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Abstract Aberrant activation of the phosphatidyl-inositol-3-kinase/protein kinase B (AKT) pathway has clinical relevance to radiation resistance, but the underlying mechanisms are incompletely understood

Key Points Aberrant c-MET pathway activation occurs frequently in gastrointestinal tumours and can result from multiple mechanisms, including c-MET protein overexpression, MET amplification or enhanced transcription and/or aberrant autocrine or paracrine secretion of HGF Activated c-MET signalling results in enhanced cancer cell proliferation, survival and invasion