The results showed the average survival of gliosarcoma-bearing (MBR 614 or U87) mice receiving BSA/PTX NPs incorporated hydrogel<sub>Gd</sub>/EPI increased to 63 days or 69 days with no tumor recurrence observed.
We demonstrate that gliosarcoma bears somatic alterations in gene coding for PI3K/Akt (<i>PTEN</i>, <i>PI3K</i>) and RAS/MAPK (<i>NF1</i>, <i>BRAF</i>) signaling pathways that are crucial for tumor growth.
These results are the first to describe the presence of Wnt signaling pathway abnormalities, manifested by nuclear β-catenin, in a subset, as well as the lack of BRAF<sup>V600E</sup> mutation in GS.
We demonstrate that gliosarcoma bears somatic alterations in gene coding for PI3K/Akt (<i>PTEN</i>, <i>PI3K</i>) and RAS/MAPK (<i>NF1</i>, <i>BRAF</i>) signaling pathways that are crucial for tumor growth.
In conclusion, this study demonstrates that concomitant TMZ together with radiation therapy increases GSM-patient survival independent of MGMT promoter methylation.
In the present study, we determined the status of MGMT using methylation-specific polymerase chain reaction (PCR) and immunohistochemistry on paraffin-embedded specimens in 12 human gliosarcomas, and these results were then related to overall survival (OS) and response to alkylating agents.
A study of clinico-pathological parameters and O⁶-methylguanine DNA methyltransferase (MGMT) promoter methylation status in the prognostication of gliosarcoma.
Abnormalities identified by immunohistochemistry included p21 immunonegativity (60%, 25%, 93%), which was most frequent in TE-GBM (P = .008), strong nuclear p53 staining (29%, 29%, 41%), strong membranous staining for epidermal growth factor receptor (EGFR) (21%, 63%, 19%), which was most frequent in E-GBM (P = .03), and an increased frequency of p27 immunonegativity in gliosarcomas (15% negative, 85% focal) compared with tumors without sarcoma (38% strongly positive) (P = .009).
The aim of this study was to evaluate the effect of VEGF-A expression on tumor growth, perfusion, and chemotherapeutic efficacy in orthotopic 9L gliosarcomas.
Both genes are induced in biologically and genetically heterogenous glioblastoma cell lines (LN-229, LN-Z308, U87MG, T98G), whereas, in gliosarcoma cells (D247MG), only the VEGF gene is induced.
Abnormalities identified by immunohistochemistry included p21 immunonegativity (60%, 25%, 93%), which was most frequent in TE-GBM (P = .008), strong nuclear p53 staining (29%, 29%, 41%), strong membranous staining for epidermal growth factor receptor (EGFR) (21%, 63%, 19%), which was most frequent in E-GBM (P = .03), and an increased frequency of p27 immunonegativity in gliosarcomas (15% negative, 85% focal) compared with tumors without sarcoma (38% strongly positive) (P = .009).
Identification of a NFKBIA polymorphism associated with lower NFKBIA protein levels and poor survival outcomes in patients with glioblastoma multiforme.
Over-representation of PPARgamma sequence variants in sporadic cases of glioblastoma multiforme: preliminary evidence for common low penetrance modifiers for brain tumour risk in the general population.
Here, we have analyzed the localization of COX-1 and COX-2 in rat experimental autoimmune encephalomyelitis (EAE), C6 glioblastoma and 9L gliosarcoma by immunohistochemistry.
Here, we have analyzed the localization of COX-1 and COX-2 in rat experimental autoimmune encephalomyelitis (EAE), C6 glioblastoma and 9L gliosarcoma by immunohistochemistry.
Gastrin significantly decreased the overall growth rate in the rat C6 and the human U373 high-grade astrocytic tumor models with either CCK(B) or CCK(C) gastrin receptor but not in the 9L rat gliosarcoma, which had no CCK(B) gastrin receptor (but had CCK(A) receptor) and only weak amounts of CCK(C) receptor.
The presence of the three CCK receptor subtypes was also assayed on three experimental models, i.e. the U373 human glioma, the C6 rat glioma and the 9L rat gliosarcoma.