Evidence map›Paper›PMID 29695998›Full record

ReviewFrontiers in endocrinology2018

The p53 Tumor Suppressor in the Control of Metabolism and Ferroptosis.

Keerthana Gnanapradeepan, Subhasree Basu, Thibaut Barnoud, Anna Budina-Kolomets, Che-Pei Kung, Maureen E Murphy

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in endocrinology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed, 1 pooled it
14.3field-weighted citation impact, top 1% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

95 citing papers in PubMed, 1 synthesis or guideline pooled it, 177 citations in OpenAlex.

  1. Review of ferroptosis in colorectal cancer: Friends or foes?World journal of gastroenterology · 2023
    Pooled it
  2. Elucidating the Role ofCurrent issues in molecular biology · 2025
    Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Alleviated NCOA4-mediated ferritinophagy protected RA FLSs from ferroptosis in lipopolysaccharide-induced inflammation under hypoxia.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Article
  12. Article
  13. Review
  14. Evaluation ofAdvanced biomedical research · 2024
    Article
  15. Review
  16. Review
  17. Ferroptosis: An Emerging Target for Bladder Cancer Therapy.Current issues in molecular biology · 2023
    Review
  18. Review
  19. The African-centric P47S Variant ofCancer research communications · 2023
    Article
  20. Review

35 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Keerthana GnanapradeepanProgram in Molecular and Cellular Oncogenesis, The Wistar Institute, Philadelphia, PA, United States.
Subhasree BasuProgram in Molecular and Cellular Oncogenesis, The Wistar Institute, Philadelphia, PA, United States.
Thibaut BarnoudProgram in Molecular and Cellular Oncogenesis, The Wistar Institute, Philadelphia, PA, United States.
Anna Budina-KolometsProgram in Molecular and Cellular Oncogenesis, The Wistar Institute, Philadelphia, PA, United States.
Che-Pei KungDepartment of Internal Medicine, School of Medicine, Washington University in St. Louis, St Louis, MO, United States.
Maureen E MurphyProgram in Molecular and Cellular Oncogenesis, The Wistar Institute, Philadelphia, PA, United States.
The Wistar Institute · USWashington University in St. Louis · US

Funding

TRAINING PROGRAM IN BASIC CANCER RESEARCHT32CA009171 · NCI · WISTAR INSTITUTE · PI Alessandro Gardini · 1985 to 2026
$15.3M
Washington University Institute of Clinical and Translational Sciences (TL1)TL1TR002344 · NCATS · WASHINGTON UNIVERSITY · PI Jay F. Piccirillo · 2017 to 2026
$8.5M
Functional Analysis of p53 Polymorphic Variants - Diversity SupplementR01CA102184 · NCI · WISTAR INSTITUTE · PI Maureen E. Murphy · 2005 to 2026
$7.4M
p53 Variants in Cancer Risk and TherapyR01CA201430 · NCI · WISTAR INSTITUTE · PI MURPHY, MAUREEN E. · 2016 to 2020
$2.2M
NCATS NIH HHS TL1 TR002344NCI NIH HHS R01 CA102184NCI NIH HHS R01 CA201430NCI NIH HHS T32 CA009171
6 · The paper itself

Abstract

The p53 tumor suppressor continues to be distinguished as the most frequently mutated gene in human cancer. It is widely believed that the ability of p53 to induce senescence and programmed cell death underlies the tumor suppressor functions of p53. However, p53 has a number of other functions that recent data strongly implicate in tumor suppression, particularly with regard to the control of metabolism and ferroptosis (iron- and lipid-peroxide-mediated cell death) by p53. As reviewed here, the roles of p53 in the control of metabolism and ferroptosis are complex. Wild-type (WT) p53 negatively regulates lipid synthesis and glycolysis in normal and tumor cells, and positively regulates oxidative phosphorylation and lipid catabolism. Mutant p53 in tumor cells does the converse, positively regulating lipid synthesis and glycolysis. The role of p53 in ferroptosis is even more complex: in normal tissues, WT p53 appears to positively regulate ferroptosis, and this pathway appears to play a role in the ability of basal, unstressed p53 to suppress tumor initiation and development. In tumors, other regulators of ferroptosis supersede p53's role, and WT p53 appears to play a limited role; instead, mutant p53 sensitizes tumor cells to ferroptosis. By clearly elucidating the roles of WT and mutant p53 in metabolism and ferroptosis, and establishing these roles in tumor suppression, emerging research promises to yield new therapeutic avenues for cancer and metabolic diseases.

Indexed as

apoptosisferroptosismetabolismp53tumor suppressor

Identifiers

PMID29695998
PMCPMC5904197
OpenAlexW2796592069

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.