ArticleTranslational cancer research2016
The IGF-1R/AKT pathway determines cell fate in response to p53.
Article in Translational cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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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.
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
20 citing papers in PubMed.
- Insulin Resistance and Inflammation.International journal of molecular sciences · 2026Review
- Anti-senescence therapies: a new concept to address cardiovascular disease.Cardiovascular research · 2025Review
- White Adipocyte Stem Cell Expansion Through Infant Formula Feeding: New Insights into Epigenetic Programming Explaining the Early Protein Hypothesis of Obesity.International journal of molecular sciences · 2025Review
- Antitumor Activity, Mechanisms of Action and Phytochemical Profiling of Sub-Fractions Obtained fromMolecules (Basel, Switzerland) · 2025Article
- Insulin-like Growth Factor 1 (IGF1) and Its Isoforms: Insights into the Mechanisms of Endometrial Cancer.Cancers · 2025Review
- Initial Characterization of WDR5B Reveals a Role in the Proliferation of Retinal Pigment Epithelial Cells.Cells · 2024Article
- GRP94 is an IGF-1R chaperone and regulates beta cell death in diabetes.Cell death & disease · 2024Article
- Review
- Tocotrienol-rich fraction reduces retinal inflammation and angiogenesis in rats with streptozotocin-induced diabetes.BMC complementary medicine and therapies · 2023Article
- The protective impact of growth hormone against rotenone-induced apoptotic cell death via acting on endoplasmic reticulum stress and autophagy axis.Turkish journal of biology = Turk biyoloji dergisi · 2023Article
- Article
- Cytochrome P450 27C1 Level Dictates Lung Cancer Tumorigenicity and Sensitivity towards Multiple Anticancer Agents and Its Potential Interplay with the IGF-1R/Akt/p53 Signaling Pathway.International journal of molecular sciences · 2022Article
- Combinatorial antitumor effects of amino acids and epigenetic modulations in hepatocellular carcinoma cell lines.Naunyn-Schmiedeberg's archives of pharmacology · 2021Article
- RFX1: a promising therapeutic arsenal against cancer.Cancer cell international · 2021Review
- Metabolic Rewiring in Radiation Oncology Toward Improving the Therapeutic Ratio.Frontiers in oncology · 2021Review
- Transforming activities of theHaematologica · 2020Article
- Article
- Polyphyllin I and VII potentiate the chemosensitivity of A549/DDP cells to cisplatin by enhancing apoptosis, reversing EMT and suppressing the CIP2A/AKT/mTOR signaling axis.Oncology letters · 2019Article
- Embryonic stem cell-derived extracellular vesicles enhance the therapeutic effect of mesenchymal stem cells.Theranostics · 2019Article
- miR-598 acts as a tumor suppressor in human gastric cancer by targeting IGF-1R.OncoTargets and therapy · 2018Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
p53 that is activated in response to DNA-damaging stress can induce apoptosis or either transient or permanent cell cycle arrests. Apoptosis and permanent cell cycle arrest (senescence) are bona-fide tumor suppressor mechanisms through which p53 inhibits cancer cell survival. In contrast, transient cell cycle arrests induced by p53 can increase survival by allowing cells time to repair their DNA before proceeding with cell division. Mechanisms that control the choice of response to p53 (apoptosis vs arrest) are not fully understood. There is abundant crosstalk between p53 and the IGF-1R/AKT/mTORC1 signaling pathway. Recent studies indicate this crosstalk can determine the choice of response to p53. These findings have clear implications for the potential use of IGF-1R pathway inhibitors against p53 wild-type or p53-null or mutant cancers.
Identifiers
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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.