Increased phosphorylation of AKT in high-risk gastric mucosa.

摘要: Aim: To establish the role of oxidative stress and v- akt murine thymoma viral oncogene homolog (AKT) activation in gastric cancer development, we examined levels phosphorylated AKT (pAKT), inducible nitric oxide synthase (iNOS), nitrotyrosine (NT), human telomerase reverse transcriptase (hTERT) by enzyme-linked immunosorbent assay 73 non-cancerous mucosa 10 carcinomas. We found that pAKT were associated with iNOS, NT, hTERT. Gastric was classified into four categories: chronic gastritis without Helicobacter pylori (CG), active H. (CAG), metaplastic (CMG), atypia (CGA). increasing pAKT, NT order CG, CAG, CMG, CGA. hTERT detected only These findings suggest might be induction CGA confer a high-risk status for carcinogenesis. v-Akt is pivotal regulator cell survival, proliferation, differentiation. It member phosphatidylinositol-3 kinase (PI3K) signaling pathway. Stimulation receptor tyrosine kinases or G-proteins activates PI3K, which turn AKT. phosphorylation maintained heat- shock protein-90, dephosphorylated protein phosphatase-2A. regulates via various growth factors cytokines. In particular, insulin-like factor-1 receptor, epidermal factor receptor-2, are important progression, activate (3, 15). also biomarker predicts metastasis