Hypermethylation of the CPG island of p16 gene correlates with gene inactivation in brain glioma

2002 ◽  
Vol 1 (4) ◽  
pp. 226-229
Author(s):  
Jiao Baohua ◽  
Geng Shaomei ◽  
Yao Zhigang
Keyword(s):  
Cpg Island ◽  
Gene Inactivation ◽  
Brain Glioma ◽  
P16 Gene

scholarly journals Frequent aberrant methylation of p16INK4a in primary rat lung tumors.

1997 ◽  
Vol 17 (3) ◽  
pp. 1366-1374 ◽  
Author(s):  
D S Swafford ◽  
S K Middleton ◽  
W A Palmisano ◽  
K J Nikula ◽  
J Tesfaigzi ◽  
...  
Keyword(s):  
Cell Lines ◽  
Cpg Island ◽  
Homozygous Deletion ◽  
Lung Tumors ◽  
Aberrant Methylation ◽  
Rat Lung ◽  
Small Cell Lung ◽  
Gene Methylation ◽  
P16 Gene ◽  
Primary Tumors

The p16INK4a (p16) tumor suppressor gene is frequently inactivated by homozygous deletion or methylation of the 5' CpG island in cell lines derived from human non-small-cell lung cancers. However, the frequency of dysfunction in primary tumors appears to be significantly lower than that in cell lines. This discordance could result from the occurrence or selection of p16 dysfunction during cell culture. Alternatively, techniques commonly used to examine tumors for genetic and epigenetic alterations may not be sensitive enough to detect all dysfunctions within the heterogeneous cell population present in primary tumors. If p16 inactivation plays a central role in development of non-small-cell lung cancer, then the frequency of gene inactivation in primary tumors should parallel that observed in cell lines. The present investigation addressed this issue in primary rat lung tumors and corresponding derived cell lines. A further goal was to determine whether the aberrant p16 gene methylation seen in human tumors is a conserved event in this animal model. The rat p16 gene was cloned and sequenced, and the predicted amino acid sequence of its product found to be 62% homologous to the amino acid sequence of the human analog. Homozygous deletion accounted for loss of p16 expression in 8 of 20 cell lines, while methylation of the CpG island extending throughout exon 1 was observed in 9 of 20 cell lines. 2-Deoxy-5-azacytidine treatment of cell lines with aberrant methylation restored gene expression. The methylated phenotype seen in cell lines showed an absolute correlation with detection of methylation in primary tumors. Aberrant methylation was also detected in four of eight primary tumors in which the derived cell line contained a deletion in p16. These results substantiate the primary tumor as the origin for dysfunction of the p16 gene and implicate CpG island methylation as the major mechanism for inactivating this gene in the rat lung tumors examined. Furthermore, rat lung cancer appears to be an excellent model in which to investigate the mechanisms of de novo gene methylation and the role of p16 dysfunction in the progression of neoplasia.

Quantitate Detect of the Methylation of Three Hematopathy Patients’ P16 Gene

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 4499-4499
Author(s):  
Bao-An Chen ◽  
Bei-ming Shou ◽  
Dong-rui Zhou ◽  
De-long Liu ◽  
Jia-hua Ding ◽  
...  
Keyword(s):  
Cpg Island ◽  
Gene Chip ◽  
The Other ◽  
P16 Gene ◽  
Precise Method ◽  
Patient Sample ◽  
Standard Curve

Abstract Objective: The changes of methylation of CpG Island are the frequent changes in epigenetic. Nowadays, there are many methods to detect the changes of methylation, but all these method are hard to quantitate precisely. In our experiment, we will establish a new precise method. Methods: Use hydrosulfite to handle the DNA, and then do PCR. The cytosine will change to thymine, if it hasn’t been methylation. On the other side, the cytosine will maintain its state if it has been methylation. Design a pair of probe, which contain one methylation probe and one un methylation probe. This pair of probe will detect three consecutive sites of CpG island in P16. Our experiment will use gene chip. Mix the the DNA of methylation and unmethylation with different ratio, then build the standard curve. Contrast the patient sample with standard curve will get the quantitate result. Results: We detected three patients, the methylation degree of the patients is 84.3%, 0%, 17.7%. Conclusion: The method we used can detect methylation degree of three consecutive sites of P16 quantitate precisely. Solve the problem of quantitate precisely.

Deletion and 5’CPG island methylation of pl5 gene in brain glioma

2000 ◽  
Vol 12 (2) ◽  
pp. 152-154
Author(s):  
Guang Zhai ◽  
Xian-hou Yuan ◽  
Jin-qing Qi
Keyword(s):  
Cpg Island ◽  
Brain Glioma ◽  
Cpg Island Methylation

Hypermethylation of promoter 5′CpG island of p16 gene in glioma tissue and plasma

2008 ◽  
Vol 7 (4) ◽  
pp. 241-244
Author(s):  
Chengdong Wang ◽  
Lili Wu ◽  
Lixue Guan ◽  
Daokui Wang ◽  
Yuting Wang ◽  
...  
Keyword(s):  
Cpg Island ◽  
Glioma Tissue ◽  
P16 Gene
Sign in / Sign up

Export Citation Format

Share Document