Established and emerging variants of glioblastoma multiforme: review of morphological and molecular features

Karsy, Michael; Gelbman, Marshall; Shah, Paarth; Balumbu, Odessa; Moy, Fred; Arslan, Erol

doi:10.5114/fn.2012.32361

Cited by 93 publications

(79 citation statements)

References 148 publications

(175 reference statements)

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“…Further, the lack of selectivity of these approaches towards cancer cells leads to significant side-effects and toxicity. Glioblastoma multiforme (GBM) is a highly aggressive major primary brain tumor in adults 16 and is a challenge to treat GBM 17 . Thus it becomes vital to identify novel agents that can inhibit its proliferation.…”

Section: Discussionmentioning

confidence: 99%

Ellagic acid inhibits proliferation and induces apoptosis in human glioblastoma cells

et al. 2016

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PURPOSE:To investigate the anticancer activity of ellagic acid (EA) in U251 human glioblastoma cells and its possible molecular mechanism. METHODS:The cells were treated with EA at various concentrations for different time periods. Cell viability and cell proliferation were detected by cell counting kit-8(CCK-8) assay and live/dead assay respectively. Cell apoptosis were measured with Annexin V-FITC/PI double staining method by flow cytometry and Mitochondrial membrane potential assay separately. Cell cycle was measured with PI staining method by flow cytometry. The expressions of Bcl-2, Survivin, XIAP, Caspase-3, Bax, JNK, p-JNK, ERK1/2, p-ERK1/2, p38, p-p38, DR4, DR5, CHOP and GRP78-related proteins were detected by western blot after EA treatment. RESULTS:Cell viability and proliferation of glioblastoma cells treated with EA were significantly lower than the control group. EA caused robust apoptosis of the glioblastoma cells compared to the control group. EA significantly decreased the proportion at G0/ G1 phases of cell cycling accompanied by increased populations at S phase in U251 cell lines. And the expressions of anti-apoptotic proteins were dramatically down-regulated. CONCLUSION:Ellagic acid potentially up-regulated DR4, DR5 and MAP kinases (JNK, ERK1/2 and p38). EA also caused significant increase in the expressions of CHOP and GRP78. Our findings suggest that EA would be beneficial for the treatment of glioblastoma.

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Section: Discussionmentioning

confidence: 99%

Ellagic acid inhibits proliferation and induces apoptosis in human glioblastoma cells

et al. 2016

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“…No oligodendroglial components were found in the histopathological study. According to the classical model of the molecular GB pathway, primary glioblastoma is characterized by high incidence of EGFR amplification (about 40%) and low frequency of IDH1 mutations (< 5%); additionally, TP53 mutations are less frequent in primary GB [26,27]. To ascertain that the tumors studied were primary glioblastomas we used the following molecular criteria: frequencies of EGFR amplification (37.5%), IDH1 mutation (2.4%), and TP53 mutation (26.2%); the results were partly published before (EGFR amplification and TP53 mutations) [8].…”

Section: Methodsmentioning

confidence: 99%

Association of loss of heterozygosity with shorter survival in primary glioblastoma patients

Jesionek-Kupnicka

Szybka²,

Potemski³

et al. 2013

pjp

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Loss of heterozygosity (LOH) co-deletion 1p/19q, MGMT promoter methylation and/or IDH1 mutation generally signify a better prognosis for patients with glioma. However, the influence of 1p/19q co-deletion and the LOH on other chromosomes in primary glioblastoma on survival is still debatable. The aim of our study was to identify LOH on chromosomes 1p, 19q, 9p, 10q, 13q, and 17p, and evaluate their impact either alone or 1p/19q co-deletion or by groups of LOH on the overall survival of 42 primary glioblastoma patients without an oligodendroglial component. These patients were additionally molecularly characterized for EGFR amplification, IDH1 mutations and TP53 mutations. We assessed their influence on the overall survival of glioblastoma patients. LOH in at least one of the loci on all examined chromosomes was detected in 65% of cases and was significantly associated with shorter overall survival (hazard ratio 3.07; 95% CI: 1.29-7.31, p = 0.006). 1p/19q co-deletion was infrequent (7.14%) and had no impact on overall survival. Our results indicate that in primary glioblastoma a specific LOH group analysis may be important for the prognosis. LOH 1p/19q co-deletion is rare in glioblastoma without an oligodendroglial component and has no impact on patient survival.

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“…Median survival of GB patients treated with aggressive multimodal thera py, including total resection, combined radiation and chemotherapy, and adjuvant chemotherapy is about 12 months [9,18,24,25]. Glioblastoma is actually con sidered a heterogeneous and dynamic disease [13,17,21].…”

Section: Introductionmentioning

confidence: 99%

Analysis of Olig2 and YKL-40 expression: a clinicopathological/immunohistochemical study for the distinction between subventricular zone II and III glioblastomas

Batista

Costa²,

Pablo³

et al. 2016

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Established and emerging variants of glioblastoma multiforme: review of morphological and molecular features

Cited by 93 publications

References 148 publications

Ellagic acid inhibits proliferation and induces apoptosis in human glioblastoma cells

Ellagic acid inhibits proliferation and induces apoptosis in human glioblastoma cells

Association of loss of heterozygosity with shorter survival in primary glioblastoma patients

Analysis of Olig2 and YKL-40 expression: a clinicopathological/immunohistochemical study for the distinction between subventricular zone II and III glioblastomas

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