SOCS-1 gene methylation in cancer

Details SOCS-1 gene methylation in cancer SOCS-1 gene methylation in cancer

2008-03-25

2008-03-25

Yu, Misook (Department: 1642)

Chemistry: molecular biology and microbiology

Measuring or testing process involving enzymes or...

Involving nucleic acid

Reexamination Certificate

active

07348139

ABSTRACT:
Methods are provided for identifying a cell exhibiting unregulated growth associated with methylation-silenced transcription of a suppressor of cytokine signaling (SOCS)/cytokine-inducible SH2 protein (CIS) family member (SOCS/CIS) gene such as the SOCS-1 gene. In addition, methods of treating a cancer patient, wherein cancer cells in the patient exhibit methylation-silenced transcription of SOCS/CIS gene such as a SOCS-1 gene, are provided, as are reagents for practicing such methods.

REFERENCES:
patent: WO 99/03993 (1999-01-01), None
patent: WO 99/61614 (1999-12-01), None
patent: WO 00/75326 (2000-12-01), None
Bai et al., (Dec. 10, 2004, International journal of cancer, vol. 112 issue 5, p. 846-53).
Herman et al., (Sep. 1996, Proc. Nat. Acad. Sci. USA, vol. 93, pp. 9821-9826).
Pogribny et al (Sep. 7, 1999, Biochem Biophys Res Commun., vol. 262 issue 3, pp. 624-628).
Voet et al., (1990, Biochemistry, p. 831 only.)
Church et al., (1984, Proc. Natl. Acad. Sci. USA, vol. 81, pp. 1991-1995).
Rein et al (J. Biol. Chem. vol. 272, pp. 10021-10029).
Nagai et al., (Mar. 2001, J. Hepatol., vol. 34, pp. 416-421).
Baylin, Stephen B. et al., “Abnormal Patterns of DNA Methylation In Human Neoplasia: Potential Consequences for Tumor Progression,” Cancer Cells, vol. 3, No. 10, Oct. 1991, pp. 383-390.
Esteller, Manel et al., “Inactivation of the DNA Repair Gene06Methylguanine-DNA MethyltransferaseBy Promoter Hypermethylation Is a Common Event In Primary Human Neoplasia,” Cancer Research, vol. 59, Feb. 15, 1999, pp. 793-797.
Garcia, Roy et al., “Constitutive Activation of Stat3 In Fibroblasts Transformed by Diverse Oncoproteins and In Breast Carcinoma Cells,” Cell Growth & Differentiation, vol. 8, Dec. 1997, pp. 1267-1276.
Guillerm, Gaelle et al., “p16INK4aand p15INK4bGene Methylations In Plasma Cells from Monoclonal Gammapathy of Undetermined Significance,” Blood, vol. 98, No. 1, Jul. 1, 2001, pp. 244-246.
Herman, James G. et all., “Silencing of theVHLTumor-Suppressor Gene by DNA Methylation In Renal Carcinoma,” Proc. Natl. Acad. Sci. USA, vol. 91, Oct. 1994, pp. 9700-9704.
Herman, James G. et al., “Hypermethylation-Associated Inactivation Indicates a Tumor Suppressor Role for p15INK4B1,” Cancer Research, vol. 56, Feb. 15, 1996, pp. 722-727.
Herman, James G. et al., “Distinct Patterns of Inactivationf p15INK4band p16INK4ACharacterize the Major Types of Hematological Malignancies,” Cancer Research, vol. 57, Mar. 1, 1997, pp. 837-841.
InvivoGen, Suppressor of Cytokine Signaling (SOCS), www.invivogen.com/genedescription/socs.htm, Mar. 26, 2002 (date viewed/printed).
Kramer, Jeffery A. et al., “Extended Analysis of the Region Encompassing the PRM1→PRM2→TNP2 Domain: Genomic Organization, Evolution and Gene Identification,” The Journal of Experimental Zoology, vol. 282, 1998, pp. 245-253.
Makos, Michele, “DNA Hypermethylation Is Associated with 17p Allelic Loss In Neural Tumors,” Cancer Research, vol. 53, Jun. 15, 1993, pp. 2715-2718.
Makos, Michele et al., “Distinct Hypermethylation Patterns Occur at Altered Chromosome Loci In Human Lung and Colon Cancer,” Proc. Natl. Acad. Sci. USA, vol. 89, Mar. 1992, pp. 1929-1933.
Makos, Michele et al., “Regional DNA Hypermethylation at D17S5 Precedes 17p Structural Changes in the Progression of Renal Tumors,”Cancer Research, vol. 53, Jun. 15, 1993, pp. 2719-2722.
Margaret, H. et al., “Frequent Death-Associated Protein Kinase Promoter Hypermethylation In Multiple Myeloma,” Clinical Cancer Research, vol. 7, Jun. 2001, pp. 1724-1729.
Masuhara, Masaaki et al., “Cloning and Characterization of Novel CIS Family Genes,” Biochemical and Biophysical Research Communications, vol. 239, Article No. RC977484, 1997, pp. 439-446.
Nagai, Hisaki et al., “Aberration of Genomic DNA in Association with Human Hepatocellular Carcinomas Detected by 2-Dimensional Gel Analysis,” Cancer Research, vol. 54, Mar. 15, 1994, pp. 1545-1550.
Naka, Tetsuji et al., “Structure and Function of a New STAT-Induced STAT Inhibitor,” Nature, vol. 387, Jun. 26, 1997, pp. 924-929.
Starr, Robyn et al., “A Family of Cytokine-Inducible Inhibitors of Signalling,” Nature, vol. 387, Jun. 26, 1997, pp. 917-921.
Yoshikawa, Hirohide et al., “Chromosome Assignment of AberrantNotI Restriction DNA Fragments In Primary Hepatocellular Carcinoma,” Gene, vol. 197, 1997, pp. 129-135.
Yoshikawa, Hirohide et al., “SOCS-1, A Negative Regulator of the JAK/STAT Pathway, Is Silenced By Methylation In Human Hepatocellular Carcinoma and Shows Growth-Suppression Activity,” Nature Genetics, vol. 28, May 2001, pp. 29-35.
Yoshikawa et al., “SOCS-1, a negative regulator of the JAK/STAT pathway, is silenced by methylation in human hepatocellular carcinoma and shows growth-suppression activity”Nature Genetics28:29-35 (2001).
Bender et al., “DNA Methylation as a Target for Drug Design”,Pharmaceutical Research15(2):175-187 (1998).

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