Evidence map›Paper›PMID 31062422›Full record

ReviewMolecular carcinogenesis2019

Regulatory mechanisms mediated by peroxisome proliferator-activated receptor-β/δ in skin cancer.

Jeffrey M Peters, Dae J Kim, Moses T Bility, Michael G Borland, Bokai Zhu, Frank J Gonzalez

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Molecular carcinogenesis, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 41% 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

2 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Review
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 5 institutions in 1 country.

Jeffrey M PetersDepartment of Veterinary and Biomedical Sciences, The Center of Molecular Toxicology and Carcinogenesis, The Pennsylvania State University, University Park, Pennsylvania.ORCID 0000-0003-2782-2998
Dae J KimDepartment of Molecular Science, School of Medicine, University of Texas Rio Grande Valley, Edinburg, Texas.
Moses T BilityDepartment of Infectious Diseases and Microbiology, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, Pennsylvania.
Michael G BorlandDepartment of Chemistry & Biochemistry, Bloomsburg University of Pennsylvania, Bloomsburg, Pennsylvania.
Bokai ZhuDivision of Endocrinology and Metabolism, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania.
Frank J GonzalezLaboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland.
University of Pittsburgh · USBloomsburg University · USNational Institutes of Health · USPennsylvania State University · USThe University of Texas Rio Grande Valley · US

Funding

Xenobiotic receptorsZIABC005562 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI GONZALEZ, FRANK J · 2009 to 2025
$26.9M
Modulation of skin cancer by PPARBeta/deltaR01CA124533 · NCI · PENNSYLVANIA STATE UNIVERSITY, THE · PI PETERS, JEFFREY M · 2007 to 2017
$2.4M
The role of TC-PTP in skin carcinogenesisR01ES022250 · NIEHS · UNIVERSITY OF TEXAS RIO GRANDE VALLEY · PI KIM, DAE JOON · 2013 to 2017
$1.7M
Modulation of liver cancer by PPARbeta/deltaR01CA140369 · NCI · PENNSYLVANIA STATE UNIVERSITY, THE · PI PETERS, JEFFREY M · 2010 to 2014
$1.4M
Engraftment of human hematopoietic stem cells to immunodeficient rabbitsR21OD024789 · OD · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BILITY, MOSES TURKLE, XU, JIE · 2018 to 2019
$452k
Modeling Staphylococcus aureus infection and pathogenesis in humanized miceR21AI135412 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BILITY, MOSES TURKLE, RICHARDSON, ANTHONY R. · 2018 to 2019
$430k
NCI NIH HHS R01 CA124533NCI NIH HHS R01 CA140369NIAID NIH HHS R21 AI135412NIEHS NIH HHS R01 ES022250NIH HHS R21 OD024789
6 · The paper itself

Abstract

Considerable progress has been made during the past 20 years towards elucidating the role of peroxisome proliferator-activated receptor-β/δ (PPARβ/δ) in skin cancer. In 1999, the original notion that PPARβ/δ was involved with epithelial cell function was postulated based on a correlation between PPARβ/δ expression and the induction of messenger RNAs encoding proteins that mediate terminal differentiation in keratinocytes. Subsequent studies definitively revealed that PPARβ/δ could induce terminal differentiation and inhibit proliferation of keratinocytes. Molecular mechanisms have since been discovered to explain how this nuclear receptor can be targeted for preventing and treating skin cancer. This includes the regulation of terminal differentiation, mitotic signaling, endoplasmic reticulum stress, and cellular senescence. Interestingly, the effects of activating PPARβ/δ can preferentially target keratinocytes with genetic mutations associated with skin cancer. This review provides the history and current understanding of how PPARβ/δ can be targeted for both nonmelanoma skin cancer and melanoma and postulates how future approaches that modulate PPARβ/δ signaling may be developed for the prevention and treatment of these diseases.

Indexed as

AnimalsCell DifferentiationCell ProliferationHumansKeratinocytesMelanomaPPAR-betaPPAR deltaRNA, MessengerSignal TransductionSkin NeoplasmsPPAR-betaPPAR deltaRNA, Messengercell cycledifferentiationperoxisome proliferator-activated receptor-β/δskin cancer

Identifiers

PMID31062422
PMCPMC6692234
OpenAlexW2944370159

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.