Table 2.
EGFRvIII issue/process | Mechanism/way to address | Selected references |
---|---|---|
EGFRvIII presence in tumors/cancers | GB in about 40%, rarely in HNCSCC, lung prostate, colorectal cancer, breast cancer | [27, 33–41, 43] |
EGFRvIII mechanism of mutation | Deletion of EGFR exons 2–7 | [26–29, 43] |
EGFRvIII mechanism of action | Several models: (1) Heterodimerization with EGFRWT (2) Homodimerization (3) EGFRvIII and MET cooperation, FAK involved (4) OSMR mechanism Resistant to degradation important for all models |
[16, 17, 121–126, 142, 143] |
EGFRvIII biological role | Extreme opinions: from lack of important role at advanced cancer (tumor) stages, to role in self-renewal, survival, and proliferation of cancer stem cells | [33, 147, 150, 152–158, 164, 165] |
EGFRvIII cell culture models | 3D primary cell cancer cell models, DK-MG model, genetically modified cancer cell lines | [21, 150, 153, 167, 242–244, 246–248] |