scholarly journals Expression in bladder transitional cell carcinoma by real-time quantitative reverse transcription polymerase chain reaction array of 65 genes at the tumor suppressor locus 9q34.1-2: Identification of 5 candidates tumor suppressor genes

2004 ◽  
Vol 111 (4) ◽  
pp. 539-542 ◽  
Author(s):  
Najla Amira ◽  
G�raldine Cancel-Tassin ◽  
St�phane Bernardini ◽  
B�atrix Cochand-Priollet ◽  
Hugues Bittard ◽  
...  
Keyword(s):  
Polymerase Chain Reaction ◽  
Tumor Suppressor ◽  
Transitional Cell Carcinoma ◽  
Cell Carcinoma ◽  
Reverse Transcription ◽  
Tumor Suppressor Genes ◽  
Transitional Cell ◽  
Bladder Transitional Cell Carcinoma ◽  
Chain Reaction ◽  
Polymerase Chain

scholarly journals Differential genome-wide array–based methylation profiles in prognostic subsets of chronic lymphocytic leukemia

Blood ◽  
2010 ◽  
Vol 115 (2) ◽  
pp. 296-305 ◽  
Author(s):  
Meena Kanduri ◽  
Nicola Cahill ◽  
Hanna Göransson ◽  
Camilla Enström ◽  
Fergus Ryan ◽  
...  
Keyword(s):  
Polymerase Chain Reaction ◽  
Chronic Lymphocytic Leukemia ◽  
Tumor Suppressor ◽  
Tumor Suppressor Genes ◽  
Lymphocytic Leukemia ◽  
Chain Reaction ◽  
Global Methylation ◽  
Suppressor Genes ◽  
Genome Wide ◽  
Polymerase Chain

Abstract Global hypomethylation and regional hypermethylation are well-known epigenetic features of cancer; however, in chronic lymphocytic leukemia (CLL), studies on genome-wide epigenetic modifications are limited. Here, we analyzed the global methylation profiles in CLL, by applying high-resolution methylation microarrays (27 578 CpG sites) to 23 CLL samples, belonging to the immunoglobulin heavy-chain variable (IGHV) mutated (favorable) and IGHV unmutated/IGHV3-21 (poor-prognostic) subsets. Overall, results demonstrated significant differences in methylation patterns between these subgroups. Specifically, in IGHV unmutated CLL, we identified methylation of 7 known or candidate tumor suppressor genes (eg, VHL, ABI3, and IGSF4) as well as 8 unmethylated genes involved in cell proliferation and tumor progression (eg, ADORA3 and PRF1 enhancing the nuclear factor-κB and mitogen-activated protein kinase pathways, respectively). In contrast, these latter genes were silenced by methylation in IGHV mutated patients. The array data were validated for selected genes using methylation-specific polymerase chain reaction, quantitative reverse transcriptase–polymerase chain reaction, and bisulfite sequencing. Finally, the significance of DNA methylation in regulating gene promoters was shown by reinducing 4 methylated tumor suppressor genes (eg, VHL and ABI3) in IGHV unmutated samples using the methyl-inhibitor 5-aza-2′-deoxycytidine. Taken together, our data for the first time reveal differences in global methylation profiles between prognostic subsets of CLL, which may unfold epigenetic silencing mechanisms involved in CLL pathogenesis.

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