Imperial College London

DrGeorgiosGiamas

Faculty of MedicineDepartment of Surgery & Cancer

Visiting Professor
 
 
 
//

Contact

 

+44 (0)20 7594 2804g.giamas Website

 
 
//

Location

 

Hammersmith HospitalHammersmith Campus

//

Summary

 

Publications

Citation

BibTex format

@article{Simon:2018:10.1186/s12943-018-0878-x,
author = {Simon, T and Pinioti, S and Schellenberger, P and Rajeeve, V and Wendler, F and Cutillas, PR and King, A and Stebbing, J and Giamas, G},
doi = {10.1186/s12943-018-0878-x},
journal = {Molecular Cancer},
title = {Shedding of bevacizumab in tumour cells-derived extracellular vesicles as a new therapeutic escape mechanism in glioblastoma},
url = {http://dx.doi.org/10.1186/s12943-018-0878-x},
volume = {17},
year = {2018}
}

RIS format (EndNote, RefMan)

TY  - JOUR
AB - Glioblastoma (GBM) is the most aggressive type of primary brain tumours. Anti-angiogenic therapies (AAT), such as bevacizumab, have been developed to target the tumour blood supply. However, GBM presents mechanisms of escape from AAT activity, including a speculated direct effect of AAT on GBM cells. Furthermore, bevacizumab can alter the intercellular communication of GBM cells with their direct microenvironment. Extracellular vesicles (EVs) have been recently described as main acts in the GBM microenvironment, allowing tumour and stromal cells to exchange genetic and proteomic material. Herein, we examined and described the alterations in the EVs produced by GBM cells following bevacizumab treatment. Interestingly, bevacizumab that is able to neutralise GBM cells-derived VEGF-A, was found to be directly captured by GBM cells and eventually sorted at the surface of the respective EVs. We also identified early endosomes as potential pathways involved in the bevacizumab internalisation by GBM cells. Via MS analysis, we observed that treatment with bevacizumab induces changes in the EVs proteomic content, which are associated with tumour progression and therapeutic resistance. Accordingly, inhibition of EVs production by GBM cells improved the anti-tumour effect of bevacizumab. Together, this data suggests of a potential new mechanism of GBM escape from bevacizumab activity.
AU - Simon,T
AU - Pinioti,S
AU - Schellenberger,P
AU - Rajeeve,V
AU - Wendler,F
AU - Cutillas,PR
AU - King,A
AU - Stebbing,J
AU - Giamas,G
DO - 10.1186/s12943-018-0878-x
PY - 2018///
SN - 1476-4598
TI - Shedding of bevacizumab in tumour cells-derived extracellular vesicles as a new therapeutic escape mechanism in glioblastoma
T2 - Molecular Cancer
UR - http://dx.doi.org/10.1186/s12943-018-0878-x
UR - http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000443533800001&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=1ba7043ffcc86c417c072aa74d649202
UR - http://hdl.handle.net/10044/1/62586
VL - 17
ER -