ReviewOncotarget2018
p53 and metabolism: from mechanism to therapeutics.
Review in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 85 papers.
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
85 citing papers in PubMed, 148 citations in OpenAlex.
- Metabolic vulnerabilities in pleural mesothelioma.Oncogenesis · 2026Review
- P53 - a new player in the metabolic adaptation of colorectal carcinoma cells under hypoxia.BMC cancer · 2026Article
- Unraveling the role ofHemaSphere · 2026Review
- Cancer Metabolism and Its Historical & Molecular Foundations: An Overview.Drugs and drug candidates · 2026Article
- The guardian of the genome meets immunotherapy: p53-based strategies.Frontiers in immunology · 2026Review
- The antitumor effect of tlr4 inhibition in head and neck cancer cell lines.Scientific reports · 2025Article
- Somatic CRISPR tumorigenesis and multiomic analysis reveal a pentose phosphate pathway disruption vulnerability in MPNSTs.Science advances · 2025Article
- Assessing the influence of TP53 polymorphisms and haplotypes on bioelectrical impedance analysis parameters and nutritional status in aging Iranian population.Molecular biology reports · 2025Article
- Review
- Unveiling the role of Ndrg1 gene on the oxidative stress induction behind the anticancer potential of styrylquinazoline derivatives.Scientific reports · 2025Article
- Review
- Exploration of the clinical prognostic model of BRCA based on PCAT7.Frontiers in oncology · 2025Article
- Chemosensitizing effect of apigenin on T-ALL cell therapy.Frontiers in pharmacology · 2025Article
- Asparagine Dependency Is a Targetable Metabolic Vulnerability in TP53-Altered Castration-Resistant Prostate Cancer.Cancer research · 2024Article
- Ferroptosis in radiation-induced brain injury: roles and clinical implications.Biomedical engineering online · 2024Review
- p53 Orchestrates Cancer Metabolism: Unveiling Strategies to Reverse the Warburg Effect.Bulletin of mathematical biology · 2024Article
- Insights into gemcitabine resistance in pancreatic cancer: association with metabolic reprogramming and TP53 pathogenicity in patient derived xenografts.Journal of translational medicine · 2024Article
- Metabolic signature and response to glutamine deprivation are independent of p53 status in B cell malignancies.iScience · 2024Article
- Hepa-ToxMOA: a pathway-screening method for evaluating cellular stress and hepatic metabolic-dependent toxicity of natural products.Scientific reports · 2024Article
- MicroRNA regulation of the serine synthesis pathway in endocrine-resistant breast cancer cells.Endocrine-related cancer · 2023Article
25 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The tumor cell changes itself and its microenvironment to adapt to different situations, including action of drugs and other agents targeting tumor control. Therefore, metabolism plays an important role in the activation of survival mechanisms to keep the cell proliferative potential. The Warburg effect directs the cellular metabolism towards an aerobic glycolytic pathway, despite the fact that it generates less adenosine triphosphate than oxidative phosphorylation; because it creates the building blocks necessary for cell proliferation. The transcription factor p53 is the master tumor suppressor; it binds to more than 4,000 sites in the genome and regulates the expression of more than 500 genes. Among these genes are important regulators of metabolism, affecting glucose, lipids and amino acids metabolism, oxidative phosphorylation, reactive oxygen species (ROS) generation and growth factors signaling. Wild-type and mutant p53 may have opposing effects in the expression of these metabolic genes. Therefore, depending on the p53 status of the cell, drugs that target metabolism may have different outcomes and metabolism may modulate drug resistance. Conversely, induction of p53 expression may regulate differently the tumor cell metabolism, inducing senescence, autophagy and apoptosis, which are dependent on the regulation of the PI3K/AKT/mTOR pathway and/or ROS induction. The interplay between p53 and metabolism is essential in the decision of cell fate and for cancer therapeutics.
Indexed as
Identifiers
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.