P16 deletion and mutation analysis in human brain tumors.
We screened human primary and recurrent malignant glioma, juvenile pilocytic astrocytoma, medulloblastoma, and meningioma tissue specimens for alterations in p16 gene structure. Single strand conformation polymorphism (SSCP) analysis was used to screen for point mutations, and a quantitative polymerase chain reaction-based assay was used to screen for homozygous gene deletions. In malignant glioma specimens, homozygous p16 gene deletions were significantly more common in high-grade tumors than in low-grade gliomas. Point mutations causing alteration in predicted protein structure were not detected. Medulloblastomas showed rare homozygous deletions and no point mutations. No mutations were detected in meningiomas.
Barker
F G
FG
Department of Neurological Surgery, University of California, San Francisco, USA.
Chen
P
P
Furman
F
F
Aldape
K D
KD
Edwards
M S
MS
Israel
M A
MA
D002352:Carrier Proteins / Q000235:genetics*; D002528:Cerebellar Neoplasms / Q000235:genetics*; D019941:Cyclin-Dependent Kinase Inhibitor p16; D004252:DNA Mutational Analysis; D004791:Enzyme Inhibitors / Q000378:metabolism*; D017353:Gene Deletion; D016147:Genes, Tumor Suppressor / Q000235:genetics; D006801:Humans; D008527:Medulloblastoma / Q000235:genetics*; D008577:Meningeal Neoplasms / Q000235:genetics*; D008579:Meningioma / Q000235:genetics*; D016133:Polymerase Chain Reaction; D018807:Polymorphism, Single-Stranded Conformational
D002352:Carrier Proteins; D019941:Cyclin-Dependent Kinase Inhibitor p16; D004791:Enzyme Inhibitors