Literature DB >> 15927359

Targeting programmed cell death pathways with experimental therapeutics: opportunities in high-risk neuroblastoma.

Kelly C Goldsmith1, Michael D Hogarty.   

Abstract

Neuroblastoma is a pediatric solid tumor with high morbidity and mortality in association with particular high-risk biological and clinical features (such as MYCN proto-oncogene amplification or advanced tumor stage). Such high-risk neuroblastomas may be initially responsive to cytoreductive therapies, yet the majority will ultimately demonstrate de novo or acquired chemoresistance leading to tumor progression and death. Insight into the genetic alterations responsible for these phenotypes are beginning to be gained, and subversion of inherent programmed cell death pathways is a common theme. Intact apoptosis pathways protect cells against neoplastic transformation and provide the mechanisms by which cytotoxic agents exert their effects. When these pathways are abolished through alterations in the cell death machinery, they complement deregulated oncogenes to promote tumor initiation and therapy resistance. Currently, therapeutic intensity for high-risk neuroblastoma has been advanced to near-tolerance with only modest gains in survival, and it is likely that further improvements in outcome will require innovative approaches that target key regulatory pathways that potentiate currently available therapies. Efforts to abrogate the cancer cell 'survival bias' engendered by alterations in death pathways are now a major focus in experimental cancer therapeutics, and their application to the problem of high-risk neuroblastoma form the basis of this review. These include agents that activate death receptors (TRAIL-agonists) or restore DISC competency (CDDO, DNA methyltransferase and HDAC inhibitors); reduce pro-survival Bcl2 homologues (Oblimersen sodium [AS-Bcl2], AS-Mcl1) or deliver a pro-apoptotic BH3 protein burden (BH3 peptides, gossypol, ABT737); or repress IAPs (Smac/Diablo peptides, AS-XIAP, AS-Survivin). As our knowledge of apoptosis dysregulation in neuroblastoma evolves, the possibilities for pro-apoptotic therapeutics seems not only promising, but a realistic adjunct to conventional treatments.

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Year:  2005        PMID: 15927359     DOI: 10.1016/j.canlet.2005.01.048

Source DB:  PubMed          Journal:  Cancer Lett        ISSN: 0304-3835            Impact factor:   8.679


  31 in total

Review 1.  Therapeutic targets for neuroblastomas.

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2.  HsMAD2 mRNA expression may be a predictor of sensitivity to paclitaxel and survival in neuroblastoma.

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3.  The stress protein BAG3 stabilizes Mcl-1 protein and promotes survival of cancer cells and resistance to antagonist ABT-737.

Authors:  Mariana Boiani; Cristina Daniel; Xueyuan Liu; Michael D Hogarty; Lawrence J Marnett
Journal:  J Biol Chem       Date:  2013-01-22       Impact factor: 5.157

4.  EGFR signaling defines Mcl⁻1 survival dependency in neuroblastoma.

Authors:  Srilatha Nalluri; Susan K Peirce; Rachel Tanos; Haneen A Abdella; Dipan Karmali; Michael D Hogarty; Kelly C Goldsmith
Journal:  Cancer Biol Ther       Date:  2015       Impact factor: 4.742

5.  The role of natural products in revealing NRF2 function.

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6.  From bench to bedside: the growing use of translational research in cancer medicine.

Authors:  Erin M Goldblatt; Wen-Hwa Lee
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7.  Sensitization to TRAIL-induced apoptosis in human neuroblastoma SK-N-AS cells by NF-κB inhibitors is dependent on reactive oxygen species (ROS).

Authors:  Tom Gatsinzi; Kerstin Iverfeldt
Journal:  J Neurooncol       Date:  2011-01-13       Impact factor: 4.130

8.  Stromal cell-derived CSF-1 blockade prolongs xenograft survival of CSF-1-negative neuroblastoma.

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Journal:  Int J Cancer       Date:  2010-03-15       Impact factor: 7.396

9.  Genistein induces receptor and mitochondrial pathways and increases apoptosis during BCL-2 knockdown in human malignant neuroblastoma SK-N-DZ cells.

Authors:  Joseph George; Naren L Banik; Swapan K Ray
Journal:  J Neurosci Res       Date:  2010-03       Impact factor: 4.164

10.  Chemoresistance acquisition induces a global shift of expression of aniogenesis-associated genes and increased pro-angogenic activity in neuroblastoma cells.

Authors:  Martin Michaelis; Denise Klassert; Susanne Barth; Tatyana Suhan; Rainer Breitling; Bernd Mayer; Nora Hinsch; Hans W Doerr; Jaroslav Cinatl; Jindrich Cinatl
Journal:  Mol Cancer       Date:  2009-09-29       Impact factor: 27.401

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