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. 2005 Feb 17:5:19.
doi: 10.1186/1471-2407-5-19.

V体育ios版 - Increased p53 immunopositivity in anaplastic medulloblastoma and supratentorial PNET is not caused by JC virus

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"V体育平台登录" Increased p53 immunopositivity in anaplastic medulloblastoma and supratentorial PNET is not caused by JC virus

Charles G Eberhart et al. BMC Cancer. .

Abstract (VSports app下载)

Background: p53 mutations are relatively uncommon in medulloblastoma, but abnormalities in this cell cycle pathway have been associated with anaplasia and worse clinical outcomes. We correlated p53 protein expression with pathological subtype and clinical outcome in 75 embryonal brain tumors. The presence of JC virus, which results in p53 protein accumulation, was also examined. VSports手机版.

Methods: p53 protein levels were evaluated semi-quantitatively in 64 medulloblastomas, 3 atypical teratoid rhabdoid tumors (ATRT), and 8 supratentorial primitive neuroectodermal tumors (sPNET) using immunohistochemistry V体育安卓版. JC viral sequences were analyzed in DNA extracted from 33 frozen medulloblastoma and PNET samples using quantitative polymerase chain reaction. .

Results: p53 expression was detected in 18% of non-anaplastic medulloblastomas, 45% of anaplastic medulloblastomas, 67% of ATRT, and 88% of sPNET. The increased p53 immunoreactivity in anaplastic medulloblastoma, ATRT, and sPNET was statistically significant. Log rank analysis of clinical outcome revealed significantly shorter survival in patients with p53 immunopositive embryonal tumors V体育ios版. No JC virus was identified in the embryonal brain tumor samples, while an endogenous human retrovirus (ERV-3) was readily detected. .

Conclusion: Immunoreactivity for p53 protein is more common in anaplastic medulloblastomas, ATRT and sPNET than in non-anaplastic tumors, and is associated with worse clinical outcomes VSports最新版本. However, JC virus infection is not responsible for increased levels of p53 protein. .

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Figures (VSports在线直播)

Figure 1
Figure 1
p53 Immunostaining in CNS embryonal tumors. Most p53 immunopositivity was relatively faint and present only in a small fraction of the tumor. This nodular medulloblastoma had weak staining in less than 25% of cells (A). Some anaplastic medulloblastomas had strong p53 immunostaining in a larger fraction of cells (B). Most AT/RT and supratentorial PNET contained p53 immunopositive cells, like this lesion metastatic within the CNS in which almost all cells are strongly positive (C). Note the lack pf staining in non-neoplastic stroma (Asterisk).
Figure 2
Figure 2
A statistically significant increase in p53 immunopositivity in AT/RT and sPNET Most classic and nodular medulloblastoma (MB) contained no p53 immunopositive cells. In contrast, p53 positive cells were present in many anaplastic MB, supratentorial primitive neuroectodermal tumors (sPNET) and atypical teratoid rhabdoid tumors (ATRT). Triangles represent individual tumors with negative (0), weak (1) or strong (2) p53 immunostaining. Bars represent the mean and standard error of the mean. The increase in p53 immunopositivity in the sPNET/ATRT category as compared to classical MB was statistically significant (Mann Whitney test).
Figure 3
Figure 3
JC virus sequences are not detected in embryonal brain tumors. JC virus plasmid DNA is detectable over a wide range of dilutions when added to genomic DNA (A), but was not identified in DNA extracted from a range of embryonal brain tumors (B). In contrast, the ERV-3 endogenous retrovirus is easily detected both using standard dilution curves (C) and in tumor DNA (D).

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