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Adenovirus-mediated hPNPase(old-35) gene transfer as a therapeutic strategy for neuroblastoma

Tom Van Maerken UGent, Devanand Sarkar, Franki Speleman UGent, Paul Dent, William A. Weiss and Paul B. Fisher (2009) Journal of Cellular Physiology. 219(3). p.707-715
abstract
Current treatment options for neuroblastoma fail to eradicate the disease in the majority of high-risk patients, clearly mandating development of innovative therapeutic strategies. Gene therapy represents a promising approach for reversing the neoplastic phenotype or driving tumor cells to self-destruction. We presently studied the effects of adenovirus-mediated gene transfer of human polynucleotide phosphorylase (hPNPase(old-35)), a 3',5'-exoribonuclease with growth-inhibitory properties, in neuroblastoma cells. Transgene expression was driven by either the cytomegalovirus (CMV) promoter or by a tumor-selective promoter derived from progression elevated gene-3 (PEG-3). Our data demonstrate that efficient adenoviral transduction of neuroblastoma cells and robust transgene expression are feasible objectives, that the PEG-3 promoter is capable of selectively targeting gene expression in the majority of neuroblastoma cells, and that hPNPase(old-35) induces profound growth suppression and apoptosis of malignant neuroblastoma cells, while exerting limited effects on normal neural crest-derived melanocytes. These findings support future applications of hPNPase(old-35) for targeted gene-based therapy of neuroblastoma and suggest that combination with the PEG-3 promoter holds promise for creating a potent and selective neuroblastoma therapeutic.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
PEG-3 promoter, apoptosis, neuroblastoma, hPNPase(old-35), gene therapy
journal title
Journal of Cellular Physiology
J. Cell. Physiol.
volume
219
issue
3
pages
707 - 715
Web of Science type
Article
Web of Science id
000265547900023
JCR category
PHYSIOLOGY
JCR impact factor
4.586 (2009)
JCR rank
7/75 (2009)
JCR quartile
1 (2009)
ISSN
0021-9541
DOI
10.1002/jcp.21719
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
835705
handle
http://hdl.handle.net/1854/LU-835705
date created
2010-01-23 20:52:39
date last changed
2016-12-19 15:45:58
@article{835705,
  abstract     = {Current treatment options for neuroblastoma fail to eradicate the disease in the majority of high-risk patients, clearly mandating development of innovative therapeutic strategies. Gene therapy represents a promising approach for reversing the neoplastic phenotype or driving tumor cells to self-destruction. We presently studied the effects of adenovirus-mediated gene transfer of human polynucleotide phosphorylase (hPNPase(old-35)), a 3',5'-exoribonuclease with growth-inhibitory properties, in neuroblastoma cells. Transgene expression was driven by either the cytomegalovirus (CMV) promoter or by a tumor-selective promoter derived from progression elevated gene-3 (PEG-3). Our data demonstrate that efficient adenoviral transduction of neuroblastoma cells and robust transgene expression are feasible objectives, that the PEG-3 promoter is capable of selectively targeting gene expression in the majority of neuroblastoma cells, and that hPNPase(old-35) induces profound growth suppression and apoptosis of malignant neuroblastoma cells, while exerting limited effects on normal neural crest-derived melanocytes. These findings support future applications of hPNPase(old-35) for targeted gene-based therapy of neuroblastoma and suggest that combination with the PEG-3 promoter holds promise for creating a potent and selective neuroblastoma therapeutic.},
  author       = {Van Maerken, Tom and Sarkar, Devanand and Speleman, Franki and Dent, Paul and Weiss, William A. and Fisher, Paul B.},
  issn         = {0021-9541},
  journal      = {Journal of Cellular Physiology},
  keyword      = {PEG-3 promoter,apoptosis,neuroblastoma,hPNPase(old-35),gene therapy},
  language     = {eng},
  number       = {3},
  pages        = {707--715},
  title        = {Adenovirus-mediated hPNPase(old-35) gene transfer as a therapeutic strategy for neuroblastoma},
  url          = {http://dx.doi.org/10.1002/jcp.21719},
  volume       = {219},
  year         = {2009},
}

Chicago
Van Maerken, Tom, Devanand Sarkar, Franki Speleman, Paul Dent, William A. Weiss, and Paul B. Fisher. 2009. “Adenovirus-mediated hPNPase(old-35) Gene Transfer as a Therapeutic Strategy for Neuroblastoma.” Journal of Cellular Physiology 219 (3): 707–715.
APA
Van Maerken, T., Sarkar, D., Speleman, F., Dent, P., Weiss, W. A., & Fisher, P. B. (2009). Adenovirus-mediated hPNPase(old-35) gene transfer as a therapeutic strategy for neuroblastoma. Journal of Cellular Physiology, 219(3), 707–715.
Vancouver
1.
Van Maerken T, Sarkar D, Speleman F, Dent P, Weiss WA, Fisher PB. Adenovirus-mediated hPNPase(old-35) gene transfer as a therapeutic strategy for neuroblastoma. Journal of Cellular Physiology. 2009;219(3):707–15.
MLA
Van Maerken, Tom, Devanand Sarkar, Franki Speleman, et al. “Adenovirus-mediated hPNPase(old-35) Gene Transfer as a Therapeutic Strategy for Neuroblastoma.” Journal of Cellular Physiology 219.3 (2009): 707–715. Print.