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  • 1
    Electronic Resource
    Electronic Resource
    Accumulation of wild-type p53 in astrocytomas is associated with increased p21 expression (1997)
    Springer
    Acta neuropathologica 94 (1997), S. 21-27 
    Details
    ISSN: 1432-0533
    Keywords: Key words p21 ; p53 ; Astrocytoma ; Single-strand ; conformation polymorphism ; Immunohistochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Approximately one quarter of human astrocytomas show immunohistochemical positivity for p53 protein but lack p53 gene mutations, which could reflect either an accumulation of wild-type p53 protein or an inadequate sensitivity of mutation detection. Since wild-type p53 up-regulates p21 expression, increased p21 expression in those astrocytomas with p53 accumulation in the absence of mutations would argue that the protein was wild type in these tumors. We therefore compared p21 expression with p53 gene and protein status in 48 primary human astrocytomas. Single-strand conformation polymorphism analysis and direct sequencing of the p53 gene showed mutations in 11 tumors (22.9%), while immunohistochemistry revealed positive staining in 19 cases (39.6%). Those tumors with p53 immunopositivity in the absence of p53 mutation had significantly increased p21 expression when compared to either mutant p53 or p53-immunonegative cases. Neither p53 nor p21 status correlated with proliferation indices, as assessed by Ki-67 immunohistochemistry. These results support the hypotheses that functionally wild-type p53 accumulates in some astrocytomas, and that alternative cell cycle checkpoints (such as the p16 pathway) may be more important than p21 in regulating proliferation in astrocytomas.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050667
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  • 2
    Electronic Resource
    Electronic Resource
    Homozygous deletions of the CDKN2/p16 gene in dural hemangiopericytomas (1996)
    Springer
    Acta neuropathologica 91 (1996), S. 221-225 
    Details
    ISSN: 1432-0533
    Keywords: Key words CDKN2 ; Hemangiopericytoma ; Meningioma ; p16 ; p53
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract While most authors currently classify dural-based hemangiopericytoma (HPC) as a distinct entity rather than as a subtype of meningioma, the histogenesis of HPC has long been debated. We have recently shown that meningiomas contain frequent mutations of the neurofibromatosis 2 gene, while HPCs do not, suggesting that HPC is genetically distinct from meningioma. In the present study, we evaluated a series of 31 dural HPCs (including 3 pairs of primary and recurrent tumor) and 26 meningiomas for alterations in the cell-cycle regulatory genes CDKN2/p16 and p53. Homozygous deletions of the CDKN2/p16 gene were detected using a comparative multiplex polymerase chain reaction assay in 7 of 28 primary HPCs (25%), but in only one of 26 meningiomas (P = 0.03). Among the HPCs with recurrence, 1 pair of 3 had a homozygous CDKN2/p16 deletion. The 1 meningioma with a CDKN2/p16 deletion was a meningothelial meningioma, without atypical or malignant features. Single-strand conformational polymorphism analysis of all three exons of CDKN2/p16 and exons 5–8 of p53 revealed no mutations in either HPCs or meningiomas. These results illustrate that homozygous deletions of CDKN2/p16 occur in HPCs and suggest that alterations of the p16-mediated cell-cycle regulatory pathway may underlie the formation or progression of some HPCs. The data also provide further genetic evidence that HPC is not a subtype of meningioma.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050419
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
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