The majority of therapeutic tactics for treating GBM, including surgical resection and chemotherapy, target the main tumor mass; thus, satellite lesions peripheral to the locally invasive main tumor mass are left untreated and account for tumor recurrence within 2 to 3 cm of the resected tumor margin. Chemotherapy may be effective at treating proliferating cells comprising the tumor core; however, invasive malignant cells possess a genetic profile distinct from the tumor core and capable of evading the drug's mode of action. Also referred to as the "go or grow hypothesis," invasive tumors consist of malignant cells programmed to either proliferate and give rise to main tumor masses or migrate and re-initiate tumorigenesis along white matter tracts and perivascular spaces. Invasive patterns of GBM, first described as "secondary structures of Scherer," are represented as perineuronal or perivascular satellitosis, have supine spread, and invade along the white matter tracts. The chemokine receptor CXCR4 is found to be up-regulated in
The majority of therapeutic tactics for treating GBM, including surgical resection and chemotherapy, target the main tumor mass; thus, satellite lesions peripheral to the locally invasive main tumor mass are left untreated and account for tumor recurrence within 2 to 3 cm of the resected tumor margin. Chemotherapy may be effective at treating proliferating cells comprising the tumor core; however, invasive malignant cells possess a genetic profile distinct from the tumor core and capable of evading the drug's mode of action. Also referred to as the "go or grow hypothesis," invasive tumors consist of malignant cells programmed to either proliferate and give rise to main tumor masses or migrate and re-initiate tumorigenesis along white matter tracts and perivascular spaces. Invasive patterns of GBM, first described as "secondary structures of Scherer," are represented as perineuronal or perivascular satellitosis, have supine spread, and invade along the white matter tracts. The chemokine receptor CXCR4 is found to be up-regulated in