Polymerase chain reaction-based identification of insecticide resistance genes and DNA methylation in the aphid Myzus persicae (Sulzer)

1996 ◽  
Vol 5 (3) ◽  
pp. 197-202 ◽  
Author(s):  
L. M. Field ◽  
S. E. Crlck ◽  
A. L. Devonshire
Keyword(s):  
Dna Methylation ◽  
Polymerase Chain Reaction ◽  
Insecticide Resistance ◽  
Resistance Genes ◽  
Myzus Persicae ◽  
Chain Reaction ◽  
Polymerase Chain

Expression and mutational analysis of Cip/Kip family in early glottic cancer

2015 ◽  
Vol 129 (2) ◽  
pp. 168-173 ◽  
Author(s):  
D-K Kim ◽  
J H Lee ◽  
O J Lee ◽  
C H Park
Keyword(s):  
Dna Methylation ◽  
Polymerase Chain Reaction ◽  
Kinase Inhibitors ◽  
Mutational Analysis ◽  
Glottic Cancer ◽  
Cyclin Dependent Kinase ◽  
Chain Reaction ◽  
Single Strand Conformational Polymorphism ◽  
Early Glottic Cancer ◽  
Polymerase Chain

AbstractBackground:Genetic alteration of cyclin-dependent kinase inhibitors has been associated with carcinogenesis mechanisms in various organs.Objective:This study aimed to evaluate the expression and mutational analysis of Cip/Kip family cyclin-dependent kinase inhibitors (p21CIP1/WAF1, p27KIP1 and p57KIP2) in early glottic cancer.Methods:Expressions of Cip/Kip family and p53 were determined by quantitative reverse transcription polymerase chain reaction and densitometry. For the analysis of p21 inactivation, sequence alteration was assessed using single-strand conformational polymorphism polymerase chain reaction. Additionally, the inactivation mechanism of p27 and p57 were investigated using DNA methylation analysis.Results:Reduced expression of p27 and p57 were detected in all samples, whereas the expression of p21 was incompletely down-regulated in 6 of 11 samples. Additionally, single-strand conformational polymorphism polymerase chain reaction analysis showed the p53 mutation at exon 6. Methylation of p27 and p57 was detected by DNA methylation assay.Conclusion:Our results suggest that the Cip/Kip family may have a role as a molecular mechanism of carcinogenesis in early glottic cancer.

scholarly journals Pilot study of DNA methylation in the pathogenesis of chronic rhinosinusitis with nasal polyps

2015 ◽  
Vol 53 (4) ◽  
pp. 345-352
Author(s):  
Y.B. Zheng ◽  
Y. Zhao ◽  
L.Y. Yue ◽  
P. Lin ◽  
Y.F. Liu ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Polymerase Chain Reaction ◽  
Chronic Rhinosinusitis ◽  
Nasal Polyps ◽  
Cpg Islands ◽  
Inferior Turbinate ◽  
Control Group ◽  
Chain Reaction ◽  
Bisulphite Sequencing ◽  
Polymerase Chain

Background: DNA methylation has been implicated in the pathogenesis of allergy and atopy. This study aimed to identify whether DNA methylation also plays an important role in the pathogenesis of nasal polyps (NP). Methodology: NP tissues were obtained from 32 patients with chronic rhinosinusitis with bilateral NP. Biopsies of inferior turbinate mucosa (ITM) were taken from 18 patients who underwent rhinoseptoplasty (control group). The methylated genes, which were detected by DNA methylation microarray, were validated by methylation-specific polymerase chain reaction, bisulphite sequencing, real-time polymerase chain reaction and immunohistochemistry. Results: DNA methylation microarray identified 8,008 CpG islands in 2,848 genes. One hundred and ninety-eight genes were found to have a methylated signal in the promoter region in NP samples compared with ITM samples. The four top genes that changed, COL18A1, EP300, GNAS and SMURF1, were selected for further study. The methylation frequency of COL18A1 was significantly higher in NP samples than in ITM samples. Conclusions: DNA methylation might play an important role in the pathogenesis of NP. Promoter methylation of COL18A1 was found to be significantly increased in NP tissues, further studies are necessary to confirm the significance of these epigenetic factors in the mechanisms underlying the development or persistence of NP.

Evaluation of a 7-Day Continuous Intravenous Infusion of Decitabine: Inhibition of Promoter-Specific and Global Genomic DNA Methylation

2005 ◽  
Vol 23 (17) ◽  
pp. 3897-3905 ◽  
Author(s):  
Wolfram E. Samlowski ◽  
Sancy A. Leachman ◽  
Mark Wade ◽  
Pamela Cassidy ◽  
Patricia Porter-Gill ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Polymerase Chain Reaction ◽  
Continuous Infusion ◽  
Intravenous Infusion ◽  
Genomic Dna ◽  
Quantitative Polymerase Chain Reaction ◽  
Dna Hypomethylation ◽  
Chain Reaction ◽  
Polymerase Chain

Purpose The nucleoside analog 5-aza-2′-deoxycytidine (5-aza-CdR, decitabine) is a potent inhibitor of DNA methylation in vitro. Cellular treatment with this agent induces the re-expression of methylation-silenced genes. It remains unclear to what extent this compound inhibits DNA methylation in vivo. A clinical study was designed to examine the molecular effects and toxicity of a continuous 1-week intravenous infusion of decitabine in solid tumor patients. Methods Ten patients with refractory solid tumors were included in this study. Decitabine was administered at 2 mg/m2/d via continuous infusion for 168 hours. Quantitative polymerase chain reaction and high performance liquid chromatography were utilized to measure promoter-specific and global DNA methylation in peripheral-blood cells before and after treatment. Results Transient grade III/IV neutropenia (two patients) and grade II thrombocytopenia (one patient) was observed at the lowest planned dose step (2 mg/m2/d for 7 days). Nonhematologic toxicities were not observed. Quantitative polymerase chain reaction demonstrated significant MAGE-1 promoter hypomethylation by 14 days after the start of treatment in all 13 treatment cycles examined. Significant genomic DNA hypomethylation was also seen by day 14 in 11 of 13 treatment cycles analyzed. Genomic DNA methylation reverted to baseline levels by 28 to 35 days after the start of treatment, demonstrating that inhibition of DNA methylation by decitabine is transient. Conclusion A 168-hour continuous infusion of decitabine is well tolerated and results in the inhibition of promoter-specific and genomic DNA methylation in vivo. This treatment schedule is suitable for evaluation of decitabine in combination with agents whose activity may be enhanced by the reversal of DNA methylation–mediated gene silencing.

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