Differences
This shows you the differences between two versions of the page.
| Both sides previous revision Previous revision Next revision | Previous revision | ||
|
group_2_presentation_1_-_glioblastoma [2017/10/06 19:58] morgal |
group_2_presentation_1_-_glioblastoma [2018/01/25 15:19] (current) |
||
|---|---|---|---|
| Line 1: | Line 1: | ||
| + | Link to ppt: https://docs.google.com/a/mcmaster.ca/presentation/d/1aPDGB9N-jfVw91J4yq4N44fnEg5pGluNftePloslFag/edit?usp=sharing | ||
| ====== Introduction ====== | ====== Introduction ====== | ||
| Line 127: | Line 128: | ||
| **Bevacizumab (Avastin®)** | **Bevacizumab (Avastin®)** | ||
| - | Bevacizumab (Avastin®) is a monoclonal antibody implemented in GBM chemotherapeutic regiments to target vascular endothelial growth factor (VEGF) and was approved by the FDA in 2009 after clinical trials had demonstrated excellent performance. The VEGF protein is needed for angiogenesis, a process that involves the synthesis of new vasculature from pre-existing vessels and occurs during wound healing and when cells are deficient in oxygen levels. The synthesis of new blood vessels among tumor cells mediated by VEGF leads to a greater blood and oxygen supply necessary for the proliferation of GBM cells (Gil-Gil et al. 2013). Avastin works to reduce vascular permeability and edema, enhancing delivery of oxygen to brain cells and reducing necrosis in the tumor core when administered in conjunction with radiation therapy (Davis 2016). According to Gil-Gil et al. 2013, GBM cells generate the proangiogenic factor called VEGF which binds with its tyrosine kinase receptor on the surface of endothelial cells, initiating a signal cascade resulting in angiogenesis. Figure 7 demonstrates that Bevacizumab is easily able to penetrate the selectively permeable blood-brain barrier with a molecular weight of 149 kDa and binds with a high affinity to VEGF, sterically inhibiting the factor from binding to its receptors on endothelial cells and effectively reducing angiogenesis, inhibiting tumor growth, and reducing edema in the brain. | + | Bevacizumab (Avastin®) is a monoclonal antibody implemented in GBM chemotherapeutic regiments to target vascular endothelial growth factor (VEGF) and was approved by the FDA in 2009 after clinical trials had demonstrated excellent performance. The VEGF protein is needed for angiogenesis, a process that involves the synthesis of new vasculature from pre-existing vessels and occurs during wound healing and when cells are deficient in oxygen levels. The synthesis of new blood vessels among tumor cells mediated by VEGF leads to a greater blood and oxygen supply necessary for the proliferation of GBM cells (Gil-Gil et al. 2013). Avastin works to reduce vascular permeability and edema, enhancing delivery of oxygen to brain cells and reducing necrosis in the tumor core when administered in conjunction with radiation therapy (Davis 2016). According to Gil-Gil et al. 2013, GBM cells generate the proangiogenic factor called VEGF which binds with its tyrosine kinase receptor on the surface of endothelial cells, initiating a signal cascade resulting in angiogenesis. Figure 12 demonstrates that Bevacizumab is easily able to penetrate the selectively permeable blood-brain barrier with a molecular weight of 149 kDa and binds with a high affinity to VEGF, sterically inhibiting the factor from binding to its receptors on endothelial cells and effectively reducing angiogenesis, inhibiting tumor growth, and reducing edema in the brain. |
| {{ :avastin.png?500 |}} | {{ :avastin.png?500 |}} | ||
