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Molecular architecture and signaling differences between WT EGFR and EGFRvIII in HNSCC. WT EGFR is activated by the binding of various ligands whereas EGFRvIII exhibits truncations in its extracellular domain and is constitutively active. Both WT EGFR and EGFRvIII promote tumorigenesis via pathways initiated by the phosphorylation of certain effector proteins and their respective pathways. Additionally EGFRvIII exhibits unique downstream effectors separate from WT EGFR.

Journal: Frontiers in Oncology

Article Title: EGFRvIII expression in head and neck squamous cell carcinoma: clinical significance and sources of frequency variation across studies

doi: 10.3389/fonc.2026.1790296

Figure Lengend Snippet: Molecular architecture and signaling differences between WT EGFR and EGFRvIII in HNSCC. WT EGFR is activated by the binding of various ligands whereas EGFRvIII exhibits truncations in its extracellular domain and is constitutively active. Both WT EGFR and EGFRvIII promote tumorigenesis via pathways initiated by the phosphorylation of certain effector proteins and their respective pathways. Additionally EGFRvIII exhibits unique downstream effectors separate from WT EGFR.

Article Snippet: 13. , Chang ( ) , 2013 , 108 , Taiwan , Oral cavity 32.4% tongue, 43.5% buccal mucosa, remaining unspecified oral sites. , FFPE , IHC , WT EGFR (Novocastra RTU-EGFR-384), EGFRvIII (4-5H), PTEN (138G8), pAKT (Ser473 D9E) , 75% (31.5% high expression) , >5% membranous (WT EGFR), >5% cytoplasmic (EGFRvIII, PTEN, pAKT); EGFRvIII scored 0–4+ Classified into five groups according to the extent of moderate to strong cytoplasmic reactivity: 0, (none); 1+, (1 ~ 24%); 2+, (25 ~ 49%); 3+, (50 ~ 74%); and 4+, (75 ~ 100%) , EGFRvIII correlated with tumor T classification and TNM stage; EGFRvIII and pAKT were independent predictors of patient survival.

Techniques: Binding Assay, Phospho-proteomics