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Object  Several genes have been shown to carry mutations in human malignant gliomas, including the  phosphatase and tensin homolog (PTEN)  deleted on chromosome 10 and  p16  tumor suppressor genes. Alterations of this gene located on chromosome 10 q23 and 9p21, respectively, may contribute to gliomagenesis. In this study, the authors analyzed 20 cases of malignant gliomas obtained in patients living on the east coast of Malaysia to investigate the possibilities of involvement of the  PTEN  and  p16  genes.    Methods  Samples of DNA were amplified by polymerase chain reaction (PCR), analyzed by single-stranded conformation polymorphism (SSCP), and subsequently by sequencing. Two cases of glioblastoma multiforme, three cases of anaplastic astrocytoma, one case of anaplastic pleomorphic xanthoastrocytoma, and one case of anaplastic ependymoma showed SSCP band shifts in  PTEN  mutational analyses. The DNA sequencing analyses of these samples revealed missense and nonsense mutations, with cluster of mutations in the region 5' to the core phosphatase motif of exon 5 and the 5'-end of exon 6. No abnormal migration shifts were detected in the glioma samples analyzed for point mutations of the  p16  gene. Homozygous deletions of  p16  were also not detected in all samples.    Conclusions  These findings indicate that mutations of the  PTEN  genes were likely to contribute to the tumorigenesis and morphological transformations of gliomas. In addition, the alterations of the  p16  gene might not play a major role in tumorigenesis of malignant gliomas in Malaysian patients.

Molecular genetic analysis of phosphatase and tensin homolog and p16 tumor suppressor genes in patients with malignant glioma