Glioblastoma (GBM) is considered a primary brain tumor which is extremely aggressive and difficult to treat. Glioblastoma is demarcated by highly aggressive proliferation with great invasive potential as well as refractory to present treatments due to suppression of pro-apoptotic pathways (Karmakar et al., 2007). Such factors up-regulated in cancer involve cell proliferation, cell invasion, metastasis, angiogenesis, and resistance to chemo and radiotherapy (Kunnumakkara et al., 2008). Treatments for glioblastoma include chemotherapy, surgery, and radiotherapy, yet survival rates with these treatments remain small. To improve the prognosis for patients with Glioblastoma, an effective treatment is required. Determination of how treatments may interact with apoptotic pathways may be essential to finding a therapy to control and prevent glioblastoma proliferation. Cell survival signaling mechanisms such as overexpression of nuclear factor kappa B (NKB) and anti-apoptotic Bcl-2 proteins may play important roles to prevent apoptosis. However, inhibition of these factors favor apoptosis and may provide a strategy for treating such cancers as glioblastomas (Biswas et al., 2003). Finding a therapeutic approach which can inhibit anti-apoptotic
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Apoptosis can be triggered by two major pathways which include a death receptor-associated extrinsic pathway and a mitochondria-
Apoptosis can be triggered by two major pathways which include a death receptor-associated extrinsic pathway and a mitochondria-