Evidence map›Paper›PMID 27613337›Full record

ReviewThe Journal of endocrinology2016

The role of the p53 tumor suppressor in metabolism and diabetes.

Che-Pei Kung, Maureen E Murphy

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of endocrinology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.

0numbers the graph read from it
0cells of the map it votes in
93citing papers in PubMed
5.6field-weighted citation impact, top 3% 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

93 citing papers in PubMed, 187 citations in OpenAlex.

  1. Article
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  4. Review
  5. Insulin Resistance and Inflammation.International journal of molecular sciences · 2026
    Review
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33 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

2 authors at 2 institutions in 1 country.

Che-Pei KungDepartment of Internal MedicineWashington University School of Medicine, St Louis, Missouri, USA patkung@wustl.edu mmurphy@wistar.org.
Maureen E MurphyDepartment of Internal MedicineWashington University School of Medicine, St Louis, Missouri, USA patkung@wustl.edu mmurphy@wistar.org.
The Wistar Institute · USUniversity of Missouri–St. Louis · US

Funding

Tumor Microenvironment and MetastasisP30CA010815 · NCI · WISTAR INSTITUTE · PI Maureen E. Murphy · 1985 to 2026
$75.9M
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
NCI NIH HHS P30 CA010815NCI NIH HHS R01 CA102184NCI NIH HHS R01 CA201430
6 · The paper itself

Abstract

In the context of tumor suppression, p53 is an undisputedly critical protein. Functioning primarily as a transcription factor, p53 helps fend off the initiation and progression of tumors by inducing cell cycle arrest, senescence or programmed cell death (apoptosis) in cells at the earliest stages of precancerous development. Compelling evidence, however, suggests that p53 is involved in other aspects of human physiology, including metabolism. Indeed, recent studies suggest that p53 plays a significant role in the development of metabolic diseases, including diabetes, and further that p53's role in metabolism may also be consequential to tumor suppression. Here, we present a review of the literature on the role of p53 in metabolism, diabetes, pancreatic function, glucose homeostasis and insulin resistance. Additionally, we discuss the emerging role of genetic variation in the p53 pathway (single-nucleotide polymorphisms) on the impact of p53 in metabolic disease and diabetes. A better understanding of the relationship between p53, metabolism and diabetes may one day better inform the existing and prospective therapeutic strategies to combat this rapidly growing epidemic.

Indexed as

ApoptosisModels, BiologicalAmino Acid SubstitutionAnimalsDiabetes Mellitus, Type 1Diabetes Mellitus, Type 2Genetic Predisposition to DiseaseHumansInsulinInsulin ResistanceInsulin-Secreting CellsInsulin SecretionLiverMuscle, SkeletalPancreasPolymorphism, Single NucleotideInsulinTP53 protein, humanTumor Suppressor Protein p53diabetesinsulin resistancemetabolismp53

Identifiers

PMID27613337
PMCPMC5148674
OpenAlexW2510683099

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.