Séminaire médico-scientifique CRCL/CLB
vendredi 13 février 2015
Le prochain séminaire médico-scientifique CRCL/CLB se tiendra le vendredi 5 mai à 11h30 dans la salle ONCORA (Centre Léon Bérard, 2e étage). Nous serons heureux d'accueillir le Pr Cathrin Brisken (EPFL Lausanne). Plus d'informations prochainement.
WIN Symposium June Paris
mardi 21 février 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
lundi 2 janvier 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).
Information and registration: click here
A stemness-related ZEB1-MSRB3 axis governs cellular pliancy and breast cancer genome stability
mardi 11 avril 2017
Morel AP et al. Nature Medecine Avril 2017. Cette publication est issue des travaux de l'équipe d'Alain Puisieux.
Chromosomal instability (CIN), a feature of most adult neoplasms from their early stages onward, is a driver of tumorigenesis. However, several malignancy subtypes, including some triple-negative breast cancers, display a paucity of genomic aberrations, thus suggesting that tumor development may occur in the absence of CIN. Here we show that the differentiation status of normal human mammary epithelial cells dictates cell behavior after an oncogenic event and predetermines the genetic routes toward malignancy. Whereas oncogene induction in differentiated cells induces massive DNA damage, mammary stem cells are resistant, owing to a preemptive program driven by the transcription factor ZEB1 and the methionine sulfoxide reductase MSRB3. The prevention of oncogene-induced DNA damage precludes induction of the oncosuppressive p53-dependent DNA-damage response, thereby increasing stem cells' intrinsic susceptibility to malignant transformation. In accord with this model, a subclass of breast neoplasms exhibit unique pathological features, including high ZEB1 expression, a low frequency of TP53 mutations and low CIN.
PubMed access: click here
Structural Decoding of the Netrin-1/UNC5 Interaction and its Therapeutical Implications in Cancers
vendredi 25 mars 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