Evidence map›Paper›PMID 34840111›Full record

ReviewAdvances in biological regulation2022

Mechanistic roles of mutant p53 governing lipid metabolism.

Ryan M Loughran, Brooke M Emerling

Open access · greenAbstract readReview
In one paragraph

Review in Advances in biological regulation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.8field-weighted citation impact, top 33% 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

14 citing papers in PubMed, 15 citations in OpenAlex.

  1. Revisiting tumor immunogenicity through the lens of mutant p53: Implications for cancer immunotherapy.Apoptosis : an international journal on programmed cell death · 2026
    Review
  2. Review
  3. Review
  4. Review
  5. Noncanonical PI(4,5)PScience advances · 2026
    Article
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  13. Review
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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 1 institution in 1 country.

Ryan M LoughranCell and Molecular Biology of Cancer Program, Sanford Burnham Prebys, La Jolla, CA, 92037, USA.
Brooke M EmerlingCell and Molecular Biology of Cancer Program, Sanford Burnham Prebys, La Jolla, CA, 92037, USA. Electronic address: bemerling@sbpdiscovery.org.
Discovery Institute · US

Funding

Tumor Microenvironment and Cancer ImmunologyP30CA030199 · NCI · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI ELENA B PASQUALE · 1985 to 2026
$107.2M
Non-Canonical Phosphatidylinositol Kinases in Triple Negative Breast CancerR01CA237536 · NCI · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI EMERLING, BROOKE M · 2020 to 2024
$2.2M
Cancer Targets and Drug DiscoveryT32CA211036 · NCI · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI COSFORD, NICHOLAS DAVID · 2018 to 2022
$1.2M
NCI NIH HHS P30 CA030199NCI NIH HHS R01 CA237536NCI NIH HHS T32 CA211036
6 · The paper itself

Abstract

Metabolic reprogramming of cancer cells by various acquired mutations provides support for rapid proliferation and growth in the tumor microenvironment. Mutations in the TP53 gene are the most common mutation found across all human cancers. Commonly referred to as "the guardian of the genome", p53 has a well-established role as a tumor suppressor by mediating checkpoint integrity and protecting cells from DNA damage. To date, the many functional roles of p53 extending beyond its classical function and exerting control over metabolic processes continues to confound the field. Recently, emerging roles for p53 in mediating lipid metabolism have come to light with intriguing metabolic roles in regulating cholesterol homeostasis and lipid droplet formation. Herein, we will seek to unify the mechanisms by which absence of functional p53, as well as stable mutant forms of p53, exert control over these lipid metabolism programs. Of equal importance, synthetic lethal phenotypes in the context of mutant p53 and aberrant lipid homeostasis offer new possible targets in the therapeutic landscape. This review aims to characterize the mechanisms by which p53 exerts control over these pathways and examine how precision medicine may benefit from tumor subtyping of p53 mutations.

Indexed as

NeoplasmsTumor Suppressor Protein p53AnimalsGenes, p53HumansLipid MetabolismMutationTumor MicroenvironmentTumor Suppressor Protein p53CancerCholesterolLipid dropletMetabolismMevalonateSynthetic lethality

Identifiers

PMID34840111
PMCPMC8858851
OpenAlexW3214992506

What OpenQuestion 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 OpenQuestion graph.