Affiliations 

  • 1 A M Jafri, MD. Neuroscience Unit, School of Medical Sciences, Health Campus, Universiti Sains Malaysia, 16150 Kubang Kerian, Kelantan
  • 2 S Sarina, BBioMed Sc. Human Genome Center, School of Medical Sciences, Health Campus, Universiti Sains Malaysia, 16150 Kubang Kerian, Kelantan
  • 3 P Jain George, MD. Neuroscience Unit, School of Medical Sciences, Health Campus, Universiti Sains Malaysia, 16150 Kubang Kerian, Kelantan
  • 4 I Mohd Nizam, PhD. Human Genome Center, School of Medical Sciences, Health Campus, Universiti Sains Malaysia, 16150 Kubang Kerian, Kelantan
Med J Malaysia, 2004 Oct;59(4):480-5.
PMID: 15779580 MyJurnal

Abstract

Recent study has shown that activation of the telomerase and p16 gene mutation are both necessary for tumorigenesis. Our objectives were to detect telomerase activity and investigate the possibility of p16 gene mutations in various types of brain tumor. We analyzed 23 tumor tissues collected in 2000 to 2002. Telomerase activity was detected by a TRAP assay using a TRAPEZE Telomerase Detection Kit (Intergen, Co). PCR-SSCP (Single Strand Conformation Polymorphism) analysis was performed to screen for p16 gene mutation at exon 1 and 2. The activity was detected in 26.1% of the brain tumor samples and mostly present in high-grade tumors. There was a significant association between telomerase activity status and tumor grade but not with patient criteria. Telomerase activity was detected in the analyzed tumors, supporting the fact that activation of telomerase is an important feature for tumorigenesis. There was no mobility shift of p16 gene using SSCP and suggested no mutation at exon 1 and 2 occurred in all samples. These results suggest that another mechanism of p16 gene alterations could be involved and associated with detectable telomerase activity in the progression of tumors.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.