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The ETV5 oncogene is a target of activated ALK signaling in neuroblastoma

Liselot Mus UGent, Irina Lambertz, Candy Kumps, Shana Claeys UGent, Geertrui Denecker UGent, Wouter Van Loocke UGent, Christophe Van Neste UGent, Jan Koster, Rogier Versteeg, Nadine Van Roy UGent, et al. (2017) f-Tales, Abstracts.
abstract
Neuroblastoma (NB) is an aggressive childhood cancer arising from sympatho-adrenergic neuronal progenitors. Current survival rates are still disappointingly low for high risk desease indicating the need for novel therapeutic approaches. Mutant ALK is currently the most prominent druggable target being present in 10% of NB patients. Unfortunately, targeted therapies with single compounds are prone to resistance. Therefore, deeper insights into the ALK downstream pathway is critical to understand resistance mechanisms and to identify additional targets for combination therapy. As part of a broader study aimed at dissecting downstream ALK signaling, we observed robust regulation of the oncogene ETV5 in multiple NB cell lines through the ALK-activated RAS/MAPK-axis. Further functional analysis revealed that ALK-mutated NB cell lines depend on ETV5 for proliferation, invasion and colony formation. The effect of ETV5 on proliferation was further supported by mouse xenografts of a NB cell line with stable ETV5 knock-down. Next, transcriptome profiling of both ETV5 knock-down cell lines and xenografts revealed an ETV5 signature which (1) identified patients with poor overall survival, (2) was enriched for an Ewing sarcoma gene signature, suggesting a possible common perturbed gene regulatory pathway and (3) contained CXCR4, an important mediator of invasion and metastasis, and TRIM67, a negative regulator of the RAS-pathway, as possible ETV5 targets.
Please use this url to cite or link to this publication:
author
organization
year
type
conference (poster)
publication status
published
subject
in
f-Tales, Abstracts
conference name
f-Tales: Cancer : an old dog with new tricks
conference location
Leuven, Belgium
conference start
2017-03-06
conference end
2016-03-07
language
English
UGent publication?
yes
classification
C3
id
8516922
handle
http://hdl.handle.net/1854/LU-8516922
date created
2017-04-04 15:55:33
date last changed
2017-07-31 14:54:31
@inproceedings{8516922,
  abstract     = {Neuroblastoma (NB) is an aggressive childhood cancer arising from sympatho-adrenergic neuronal progenitors. Current survival rates are still disappointingly low for high risk desease indicating the need for novel therapeutic approaches. Mutant ALK is currently the most prominent druggable target being present in 10\% of NB patients.  Unfortunately, targeted therapies with single compounds are prone to resistance. Therefore, deeper insights into the ALK downstream pathway is critical to understand resistance mechanisms and to identify additional targets for combination therapy. 
As part of a broader study aimed at dissecting downstream ALK signaling, we observed robust regulation of the oncogene ETV5 in multiple NB cell lines through the ALK-activated RAS/MAPK-axis. Further functional analysis revealed that ALK-mutated NB cell lines depend on ETV5 for proliferation, invasion and colony formation. The effect of ETV5 on proliferation was further supported by mouse xenografts of a NB cell line with stable ETV5 knock-down. Next, transcriptome profiling of both ETV5 knock-down cell lines and xenografts revealed an ETV5 signature which (1) identified patients with poor overall survival, (2) was enriched for an Ewing sarcoma gene signature, suggesting a possible common perturbed gene regulatory pathway and (3) contained CXCR4, an important mediator of invasion and metastasis, and TRIM67, a negative regulator of the RAS-pathway, as possible ETV5 targets.},
  author       = {Mus, Liselot and Lambertz, Irina and Kumps, Candy and Claeys, Shana and Denecker, Geertrui and Van Loocke, Wouter and Van Neste, Christophe and Koster, Jan and Versteeg, Rogier and Van Roy, Nadine and De Wilde, Bram and Laureys, Genevieve and Schulte, Johannes and De Wever, Olivier and De Preter, Katleen and Speleman, Franki},
  booktitle    = {f-Tales, Abstracts},
  language     = {eng},
  location     = {Leuven, Belgium},
  title        = {The ETV5 oncogene is a target of activated ALK signaling in neuroblastoma},
  year         = {2017},
}

Chicago
Mus, Liselot, Irina Lambertz, Candy Kumps, Shana Claeys, Geertrui Denecker, Wouter Van Loocke, Christophe Van Neste, et al. 2017. “The ETV5 Oncogene Is a Target of Activated ALK Signaling in Neuroblastoma.” In f-Tales, Abstracts.
APA
Mus, L., Lambertz, I., Kumps, C., Claeys, S., Denecker, G., Van Loocke, W., Van Neste, C., et al. (2017). The ETV5 oncogene is a target of activated ALK signaling in neuroblastoma. f-Tales, Abstracts. Presented at the f-Tales: Cancer : an old dog with new tricks.
Vancouver
1.
Mus L, Lambertz I, Kumps C, Claeys S, Denecker G, Van Loocke W, et al. The ETV5 oncogene is a target of activated ALK signaling in neuroblastoma. f-Tales, Abstracts. 2017.
MLA
Mus, Liselot, Irina Lambertz, Candy Kumps, et al. “The ETV5 Oncogene Is a Target of Activated ALK Signaling in Neuroblastoma.” f-Tales, Abstracts. 2017. Print.