Abstract: The present invention relates to the stratification and treatment of patients suffering of cancer. Due to the fact that anti-PD1 therapy targets lymphocytes and the efficiency of anti-cancer therapy is measured by the impact on the tumor cells, the inventors postulated that studying the molecular mechanisms of resistance of anti-PD1 therapy should take into consideration existing intercellular communication between lymphocytes and tumor cells. As exosomes are the carriers for the intercellular transfer of the miRNA responsible of chemoresistance, they herein investigated whether exposure of T cells to anti-PD1 therapy might promote the expression of exosomal miRNA (exomiR) causing the chemoresistance of cancer cells. Surprisingly, they found that anti-PD1 exposure of T-cell promotes an enrichment of exosomal miRNA-4315. They also noted that exosomal miRNA-4315 induced a phenomenon of apopto-resistance to conventional chemotherapies in cancer cells receiving exosomal miRNA-4315.

Abstract: The present invention relates the treatment and prognostic of cancer like glioblastoma. Here, the inventors focused their study on the impact of presence of N6-adenosine methylation in miRNA-200b-3p in samples of patients suffering from glioblastoma multiforme (GBM). Their study was particularly focused on the impact of miRNA-200b-3p and its adenosine methylation on the expression of XIAP. XIAP acts as an anti-apoptotic protein via the inhibition of caspase-3 and -7 activation and high XIAP expression is associated with a poor survival in several solid tumors. Thus, the miR-200b-3p-mediated repression of XIAP mRNA expression appears as a mechanism governing the caspase-3 and -7 activity and the apoptosis. In theory, in the presence of miR-200b-3p, XIAP mRNA expression is repressed and caspase-3 and -7 can be activated to promote apoptosis.