ReviewPharmaceutics2023
Targeting EGFR/PI3K/AKT/mTOR Signaling in Hepatocellular Carcinoma.
Review in Pharmaceutics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.
- Clinicopathological significance of AKT and phosphorylated AKT expression in hepatocellular carcinoma: A Meta-Analysis.BMC cancer · 2025Pooled it
- FAT4 loss promotes tumor growth and ferroptosis resistance in hepatocellular carcinoma via PI3K/AKT pathway activation.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Article
- Emetine and Its Derivatives as Anticancer Agents Targeting the PI3K/AKT/mTOR Pathway: A Narrative Review of Mechanisms, Pharmacology, and Clinical Insights.Journal of cellular and molecular medicine · 2026Review
- Astragaloside IV and rapamycin co-loaded bone marrow mesenchymal stem cell-derived exosome nanocarriers for targeted modulation of the PI3K/Akt/mTOR pathway in hepatocellular carcinoma.Nanomedicine (London, England) · 2026Article
- Agomelatine versus gefitinib against HepG2 cells: Modulating PI3K/AKT and MAPK/RAF1/c-FOS pathways.Molecular biology reports · 2026Article
- Elucidating the Mechanism of Oridonin in Treating Hepatocellular Carcinoma: Network Pharmacology and Experimental Validation.Journal of cellular and molecular medicine · 2026Article
- LARS promotes hepatocellular carcinoma progression via the PI3K/AKT/mTOR pathway and interaction with RPS5, and serves as a prognostic biomarker.Molecular medicine (Cambridge, Mass.) · 2026Article
- CZC54252 overcomes Osimertinib resistance by targeting EGFRBMC pharmacology & toxicology · 2026Article
- Unsaponifiable fraction of black Vitis vinifera seed oil attenuates liver cancer progression by targeting apoptosis and key tumor-associated genes: In vitro, in vivo, and in silico studies.Scientific reports · 2026Article
- miRNA-1231 Regulated EGFR Signaling: A Potential Therapeutic Target for Hepatocellular Carcinoma.Applied biochemistry and biotechnology · 2026Article
- Exploring and validating the molecular targets and potential mechanisms of shikonin against osteomyelitis through computational analyses and animal experiments.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- mTOR in radiotherapy of lung cancer: Mechanisms of radiation resistance and therapeutic implications (Review).International journal of oncology · 2026Review
- TET1 suppresses hepatocellular carcinoma progression by modulating the PI3K/Akt signaling pathways.Scientific reports · 2026Article
- Mechanistic Research on the Crosstalk Between Macrophage Polarization and Energy Metabolic Reprogramming in Hepatocellular Carcinoma.Journal of hepatocellular carcinoma · 2026Review
- Quercetin suppresses the progression of HBV-associated hepatocellular carcinoma by modulating the EGFR signaling pathway.PloS one · 2026Article
- Harmine suppresses the malignant phenotypes of Lewis lung carcinoma cells by inhibiting EGFR phosphorylation.American journal of translational research · 2026Article
- SEMA4F Regulates the Malignant Phenotype of Hepatocellular Carcinoma Cells Through the PI3K-Akt Pathway.Journal of hepatocellular carcinoma · 2026Article
- Therapeutic Potential of Silver Nanoparticles in Hepatocellular Carcinoma: From Pathogenesis to Clinical Perspectives.International journal of nanomedicine · 2026Review
- Navigating the Labyrinth of Hepatocellular Carcinoma: Leveraging AI/ML for Precision Oncology.Oncology research · 2026Review
- Sophoricoside from sophora japonica L. is efficacious as monotherapy or in combination with lenvatinib in hepatocellular carcinoma via targeting EGFR.Scientific reports · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Hepatocellular carcinoma (HCC) poses a significant global health concern, with its incidence steadily increasing. The development of HCC is a multifaceted, multi-step process involving alterations in various signaling cascades. In recent years, significant progress has been made in understanding the molecular signaling pathways that play central roles in hepatocarcinogenesis. In particular, the EGFR/PI3K/AKT/mTOR signaling pathway in HCC has garnered renewed attention from both basic and clinical researchers. Preclinical studies in vitro and in vivo have shown the effectiveness of targeting the key components of this signaling pathway in human HCC cells. Thus, targeting these signaling pathways with small molecule inhibitors holds promise as a potential therapeutic option for patients with HCC. In this review, we explore recent advancements in understanding the role of the EGFR/PI3K/AKT/mTOR signaling pathway in HCC and assess the effectiveness of targeting this signaling cascade as a potential strategy for HCC therapy based on preclinical studies.
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What OpenQuestion holds
Registered trials
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.