Caspase 8 is deleted or silenced preferentially in childhood neuroblastomas with amplification of MYCN

Teitz, Tal; Wei, Tie; Valentine, Marcus B.; Vanin, Elio F.; Grenet, José; Valentine, Virginia; Behm, FG; Look, A. Thomas; Lahti, Jill M.; Kidd, Vincent J.

doi:10.1038/75007

Cited by 723 publications

(639 citation statements)

References 35 publications

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“…p53 is central in the DNA damage response and triggers cell death by both transcription-dependent and -independent mechanisms (Slee et al, 2004;Yee and Vousden, 2005). Other examples of apoptosis evasion include disruption of Fas death receptor pathway, upregulation of the widespread antiapoptotic family of inhibitors of apoptosis proteins (IAPs) or downregulation of caspases (Muschen et al, 2000;Teitz et al, 2000;Yang et al, 2003). The PI3K/Akt/ PTEN pathway was also shown to play a role in abrogating apoptosis.…”

Section: Mitochondrial Apoptosis and Its Subversion In Oncogenesismentioning

confidence: 99%

Mitochondria and cancer: is there a morphological connection?

2006

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Mitochondria are key players in several cellular functions including growth, division, energy metabolism, and apoptosis. The mitochondrial network undergoes constant remodelling and these morphological changes are of direct relevance for the role of this organelle in cell physiology. Mitochondrial dysfunction contributes to a number of human disorders and may aid cancer progression. Here, we summarize the recent contributions made in the field of mitochondrial dynamics and discuss their impact on our understanding of cell function and tumorigenesis.

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Section: Mitochondrial Apoptosis and Its Subversion In Oncogenesismentioning

confidence: 99%

Mitochondria and cancer: is there a morphological connection?

2006

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“…In the case of disseminated neuroendocrine tumors, such as small-cell carcinoma and neuroblastoma, the loss of caspase 8 is associated with malignant disease. 113,114 Importantly, the frequency with which these events are observed in established tumors suggests that the requirement for integrin ligation by the local ECM imposes an important hurdle that must be overcome during oncogenesis (Figure 3).…”

Section: Physiological Roles For Cellular 'Dependence' On the Ecmmentioning

confidence: 99%

Integrins as a distinct subtype of dependence receptors

Stupack

2005

Cell Death Differ

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In the absence of their cognate ligand, dependence receptors trigger programmed cell death. This function is the defining feature of dependence receptors, which include members of several different protein families. The integrins are a family of heterodimeric receptors for extracellular matrix (ECM) proteins, mediating cell anchorage and migration. Integrins share characteristics with dependence receptors, and integrin binding to substrate ECM ligands is essential for cell survival. Although integrins do not conform in all characteristics to the established definitions of dependence receptors, alterations in the expression of integrins and their ligands during physiological and pathological events, such as wound healing, angiogenesis and tumorigenesis, do regulate cell fate in a ligand-dependent manner. This biosensory function of integrins fits well with our current concept of dependence receptor action, and thus integrins may rightly be considered to comprise a distinct subclass of dependence receptor.

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“…However, for this experiment, we could not use BJAB-FADD-DN, since this cell line does not form tumours in nude mice. Therefore, we used apoptosis-resistant neuroblastoma (Kelly) cells defective in death receptor signalling due to a hypermethylated and downregulated caspase-8 gene (Teitz et al, 2000;Fulda et al, 2001). Kelly xenografts were treated as described above.…”

Section: Jurkat-trail Cells Inhibit Tumour Growth Of Trailsensitive Hmentioning

confidence: 99%

Induction of apoptosis in experimental human B cell lymphomas by conditional TRAIL-expressing T cells

et al. 2003

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In the present study, we demonstrate the utility of a non-tumour-forming T-cell line for the inducible gene transfer of tumour necrosis factor (TNF)-related apoptosis-inducing ligand (Apo2L/TRAIL), which has been shown to selectively induce apoptosis in malignant but not in normal cells. To generate T cells inducible for TRAIL expression, we stably transfected Jurkat cells with TRAIL in the context of the Tet-On system. The switched on cells strongly expressed TRAIL mRNA, whose protein product was expressed on the cell surface. Paracrine induction of apoptosis in human target tumour cells was solely found for membrane-bound TRAIL. The Jurkat-TRAIL cells itself survived due to clonal selection of TRAIL-resistant cells. Jurkat-TRAIL cells had an additive effect with cytotoxic drugs in vitro, since cell death was enhanced. To elucidate the antitumoral activity of these Jurkat-TRAIL cells in vivo, we injected them intratumorally in xenografts of human Burkitt lymphomas. Switching on expression of TRAIL by adding tetracycline to the drinking water of the mice strongly reduced tumour growth by apoptosis in a caspase-dependent manner. Thus, non-tumourforming T-cell lines offer a novel method for gene transfer and inducible expression of TRAIL in tumour therapy.

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Caspase 8 is deleted or silenced preferentially in childhood neuroblastomas with amplification of MYCN

Cited by 723 publications

References 35 publications

Mitochondria and cancer: is there a morphological connection?

Mitochondria and cancer: is there a morphological connection?

Integrins as a distinct subtype of dependence receptors

Induction of apoptosis in experimental human B cell lymphomas by conditional TRAIL-expressing T cells

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