in the lung cancer region on chromosome 3p21.3 has the MYND Zn finger-like module—Human Blu protein (Blu) mRNA, completed cds,” Abstract, Database EMBL Sequence Library, Database Accession No. U70824, XP002207890, 1998.
Duh et al., “A novel gene (Blu) that resides in the lung cancer region on chromosome 3p21.3 has the MYND Zn finger-like module—Human Blu protein testis isoform (Blu) mRNA, complete cds,” Abstract, Database EMBL Sequence Library, Database Accession No. U70880, XP002207891, 1998.
Forgacs et al., “Mutation analysis of the PTEN/MMAC1 gene in lung cancer,”Oncogene, 17:1557-1565, 1998.
Gazdar et al., “Characterization of paired tumor and non-tumor cell lines established from patients with breast cancer,”Internatl J Cancer, 78:766-774, 1998.
Gazdar et al., “Molecular genetic changes found in human lung cancer and its precursor lesions,”Cold Spring Harbor Sym Quant Biol, 59:565-572, 1994.
Gorunova et al., “Cytogenetic analysis of pancreatic carcinomas: Intratumor heterogeneity and nonrandom pattern of chromosome aberrations,”Genes Chrom Cancer, 23:81-99, 1998.
Gromeier et al., “Viruses for the treatment of malignant glioma,”Curr. Opin. Mol. Ther., 3:503-508, 2001.
Gura, “Sytems for identifying new drugs are often faulty,”Science, 278:1041-1042, 1997.
Hibi et al., “Three distinct regions involved in 3p deletion in human lung cancer,”Oncogene, 7:445-449, 1992.
Hsieh et al., “Differential effects on growth, cell cycle arrest, and induction of apoptosis by resveratrol in human prostate cancer cell lines,”Exp. Cell Res., 249:109-115, 1999.
Hughson et al., “Clear-cell and papillary carcinoma of the kidney: An analysis of chromosome 3, 7, and 17 abnormalities by microsatellite amplification, cytogenetics, and fluorescence in situ hybridization,”Cancer Genet Cytogenet, 106:93-104, 1998.
Hung et al., “Allele-specific chromosome 3p deletions occur at an early stage in the pathogenesis of lung carcinoma,”JAMA, 273:558-563, 1995, Correction:JAMA, 273:1908, 1995.
Janmaat et al., “Response to epidermal growth factor receptor inhibitors in non-small cell lung cancer cells: limited antiproliferative effects and absence of apoptosis associated with persistent activity of extracellular signal-regulated kinase or Akt kinase pathways,”Clin. Cancer Res., 9:2316-2326, 2003.
Ji et al., “3p21.3 tumor suppressor cluster: prospects for translational applications,”Future Oncol., 1:79-92, 2005.
Kersemaekers et al., “Allelic loss and prognosis in carcinoma of the uterine cervix,”Internatl J Cancer, 79:411-417, 1998.
Killary and Fournier, “Microcell fusion,”Methods in Enzymology, 254:133-152, 1995.
Killary et al., “Definition of a tumor suppressor locus within a human chromosome 3p21-p22,”Proc. Natl. Acad. Sci., 89:10877-10881, 1992.
Kohno et al., “p53 mutation and allelic loss of chromosome 3p, 9p of preneoplastic lesions in patients with nonsmall cell lung carcinoma,”Cancer, 85:341-347, 1999.
Kok et al., “A homozygous deletion in a small cell lung cancer cell line involving a 3p21 region with a marked instability in yeast artificial chromosomes”,Cancer Res., 54:4183-4187, 1994.
Kok et al., “Deletion of a DNA sequence at the chromosomal region 3p21 in all major types of lung cancer,”Nature, 330:578-581, 1987.
Kok et al., “Deletions of the short arm of chromosome 3 in solid tumors and the search for suppressor genes,”Adv Cancer Res, 71:27-92, 1997.
Kondo et al., “Overexpression of candidate tumor suppressor gene FUS1 isolated from the 3p21.3 homozyogous deletion region leads to G1 arrest and growth inhibition of lung cancer cells,”Oncogene, 20:6258-6262, 2001.
Latif et al., “FUS1, a highly conserved gene, is located in the smalletst lung cancer region on 3p21.3—Homo sapiens lung cancer candidate FUS1 (FUS1) mRNA, complete cds,” GenBank Accession No. AF055479, 1998.
Lerman and Minna, “The 630-kb lung cancer homozygous deletion region on human chromosome 3p21.3: identification and evaluation of the resident candidate tumor suppressor genes,”Cancer Res, 60:6116-6133, 2000.
Lin et al., “Expression of several genes in the human chromosome 3p2I.3 homozygous deletion region by an adenovirus vector results in tumor suppressor activities in vitro and in vivo,”Cancer Research, 62:2715-2720, 2002.
Lu et al., “Systemic therapy with tumor suppressor FUS1-nanoparticles for stage IV lung cancer,” 2007 AACR Annual Meeting, Apr. 14-18, 2007 (Abstract No. LB-348).
Minna et al., “Cancer of the Lung: Section 1: Molecular Biology of Lung Cancer,” In: DeVita Jr., et al., (editors.)Cancer: Principles and Practice of Oncology. 5 ed. Philadelphia: Lippincott-Raven Publishers, 849-857, 1997.
Mizuguchi and Kay, “Efficient construction of a recombinant adenovirus vector by an improved in vitro ligation method,”Hum.Gene Therap., 9:2577-2583, 1998.
Nayl
Ji Lin
Lerman Michael
Minna John Dorrance
Roth Jack
Board of Regents of the University of Texas System
Fulbright & Jaworski L.L.P.
Joike Michele K
The United States of America as represented by the Department of
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