ArticleCancer biology & therapy2013
Dysregulation of the mTOR pathway in p53-deficient mice.
Article in Cancer biology & therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- Genetic polymorphisms of mTOR and cancer risk: a systematic review and updated meta-analysis.Oncotarget · 2016Pooled it
- Regulatory Interplay of p53, AMPK, and mTOR in Decidualization: Implications for Reproductive Competence and Cancer Biology.Reproductive sciences (Thousand Oaks, Calif.) · 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
- Review
- As expected, based on rapamycin-like p53-mediated gerosuppression, mTOR inhibition acts as a checkpoint in p53-mediated tumor suppression.Oncoscience · 2022Article
- Au-Pt Nanoparticle Formulation as a Radiosensitizer for Radiotherapy with Dual Effects.International journal of nanomedicine · 2021Article
- Mechanistic target of rapamycin signaling in mouse models of accelerated aging.The journals of gerontology. Series A, Biological sciences and medical sciences · 2020Review
- Is cellular senescence involved in cystic fibrosis?Respiratory research · 2019Review
- p53 Functions in Adipose Tissue Metabolism and Homeostasis.International journal of molecular sciences · 2018Review
- A role for cellular senescence in birth timing.Cell cycle (Georgetown, Tex.) · 2017Review
- Somatic polyploidy is associated with the upregulation of c-MYC interacting genes and EMT-like signature.Oncotarget · 2016Article
- Article
- Rejuvenating immunity: "anti-aging drug today" eight years later.Oncotarget · 2015Article
- p53 and rapamycin are additive.Oncotarget · 2015Article
- Quantitative analysis of male germline stem cell differentiation reveals a role for the p53-mTORC1 pathway in spermatogonial maintenance.Cell cycle (Georgetown, Tex.) · 2015Article
- Tumor promoter-induced cellular senescence: cell cycle arrest followed by geroconversion.Oncotarget · 2014Article
- Genetic prevention of lymphoma in p53 knockout mice allows the early development of p53-related sarcomas.Oncotarget · 2014Article
- Article
- p70 S6 kinase drives ovarian cancer metastasis through multicellular spheroid-peritoneum interaction and P-cadherin/b1 integrin signaling activation.Oncotarget · 2014Article
- Weekly administration of rapamycin improves survival and biomarkers in obese male mice on high-fat diet.Aging cell · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Mammalian or mechanistic target of rapamycin (mTOR) is involved in growth, aging, and age-related diseases including cancer. There is an extensive cross talk between p53 and mTOR. In cell culture, p53 inhibits the mTOR pathway in a cell type-dependent manner. p53-deficient mice develop pro-inflammation and cancer. We have shown that rapamycin delayed cancer and extended lifespan, thus partially substituting for p53. Here we show that a marker of mTOR activity, phosphorylated S6 (p-S6), is increased in the hearts of p53-deficient mice. Furthermore, cardiac p-S6 correlated with body weight. Also, p53(-/-) mice were slightly hyperinsulinemic with a tendency to elevated IGF-1. Radiation exacerbated the difference between IGF-1 levels in normal and p53(-/-) mice. Noteworthy, radiation induced Thr-308 Akt phosphorylation in the livers (but not in the hearts) of both p53(+/+) and p53(-/-) mice. Simultaneously, radiation decreased p-S6 in the livers of normal mice, consistent with the negative effect of p53 on mTOR. Our data indicate that the activity of mTOR is increased in some but not all tissues of p53(-/-) mice, associated with the tendency to increased insulin and IGF-1 levels. Therefore, the absence of p53 may create oncophilic microenvironment, favoring cancer.
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.