Survival of children with neuroblastoma

Spix, Claudia; Aareleid, Tiiu; Stiller, Charles; Magnani, Cinzia; Kaatsch, Peter; Michaelis, Jörg

doi:10.1016/s0959-8049(01)00003-x

Cited by 44 publications

(9 citation statements)

References 25 publications

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“…Treatment choices are therefore limited. Intensive chemotherapy is often successful in achieving disease remission; however, relapses are common and difficult to treat, making neuroblastoma one of the most lethal of all childhood cancers (44). Immunotherapy with humanized monoclonal anti-GD2 antibodies has showed promise (reviewed in (45)); however, as with chemotherapy, relapse and resistance are common.…”

Section: Discussionmentioning

confidence: 99%

Modulation of CD59 Expression by Restrictive Silencer Factor–Derived Peptides in Cancer Immunotherapy for Neuroblastoma

Donev¹,

Gray

Sivasankar³

et al. 2008

Cancer Research

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Tumor cells escape clearance by complement by abundantly expressing CD59 and other membrane complement regulators. Existing strategies for blocking/knocking down these regulators can contribute to tumor immunoclearance in vitro; however, there are numerous difficulties restricting their use in vivo. Here, we report a new strategy for suppression of CD59 expression in neuroblastoma using peptides that target regulators of CD59 expression. We identified the neuralrestrictive silencer factor (REST) as a target for modulation of CD59 expression in neuroblastoma. We next designed plasmids that encoded peptides comprising different DNA-binding domains of REST and transfected them into neuroblastoma cell lines. These peptides suppressed CD59 expression, sensitizing neuroblastoma to complement-mediated killing triggered by anti-GD2 therapeutic monoclonal antibody. These CD59-modulating peptides might be effective therapeutic adjuvants to therapeutic monoclonal antibodies used for treatment of neuroblastoma and other cancer types sharing the same mechanism for regulation of CD59 expression.

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Section: Discussionmentioning

confidence: 99%

Modulation of CD59 Expression by Restrictive Silencer Factor–Derived Peptides in Cancer Immunotherapy for Neuroblastoma

Donev¹,

Gray

Sivasankar³

et al. 2008

Cancer Research

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“…Children over 1 year of age with stage IV NB tumors respond poorly to treatment, with a 5 year survival rate of only 30% (Spix et al, 2001), whereas low stage tumors in infants frequently undergo spontaneous remission. Failure to undergo programmed cell death is a putative mechanism for cancer cell resistance to chemotherapy, while in contrast spontaneous remission is thought to be a result of increased apoptosis (Oue et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

Doxorubicin-induced death in neuroblastoma does not involve death receptors in S-type cells and is caspase-independent in N-type cells

et al. 2002

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Death induced by doxorubicin (dox) in neuroblastoma (NB) cells was originally thought to occur via the Fas pathway, however since studies suggest that caspase-8 expression is silenced in most high stage NB tumors, it is more probable that dox-induced death occurs via a different mechanism. Caspase-8 silenced N-type invasive NB cell lines LAN-1 and IMR-32 were investigated for their sensitivity to dox, and compared to S-type noninvasive SH-EP NB cells expressing caspase-8. All cell lines had similar sensitivities to dox, independently of caspase-8 expression. Dox induced caspase-3, -7, -8 and -9 and Bid cleavage in S-type cells and death was blocked by caspase inhibitors but not by oxygen radical scavenger BHA. In contrast, dox-induced death in Ntype cells was caspase-independent and was inhibited by BHA. Dox induced a drop in mitochondrial membrane permeability in all cell lines. Dox-induced death in Stype cells gave rise to apoptotic nuclei, whereas in Ntype cells nuclei were non-apoptotic in morphology. Transfection of SH-EP cells with a dominant negative FADD mutant inhibited TRAIL-induced death, but had no effect on dox-induced apoptosis. These results suggest that S-type cells undergo apoptosis after dox treatment independently of death receptors, whereas N-type cells are killed by a caspase-independent mechanism.

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“…The 5-year survival rate for children (1-14 years) is approximately 30%. 96 Immunotherapies have been used with limited success. The humanized monoclonal anti-GD2 antibody has been used in numerous studies with initial success, but as with chemotherapy, relapse and resistance are common.…”

Section: Targeting Nf-jb In Diseasementioning

confidence: 99%

Targeting transcription factors for therapeutic benefit

2008

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Transcription factors are a large class of biological molecules that are important for health and disease. Despite that there are challenges to targeting them therapeutically and most approaches alter their activity indirectly. Research at the chemical biology interface has led to the development of new ways of targeting transcription factors including blocking transcription factor dimerisation, targeting specific DNA sequences and DNA decoys. This review discusses these issues with a view to inspiring the development of new agents that could be useful for the treatment of cancer.

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Survival of children with neuroblastoma

Cited by 44 publications

References 25 publications

Modulation of CD59 Expression by Restrictive Silencer Factor–Derived Peptides in Cancer Immunotherapy for Neuroblastoma

Modulation of CD59 Expression by Restrictive Silencer Factor–Derived Peptides in Cancer Immunotherapy for Neuroblastoma

Doxorubicin-induced death in neuroblastoma does not involve death receptors in S-type cells and is caspase-independent in N-type cells

Targeting transcription factors for therapeutic benefit

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