Preferential expression of Fas/APO1 (CD95) and apoptotic cell death in perinecrotic cells of glioblastoma multiforme

Tachibana, Osamu; Lampe, Johannes; Kleihues, Paul; Ohgaki, Hideaki

doi:10.1007/s004010050542

Cited by 64 publications

(30 citation statements)

References 27 publications

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“…In astrocytic tumors, the incidence of apoptotic cell death in situ has been shown to correlate with tumor grade, with the proportion of cells undergoing apoptosis being greater in anaplastic astrocytomas and GBMs than in lower-grade astrocytomas (Kordek et al, 1996). Apoptosis also occurs more frequently in GBM cells within perinecrotic areas (Kordek et al, 1996;Tachibana et al, 1996). Further, Yin et al (1999) have observed that Cdk5 protein and kinase activity were increased in human head and neck squamous cell carcinoma xenografts undergoing spontaneous apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Expression and localization of cyclin-dependent kinase 5 in apoptotic human glioma cells

Catania¹

2001

Neuro-Oncology

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Neuro-Oncology nA P R I L 2 0 0 1 89 Cyclin-dependent kinase 5 (Cdk5), a member of the cyclin-dependent kinase family, is expressed predominately in mature neurons and is implicated in neurite extension, neuronal migration, and neuronal differentiation. Cdk5 protein expression also has been associated with apoptosis in a number of nonneuronal model systems. In normal brain, substrates for Cdk5 include neuro lament and tau proteins. Because human tumors of glial origin can express neuronal proteins, we examined whether Cdk5 and its activator protein, P35, are present in early passage human glioblastoma multiforme (GBM) cells lines and primary tumor specimens. Here we report the expression of Cdk5 and an "active" proteolytic form of P35 in human GBM cells and demonstrate kinase activity of the holoenzyme. We also show that Cdk5 kinase activity and expression of its activator protein, P35, is increased in the human GBM cell line M059J after exposure to ionizing radiation and that P35 is localized within M059J cells undergoing apoptosis. These results suggest a possible role for Cdk5 in mediating apoptosis in human GBM cells. Neuro-Oncology 3, 89-98, 2001 (Posted to Neuro-Oncology [serial online], Doc. 00-038, February 15, 2001

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Section: Discussionmentioning

confidence: 99%

Expression and localization of cyclin-dependent kinase 5 in apoptotic human glioma cells

Catania¹

2001

Neuro-Oncology

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“…Total RNA was isolated by Trizol Reagent (GIBCO͞BRL). The first strand of cDNA was synthesized with oligo(dT) primers and Moloney murine leukemia virus reverse transcriptase (GIBCO͞BRL) (19). PCR amplification was performed with Fas primers (5Ј-CACTATTGCTGGAGTCATG-3Ј and 5ЈCTGAGTCACT-AGTAATGTCC-3Ј) or ␤-actin primers (5Ј-CATCCTCAC-CCTGA AGTACC-3Ј and 5Ј-GGTGAGGATCT TCAT-GAGGT-3Ј) for 30 cycles at 94°C for 15 sec, 60°C for 30 sec, 72°C for 1 min, and 72°C for 5 min using AmpliTaq DNA polymerase and the 9600 GeneAmp PCR system (PerkinElmer).…”

Section: Methodsmentioning

confidence: 99%

Tat protein induces self-perpetuating permissivity for productive HIV-1 infection

Ueda

Shi

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

106

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We report that human immunodeficiency virus type 1 (HIV-1) has evolved a self-perpetuating mechanism to actively generate cells permissive for productive and cytopathic infection. Only activated T cells can be productively infected, which leads to their rapid depletion (2 ؋ 10 9 ͞day in an infected individual). Establishment of productive HIV-1 infection therefore requires continual activations from the large pool of quiescent T cells. Tat protein, which is secreted by infected cells, activated uninfected quiescent T cells in vitro and in vivo. These Tat-activated uninfected cells became highly permissive for productive HIV-1 infection. Activation of primary T cells by Tat protein involved integrin receptors and was associated with activation of mitogen-activated protein kinases, including ERK1 and JNK kinase. Accordingly, these primary T cells progressed from G 0 to the late G 1 phase of the cell cycle.

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“…20,21 Most Fas expression in GBM is within pseudopalisades corresponding to their higher levels of apoptosis. 22,23 Contact between tumor cells expressing FasL and those expressing Fas may facilitate apoptosis. 24 Overall, however, levels of apoptosis are generally low in malignant gliomas; apoptosis accounts for a slim minority of cell death; and apoptotic rates do not correlate with prognosis.…”

Section: Necrogenesis In Gbmmentioning

confidence: 99%

Vaso-occlusive and prothrombotic mechanisms associated with tumor hypoxia, necrosis, and accelerated growth in glioblastoma

Brat

Meir

2004

Laboratory Investigation

294

276

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Glioblastoma (GBM) has explosive biologic properties with rapid clinical progression leading to death. Its distinguishing pathologic features, necrosis with surrounding pseudopalisades and microvascular hyperplasia, are believed to be instrumental to its accelerated growth. Microvascular hyperplasia arises in response to the secretion of proangiogenic factors by hypoxic pseudopalisades and allows for peripheral neoplastic expansion. Mechanisms underlying necrosis and hypoxia remain obscure, but vaso-occlusive and prothrombotic contributions could be substantial. Recent investigations on the origin of pseudopalisades suggest that this morphologic phenomenon is created by a tumor cell population actively migrating away from a central hypoxic region and that, in at least a significant subset, hypoxia-induced migration appears due to vasoocclusion caused by intravascular thrombosis. Both vascular endothelial growth factor induced vascular permeability to plasma coagulation factors and the increased neoplastic expression of tissue factor likely contribute to a prothrombotic state favoring intravascular thrombosis. In addition to prothrombotic mechanisms, vaso-occlusion could also result from angiopoietin-2-mediated endothelial cell apoptosis and vascular regression, which follows neoplastic co-option of native vessels in animal models of gliomas. Vasoocclusive and prothrombotic mechanisms in GBM could readily explain the presence of pseudopalisades and coagulative necrosis in tissue sections, the emergence of central contrast enhancement and its rapid peripheral expansion on neuroimaging, and the dramatic shift to an accelerated rate of clinical progression. Since the hypoxic induction of angiogenesis appears to support further neoplastic growth, therapeutic targeting of the underlying vascular pathology and thrombosis could provide a new means to prolong time to progression.

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Preferential expression of Fas/APO1 (CD95) and apoptotic cell death in perinecrotic cells of glioblastoma multiforme

Cited by 64 publications

References 27 publications

Expression and localization of cyclin-dependent kinase 5 in apoptotic human glioma cells

Expression and localization of cyclin-dependent kinase 5 in apoptotic human glioma cells

Tat protein induces self-perpetuating permissivity for productive HIV-1 infection

Vaso-occlusive and prothrombotic mechanisms associated with tumor hypoxia, necrosis, and accelerated growth in glioblastoma

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