Imperial College London
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Dr Olivier E. Pardo

Faculty of Medicine, Department of Surgery & Cancer

Reader in Cancer Cell Signalling
 
 
 
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Contact

 

+44 (0)20 7594 2814o.pardo Website CV

 
 
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Location

 

145ICTEM buildingHammersmith Campus

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Summary

 

Publications

Citation

BibTex format

@article{Hoeland:2014:10.1371/journal.pone.0094132,
author = {Hoeland, K and Boller, D and Hagel, C and Dolski, S and Treszl, A and Pardo, OE and Cwiek, P and Salm, F and Leni, Z and Shepherd, PR and Styp-Rekowska, B and Djonov, V and von, Bueren AO and Frei, K and Arcaro, A},
doi = {10.1371/journal.pone.0094132},
journal = {PLOS One},
title = {Targeting Class I-A PI3K Isoforms Selectively Impairs Cell Growth, Survival, and Migration in Glioblastoma},
url = {http://dx.doi.org/10.1371/journal.pone.0094132},
volume = {9},
year = {2014}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - The phosphoinositide 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway is frequently activated in human cancer and plays a crucial role in glioblastoma biology. We were interested in gaining further insight into the potential of targeting PI3K isoforms as a novel anti-tumor approach in glioblastoma. Consistent expression of the PI3K catalytic isoform PI3K p110α was detected in a panel of glioblastoma patient samples. In contrast, PI3K p110β expression was only rarely detected in glioblastoma patient samples. The expression of a module comprising the epidermal growth factor receptor (EGFR)/PI3K p110α/phosphorylated ribosomal S6 protein (p-S6) was correlated with shorter patient survival. Inhibition of PI3K p110α activity impaired the anchorage-dependent growth of glioblastoma cells and induced tumor regression in vivo. Inhibition of PI3K p110α or PI3K p110β also led to impaired anchorage-independent growth, a decreased migratory capacity of glioblastoma cells, and reduced the activation of the Akt/mTOR pathway. These effects were selective, because targeting of PI3K p110δ did not result in a comparable impairment of glioblastoma tumorigenic properties. Together, our data reveal that drugs targeting PI3K p110α can reduce growth in a subset of glioblastoma tumors characterized by the expression of EGFR/PI3K p110α/p-S6.
AU  - Hoeland,K
AU  - Boller,D
AU  - Hagel,C
AU  - Dolski,S
AU  - Treszl,A
AU  - Pardo,OE
AU  - Cwiek,P
AU  - Salm,F
AU  - Leni,Z
AU  - Shepherd,PR
AU  - Styp-Rekowska,B
AU  - Djonov,V
AU  - von,Bueren AO
AU  - Frei,K
AU  - Arcaro,A
DO  - 10.1371/journal.pone.0094132
PY  - 2014///
SN  - 1932-6203
TI  - Targeting Class I-A PI3K Isoforms Selectively Impairs Cell Growth, Survival, and Migration in Glioblastoma
T2  - PLOS One
UR  - http://dx.doi.org/10.1371/journal.pone.0094132
UR  - http://hdl.handle.net/10044/1/41912
VL  - 9
ER  -
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