13 February 2014
The next CRCL/CLB seminar will take place Friday the 3rd of March, at 11.30am in the ONCORA meeting room (Centre Léon Bérard, 2nd floor). We are pleased to welcome Silvia Giordana (Turino). More information will come soon.
WIN Symposium June Paris
21 February 2017
The WIN 2017 Symposium program will elaborate the theme ‘Expediting Global Innovation in Precision Cancer Medicine’ in six plenary sessions, divided over two days of meetings. The program will be supplemented by poster viewing sessions, not overlapping with the plenary sessions, and a plenary poster awarding ceremony.
1st European Workshop of Translational Research in Bone Sarcoma - 19-20 June 2017
02 January 2017
This 2-d European workshop is aimed at young researchers (post-docs, PhD, etc.) working on Bone Sarcoma/Sarcoma. The meeting aims to provide training in bone sarcoma and more specifically osteosarcoma, chondrosarcoma and Ewing sarcoma. Invited speaker presentations will be complemented by oral communications and poster presentations from attending delegates (priority given to young researchers).
ZEB1-mediated melanoma cell plasticity enhances resistance to MAPK inhibitors
29 November 2016
This work involved the team of Alain Puisieux.
Targeted therapies with MAPK inhibitors (MAPKi) are faced with severe problems of resistance in BRAF-mutant melanoma. In parallel to the acquisition of genetic mutations, melanoma cells may also adapt to the drugs through phenotype switching. The ZEB1 transcription factor, a known inducer of EMT and invasiveness, is now considered as a genuine oncogenic factor required for tumor initiation, cancer cell plasticity, and drug resistance in carcinomas. Here, we show that high levels of ZEB1 expression are associated with inherent resistance to MAPKi in BRAFV600-mutated cell lines and tumors.
PubMed access: click here
Structural Decoding of the Netrin-1/UNC5 Interaction and its Therapeutical Implications in Cancers
25 March 2016
This study involves the team of Patrick Mehlen.
Netrin-1 has been shown to be up-regulated in a fraction of human cancers as a mechanism to allow these tumors to escape the pro-apoptotic activity of some of its main dependence receptors, the UNC5 homologs (UNC5H). Here we identify the V-2 domain of netrin-1 to be important for its interaction with the Ig1/Ig2 domains of UNC5H2. We generate a humanized anti-netrin-1 antibody that disrupts the interaction between netrin-1 and UNC5H2 and triggers death of netrin-1-expressing tumor cells in vitro. We also present evidence that combining the anti-netrin-1 antibody with epidrugs such as decitabine could be effective in treating tumors showing no or modest netrin-1 expression. These results support that this antibody is a promising drug candidate.
PubMed access: click here