ReviewJournal of carcinogenesis2013
p53 and regulation of tumor metabolism.
Review in Journal of carcinogenesis, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 28 citations in OpenAlex.
- Critical Role for Malic Enzymes in MYC-Mediated Cellular Adaptation to Glutamine Depletion.Metabolites · 2026Article
- Doxorubicin Attenuates Free Fatty Acid-Induced Lipid Accumulation via Stimulation of p53 in HepG2 Cells.Biomolecules & therapeutics · 2024Article
- N-Acetyl-L-Cysteine Reduces Cervical Carcinogenesis by Promoting Apoptosis.Drugs in R&D · 2023Article
- Extracellular citrate and metabolic adaptations of cancer cells.Cancer metastasis reviews · 2021Review
- Molecular and cellular pathways contributing to brain aging.Behavioral and brain functions : BBF · 2021Review
- Tumor-Educated Platelet miR-18a-3p as a Novel Liquid-Biopsy Biomarker for Early Diagnosis and Chemotherapy Efficacy Monitoring in Nasopharyngeal Carcinoma.Frontiers in oncology · 2021Article
- Metabolic reprogramming as an emerging mechanism of resistance to endocrine therapies in prostate cancer.Cancer drug resistance (Alhambra, Calif.) · 2021Review
- Good Guy or Bad Guy? The Duality of Wild-Type p53 in Hormone-Dependent Breast Cancer Origin, Treatment, and Recurrence.Cancers · 2018Review
- Predictive biomarkers for triple negative breast cancer treated with platinum-based chemotherapy.Cancer biology & therapy · 2017Review
- Aging: Molecular Pathways and Implications on the Cardiovascular System.Oxidative medicine and cellular longevity · 2017Review
- MEGSA: A Powerful and Flexible Framework for Analyzing Mutual Exclusivity of Tumor Mutations.American journal of human genetics · 2016Article
- Regulation of the pentose phosphate pathway in cancer.Protein & cell · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The tumor suppressor p53 plays a pre-eminent role in protecting against cancer, through its ability to sense various stresses and in turn invoke anti-proliferative and repair responses. Emerging evidence suggest that p53 is both a central sentinel for metabolic stresses and a master regulator of metabolic fluxes. This newly identified function of p53, along with the ability of p53 to induce senescence, appears to be crucial for the prevention of oncogenic transformation. A better understanding of the reciprocal regulation of p53 and metabolism, as well as p53-mediated connection between metabolism and senescence, may lead to the identification of valuable targets for tumor therapy.
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.