Combination Therapy

As part of our collaboration with Weissman’s group at Stanford, our research has established a role for CD47, a cell surface marker expressed on glioma cells, in preventing tumour cells phagocytosis through binding its receptor SIRPα on macrophages (“don’t eat me” signal). Furthermore, CD47 is a prognostic marker as its expression predisposes glioma patients to a poorer survival outcome as more than 80% of patients with the most aggressive glioma subtype, GBM, highly express CD47. This has significant clinical implications. We therefore hypothesize that CD47 can be targeted to suppress brain tumour growth. Since glioma patients are severely immunocompromised however, this approach has been refined to combine anti-CD47 therapy with adjuvant radiotherapy using Gamma Knife Surgery and chemotherapy with Temozolomide, or together with infusion of ex-vivo activated macrophages. The mission of the current research is to translating brain tumour immunotherapy from the lab bench via preclinical studies to the clinic.miceTreatment with anti-CD47 antibody decreases tumor size in the xenograft mouse model.Luciferase-expressing Human GBM cells were transplanted into the brains of immunocompromised mice. When palpable tumors (0.1 cm3) formed, treatment began with anti-CD47 antibody (B6H120) or control immunoglobulin (IgG). Representative images of brain tumor engrafted mice treated with anti-CD47 mAbs (PNAS, 2012)