Mercoledì 3 aprile appuntamento con il ciclo di Seminari del DSF: "Macrophage plasticity in inflammatory diseases and cancers".
L'incontro si svolgerà dalle 13:00 alle 13:40 in aula seminari al II piano di l.go Donegani 2 (ex Wild).
Il talk sarà tenuto da Chiara Porta (UNIUPO – DSF).
Macrophage plasticity, namely the ability of macrophages to respond to microenvironmental changes with the expression of different functional programs of activation, is essential for host defense and tissue homeostasis, but it may also promotes the development of different diseases. Exploring the molecular mechanisms driving macrophage polarized activation in infectious diseases and established cancers we identified that p50 NF-κB is a key molecule for the expression of an M2-skewed phenotype. Accordingly, we have recently demonstrated that p50 NF-κB supports colorectal cancer development and progression through its commitment to the tumor-promoting (M2-like) activation of macrophages. Therefore p50 NF-κB represents both a new prognostic indicator and an attractive target for therapeutic interventions. Strategies aimed to “re-educate” tumor associated macrophages (TAM) in “M1” effector cells have recently entered clinical trials. Malignant pleura mesothelioma (MPM) is an aggressive cancer with dismal prognosis. We are now investigating whether the combination of TAM reprograming with Tazemetostat, an inhibitor of the histone methyltransferase EZH2, could represent a new therapeutic option for MPM. Our preliminary results indicate that M1-polarized monocytes can kill MPM cells enhancing the anti-tumor effect of Tazemetostat. These findings prompt us to go insight the study of potential synergistic effects of epigenetic rewiring in association with macrophage-based immunotherapy.