SynthesisFrontiers in oncology2020
Prognostic Role of the Activated p-AKT Molecule in Various Hematologic Malignancies and Solid Tumors: A Meta-Analysis.
Synthesis in Frontiers in oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
14 citing papers in PubMed, 13 citations in OpenAlex.
- The effect and mechanism of TIPE in promoting M2 polarization through DcR3 in the microenvironment of colorectal cancer.Cancer immunology, immunotherapy : CII · 2026Article
- PD-L1 in Ovarian Cancer: Immune Evasion, Tumor-Intrinsic Signaling, and Chemoresistance.Cancer medicine · 2026Review
- PIK3CA mutations and PI3K isoform expression define prognostic signatures in ovarian clear cell carcinoma.Archives of gynecology and obstetrics · 2026Article
- From Motor Proteins to Oncogenic Factors: The Evolving Role of Kinesin Superfamily Proteins in Breast Cancer Development.Molecular biotechnology · 2026Review
- HIST1H4L promotes small cell lung cancer tumorigenesis by regulating the PI3K/Akt pathway and serves as a potential diagnostic biomarker.Frontiers in oncology · 2026Article
- FAP promotes progression of oral leukoplakia via activation of PI3K/AKT pathway by interacting with ITGB1.Translational oncology · 2025Article
- Processed Products ofAnti-cancer agents in medicinal chemistry · 2025Article
- KIFC3 promotes the proliferation, migration and invasion of non-small cell lung cancer through the PI3K/AKT signaling pathway.Scientific reports · 2024Article
- ISG12a promotes immunotherapy of HBV-associated hepatocellular carcinoma through blocking TRIM21/AKT/β-catenin/PD-L1 axis.iScience · 2024Article
- ZNF191 alters DNA methylation and activates the PI3K-AKT pathway in hepatoma cells via transcriptional regulation of DNMT1.Cancer medicine · 2022Article
- Emerging Roles for AKT Isoform Preference in Cancer Progression Pathways.Molecular cancer research : MCR · 2021Review
- CK-3, A Novel Methsulfonyl Pyridine Derivative, Suppresses Hepatocellular Carcinoma Proliferation and Invasion by Blocking the PI3K/AKT/mTOR and MAPK/ERK Pathways.Frontiers in oncology · 2021Article
- EXPRESSION LEVELS OF FOXO-1, P27KIP1, MIR-27, MIR-186 AND AKT1/AKT-P PROTEINS IN WOMEN WITH ENDOMETRIAL CANCER AND HYPERPLASIA: IMPLICATIONS FOR THE HUMAN REPRODUCTIVE SYSTEM.Acta endocrinologica (Bucharest, Romania : 2005)Article
- High expression of IGHG1 promotes breast cancer malignant development by activating the AKT pathway.Cell cycle (Georgetown, Tex.)Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer is one of the main causes of human death worldwide. Recently, many studies have firmly established the causal relationship between oxidative stress and cancer initiation and progression. As a key protein in PI3K/Akt signaling pathway, p-AKT (phosphorylated Akt) participates in the process of oxidative stress and plays a prognostic role in various hematologic tumors and solid tumors. We conducted a comprehensive search of the PubMed, Embase and Cochrane libraries to identify studies published in the past decade involving cancer patients expressing p-AKT that reported overall survival (OS) during follow-up. In this study, 6,128 patients in total were evaluated from 29 enrolled articles, and we concluded that overexpression of p-AKT was closely related to worse OS in cancer patients with a hazard ratio (HR) of 2.33 (95% CI: 1.67-4.00). Furthermore, we conducted a subgroup analysis, and the results indicated that overexpression of p-AKT was associated with worse OS in hematological tumor (HR: 1.64, 95% CI: 1.41-1.92), and solid tumor (HR: 2.44, 95% CI: 1.61-5.26). High expression of p-AKT is related to poor prognosis of various hematologic tumors and solid tumors.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.