Chemistry: molecular biology and microbiology – Measuring or testing process involving enzymes or... – Involving nucleic acid
Reexamination Certificate
2004-03-17
2009-02-03
Horlick, Kenneth R. (Department: 1637)
Chemistry: molecular biology and microbiology
Measuring or testing process involving enzymes or...
Involving nucleic acid
C435S091200
Reexamination Certificate
active
07485418
ABSTRACT:
The present invention provides a method for detecting pancreatic carcinoma in a subject. The method includes contacting a nucleic acid-containing specimen from the subject with an agent that provides a determination of the methylation state of at least one gene or associated regulatory region of the gene and identifying aberrant methylation of regions of the gene or regulatory region, wherein aberrant methylation is identified as being different when compared to the same regions of the gene or associated regulatory region in a subject not having the pancreatic carcinoma, thereby detecting pancreatic carcinoma in the subject.
REFERENCES:
patent: 4683195 (1987-07-01), Mullis et al.
patent: 4683202 (1987-07-01), Mullis et al.
patent: 4800159 (1989-01-01), Mullis et al.
patent: 5786146 (1998-07-01), Herman et al.
patent: 6017704 (2000-01-01), Herman et al.
patent: 6200756 (2001-03-01), Herman et al.
patent: 6265171 (2001-07-01), Herman et al.
patent: 6953783 (2005-10-01), Besterman et al.
patent: 7153653 (2006-12-01), Goggins et al.
Ueki et al. Hypermethylation of multiple genes in pancreatic adenocarcinoma. Cancer Res. (2000) 60:1835-1839.
Fukushima et al. Diagnosing pancreatic cancer using methylation specific PCR analysis of pancreatic juice. Cancer Biol. Therapy (2003) 2:78-83.
Han et al. Identification of differently expressed genes in pancreatic cancer cells using cDNA microarray. Cancer Res. (2002) 62:2890-2896.
Bittencourt Rosas et al. Methylation status in the promoter region of the human PGP9.5 gene in cancer and normal tissues. Cancer Lett. (2001) 170:73-79.
Tezel et al. PGP9.5 as a prognostic factor in pancreatic cancer. Clin Cancer Res. (2000) 6:4764-4767.
Antequera et al., “Number of CpG Islands and Genes in Human and Mouse,”Proc Natl Acad Sci USA, 90:11995-11999 (1993).
Baylin et al., “Abnormal Patterns of DNA Methylation in Human Neoplasia: Potential Consequences for Tumor Progression,”Cancer Cells, 3:383-390 (1991).
Baylin et al., “Alterations in DNA Methylation: A Fundamental Aspect of Neoplasia,”Adv Cancer Res, 72:141-196 (1998).
Belinsky et al., “Aberrant Methylation ofp16INK4ais an Early Event in Lung Cancer and a Potential Biomarker for Early Diagnosis,”Proc Natl Acad Sci USA, 95:11891-11896 (1998).
Costello et al., “Aberrant CpG-Island Methylation Has Non-Random and Tumor-Type-Specific Paterns,”Nat Genet, 25:132-138 (2000).
De Bustros et al., “The Short Arm of Chromosome 11 is a “Hot Spot” for Hypermethylation in Human Neoplasia,”Proc Natl Acad Sci USA, 85:5693-5697 (1988).
El-Osta et al., “Precipitous Release of Methyl-CpG Binding Protein 2 and Histone Deacetylase 1 from the Methylated Human Multidrug Resistane Gene (MDR1) on Activation,”Mol Cell Biol, 22:1844-1857 (2002).
Fearon and Vogelstein et al., “A Genetic Model for Colorectal Tumorigenesis,”Cell, 61:759-767 (1990).
Fukushima et al., “Aberrant Methylation of Suppresor of Cytokine Signalling-1 (SOCS-1) Gene in Pancreatic Ductal Neoplasms,”Br J Cancer, 89:338-343 (2003).
Goggins et al., “Progress in Cancer Genetics: Lessons in Pancreatic Cancer,”Ann Oncol, 10:4-8 (1999).
Graff et al., “E-Cadherin Expression Is Silenced by DNA Hypermethylation in Human Breast and Protate Carcinomas,”Cancer Res, 55:5195-5199 (1995).
Hedrick et al., “Isolation of cDNA Clones Encoding T Cell-Specific Membrane-Associated Proteins,”Nature, 308:149-153 (1984).
Herman et al., “Silencing of theVHLTumor-Suppressor Gene by DNA Methylation in Renal Carcinoma,”Proc Natl Acad Sci USA, 91:9700-9704 (1994).
Herman et al., “Inactivation of the CDKN2/p16/MTS1 Gene Is Frequently Associated with Aberrant DNA Methylation in all Human Cancers,”Cancer Res, 55:4525-4530 (1995).
Herman et al., “Hypermethylation-Associated Inactivation Indicates a Tumor Suppressor Role forp15INK4B1,” Cancer Res, 65:722-727 (1996).
Herman et al., “Methylation-Specific PCR: A Novel PCR Assay for Methylation Status of CpG Islands,”Proc Natl Acad Sci USA, 93:9821-9826 (1996).
Holliday, Robin, “The Inheritance of Epigenetic Defects,”Science, 238:163-170 (1987).
Iacobuzio-Donahue et al., “Exploration of Global Gene Expression Patterns in Pancreatic Adenocarcinoma Using cDNA Microarrays,”Am J Path, 162:1151-1162 (2003).
Issa et al., “Methylation of the Oestrogene Receptor CpG Island Links Ageing and Neoplasia in Human Colon,”Nature Gen, 7:536-540 (1994).
Jansen et al., “Aberrant Mehylation of the 5′ CpG Island of TSLC1 Is Common in Pancreatic Ductal Adenocarcinoma and Is First Manifest in High-Grade PanINs,”Cancer Biol&Ther, 1:293-296 (2002).
Jones, Peter A., “DNA Methylation and Cancer,”Cancer Res, 46:461-466 (1986).
Jones and Buckley, “The Role of DNA Methylation in Cancer,”Adv Cancer Res, 54:1-23 (1990).
Lisitsyn et al., “Cloning the Differences Between Two Complex Genomes,”Science, 259:946-951 (1993).
Makos et al., “Distinct Hypermethylation Patterns Occur at Altered Chromosome Loci in Human Lung and Colon Cancer,”Proc Natl Acad Sci USA, 89:1929-1933 (1992).
Matsubayashi et al., “Methylation of Cyclin D2 Is Observed Frequently in Pancreatic Cancer but Is also an Age-Related Phenomenon in Gastrointestinal Tissues,”Clin Cancer Res, 9:1446-1452 (2003).
Matsubayashi et al., “DNA Methylation Alterations in the Pancreatic Juice of Patients with Suspected Pancreatic Disease,”Cancer Res, 66:1208-1217 (2006).
Merlo et al., “5′ CpG Island Methylation Is Associated with Transcriptional Silencing of the Tumor Suppressor p16/CDKN2/MTS1 in Human Cancers,”Nature Med, 1:686-692 (1995).
Ohtani-Fujita et al., “CpG Methylation Inactivates the Promoter Activity of the Human Retinoblastoma Tumor-Suppressor Gene,”Oncogene, 8:1063-1067 (1993).
Rozenblum et al., “Tumor-Suppressive Pathways in Pancreatic Carcinoma,”Cancer Res, 57:1731-1734 (1997).
Sakai et al., “Allele-Specific Hypermethylation of the Retinoblastoma Tumor-Suppressor Gene,”Am J Hum Genet, 48:880-888 (1991).
Sato et al., “Discovery of Novel Targets for Aberrant Methylation in Pancreatic Carcinoma Using High-Throughput Microarray,”Cancer Res, 63:3735-3742 (2003).
Sato et al., “Aberrant Methylation ofReprimoCorrelates with Genetic Instability and Predicts Poor Prognosis in Pancreatic Ductal Adenocarcinoma,”Cancer, 107:251-257 (2006).
Sato and Goggins, “The Role Epigenetic Alterations in Pancreatic Cancer,”J HepatobiliaryPancreat Surg, 13:286-295 (2006).
Suzuki et al., “A Genomic Screen for Genes Upregulated by Demethylation and Histone and Deacetylase Inhibition in Human Colorectal Cancer,”Nature Gen, 31:141-149 (2002).
Toyota et al., “Identification of Differentially Methylated Sequences in Colorectal Cancer by Methylated CpG Island Amplification,”Cancer Res, 59:2307-2312 (1999).
Ueki et al., “Identification and Characterization of Differentially Methylated CpG Islands in Pancreatic Carcinoma,”Cancer Res, 61:8540-8546 (2001).
Ueki et al., “Aberrant CpG Island Methylation in Cancer Cell Lines Arises in the Primary Cancers from with they were Derived,”Oncogene, 21:2114-2117 (2002).
Cameron et al., “Synergy of Demethylation and History Deacetylase Inhibition in the Re-Expression of Genes Silenced in Cancer”,Nature Genetics, 21:103-107 (1999).
Goggins Michael G.
Sato Norihiro
DLA Piper (LLP) US
Horlick Kenneth R.
The Johns Hopkins University
Thomas David C
LandOfFree
Aberrantly methylated genes in pancreatic cancer does not yet have a rating. At this time, there are no reviews or comments for this patent.
If you have personal experience with Aberrantly methylated genes in pancreatic cancer, we encourage you to share that experience with our LandOfFree.com community. Your opinion is very important and Aberrantly methylated genes in pancreatic cancer will most certainly appreciate the feedback.
Profile ID: LFUS-PAI-O-4083006