Carmustine (BCNU) plus Teniposide (VM26) in Recurrent Malignant Glioma

Mack, Frederic; Schäfer, Niklas; Kebir, Sied; Stuplich, Moritz; Schaub, Christina; Niessen, Michael; Scheffler, Björn; Herrlinger, Ulrich; Glas, Martin

doi:10.1159/000360295

Cited by 19 publications

(8 citation statements)

References 18 publications

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“…Glioma is the most common one in primary cerebral tumors, and its treatment mainly consists of surgical resection in combination with radio-and chemotherapy [1][2][3]. Glioblastoma is characterized as extensive brain invasion [4,5], whose underlying molecular mechanisms were not elucidated in detail.…”

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: CXCL12/CXCR4 Axis Upregulates Twist to Induce EMT in Human Glioblastoma

Yao

Song

et al. 2015

Mol Neurobiol

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In recent decades, the chemokine receptor CXCR4 and its ligand CXCL12 have been extensively reported to be associated with tumorigenesis. In addition, Twist signaling induces the epithelial-mesenchymal transition (EMT) process in glioblastoma development. In the present study, in vitro assays were used to investigate the role of CXCR4 and Twist in human glioblastoma. We explored the impact of CXCR4 and Twist on human glioblastoma using in vitro protein and gene assays. We found the administration of CXCL12 upregulated the expression of p-ERK, p-AKT, Twist, N-cadherin, and MMP9 in U87 cells, whereas the increase of E-cadherin protein was affected. Subsequently, Twist activity and EMT signaling were directly influenced by PD98059 and LY294002. Most importantly, the genetic silencing of Twist inhibited CXCL12-induced EMT occurrence, including proliferation, migration, and tumor formation of U87 cells. In conclusion, CXCL12/CXCR4 pathway activates ERK and PI3K/AKT signaling to upregulate Twist pathway, leading to the progression of EMT in human glioblastoma. Our study creates a new stage for molecule-targeted therapy of human glioblastoma.

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Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: CXCL12/CXCR4 Axis Upregulates Twist to Induce EMT in Human Glioblastoma

Yao

Song

et al. 2015

Mol Neurobiol

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“…For decades BCNU was the standard of care for GBM, and it is still a component of some second-line regimens. Findings from clinical studies examining the efficacy of BCNU in recurrent GBM post-TMZ treatment are inconsistent, with some suggesting BCNU remains active while others demonstrate no benefit 16 – 18 . These TMZres cell line pairs may therefore also prove to be valuable resources for defining contexts in which BCNU is or is not appropriate second-line treatment, and for identifying other, more appropriate therapies for TMZ-resistant GBM.…”

Section: Discussionmentioning

confidence: 99%

Alterations in Cell Motility, Proliferation, and Metabolism in Novel Models of Acquired Temozolomide Resistant Glioblastoma

Tiek

Rone

Graham

et al. 2018

Sci Rep

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Glioblastoma (GBM) is an aggressive and incurable tumor of the brain with limited treatment options. Current first-line standard of care is the DNA alkylating agent temozolomide (TMZ), but this treatment strategy adds only ~4 months to median survival due to the rapid development of resistance. While some mechanisms of TMZ resistance have been identified, they are not fully understood. There are few effective strategies to manage therapy resistant GBM, and we lack diverse preclinical models of acquired TMZ resistance in which to test therapeutic strategies on TMZ resistant GBM. In this study, we create and characterize two new GBM cell lines resistant to TMZ in vitro, based on the 8MGBA and 42MGBA cell lines. Analysis of the TMZ resistant (TMZres) variants in conjunction with their parental, sensitive cell lines shows that acquisition of TMZ resistance is accompanied by broad phenotypic changes, including increased proliferation, migration, chromosomal aberrations, and secretion of cytosolic lipids. Importantly, each TMZ resistant model captures a different facet of the “go” (8MGBA-TMZres) or “grow” (42MGBA-TMZres) hypothesis of GBM behavior. These in vitro model systems will be important additions to the available tools for investigators seeking to define molecular mechanisms of acquired TMZ resistance.

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“…Gliomas are the most common primary central nervous system tumor, whose treatment mainly comprises surgical resection, postoperative radiotherapy, and chemotherapy [1, 2]. According to the World Health Organization, gliomas are divided into four clinical grades (I–IV) based on the morphology of histopathology [3].…”

Section: Introductionmentioning

confidence: 99%

The Impact of MMP-2 and Its Specific Inhibitor TIMP-2 Expression on the WHO Grade and Prognosis of Gliomas in Chinese Population: a Meta-Analysis

Feng

Zhou

et al. 2016

Mol Neurobiol

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So far, the prognostic value of matrix metalloproteinase 2 (MMP-2) and tissue inhibitor of matrix metalloproteinase 2 (TIMP-2) expressions in patients with gliomas has been widely reported, especially in China. But, the results were inconsistent. Thus, we conducted a meta-analysis to determine the correlation of MMP-2 and TIMP-2 expressions with the prognosis of patients with gliomas. Identical search strategies were used to search relevant literature in electronic databases updated to May 1, 2015, and odds ratios (ORs) with 95 % confidence intervals (95 % CIs) were estimated. Funnel plots and Egger’s tests were conducted for the evaluation of publication bias, and heterogeneity and sensitivity were also analyzed. Finally, a total of 25 studies involving 1572 patients were included in the meta-analysis. Coincidentally, all these studies were conducted in Chinese population. It was found that MMP-2 expression was significantly associated with high-WHO grade gliomas (n = 24, OR = 6.54, CI = 4.98–8.60; I 2 = 0 %, P = 0.911) and poor overall survival (OS), while it did not correlate to age (n = 2, OR = 0.78, CI = 0.35–1.74; I 2 = 0 %, P = 0.621) and gender (n = 2, OR = 1.15, CI = 0.51–2.62; I 2 = 0 %, P = 0.995). Moreover, the results of the pooled analysis indicated that there was no association between TIMP-2 expression and the WHO grade of gliomas (n = 7, OR = 1.02, 95 % CI = 0.68–1.54; I 2 = 71.4 %, P = 0.002), but the ratio of MMP-2 and TIMP-2 (MMP-2/TIMP-2) rose with the increase of the WHO grade of gliomas. In conclusion, there was no correlation between TIMP-2 expression and the WHO grade of gliomas, while MMP-2 expression was potently associated with high-WHO grade of gliomas.

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Carmustine (BCNU) plus Teniposide (VM26) in Recurrent Malignant Glioma

Cited by 19 publications

References 18 publications

RETRACTED ARTICLE: CXCL12/CXCR4 Axis Upregulates Twist to Induce EMT in Human Glioblastoma

RETRACTED ARTICLE: CXCL12/CXCR4 Axis Upregulates Twist to Induce EMT in Human Glioblastoma

Alterations in Cell Motility, Proliferation, and Metabolism in Novel Models of Acquired Temozolomide Resistant Glioblastoma

The Impact of MMP-2 and Its Specific Inhibitor TIMP-2 Expression on the WHO Grade and Prognosis of Gliomas in Chinese Population: a Meta-Analysis

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