ArticleOncology letters2017
Phosphorylated AKT expression in tumor-adjacent normal tissue is associated with poor prognosis in patients with hepatocellular carcinoma.
Article in Oncology letters, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
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Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it, 6 citations in OpenAlex.
- Clinicopathological significance of AKT and phosphorylated AKT expression in hepatocellular carcinoma: A Meta-Analysis.BMC cancer · 2025Pooled it
- Diosgenin potentiates the anticancer effect of doxorubicin and volasertib via regulating polo-like kinase 1 and triggering apoptosis in hepatocellular carcinoma cells.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Article
- miR-342-3p suppresses hepatocellular carcinoma proliferation through inhibition of IGF-1R-mediated Warburg effect.OncoTargets and therapy · 2018Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The AKT pathway serves important roles in tumor cell growth. Its overexpression is associated with poor prognosis in a number of types of cancer; however, the role of AKT in the role of the pathogenesis of hepatocellular carcinoma (HCC) remains unclear. The present study was undertaken to explore the clinical relevance of phosphorylated AKT (p-AKT) in HCC. The level of p-AKT in tumor (TU) and paired adjacent normal liver (AN) tissue from 202 HCC patients was evaluated with immunohistochemistry. The results demonstrated that p-AKT was more highly expressed in TU than in AN tissue. Kaplan-Meier curves and Cox regression revealed that patients with a high expression of p-AKT (AN) exhibited reduced overall and relapse-free survival times; this was not observed at a statistically significant level in p-AKT (TU). Additionally, the high expression of p-AKT (AN) was positively correlated with hepatitis C virus (HCV) infection in HCC patients. These results support the hypothesis that AKT activation is a mechanism of HCV-induced hepatocarcinogenesis, suggesting that AKT can be a therapeutic target for the treatment of recurrent HCC subsequent to surgical resection.
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