Evidence map›Paper›PMID 20849464›Full record

ArticlePigment cell & melanoma research2010

p53 prevents progression of nevi to melanoma predominantly through cell cycle regulation.

Tamara Terzian, Enrique C Torchia, Daisy Dai, Steven E Robinson, Kazutoshi Murao, Regan A Stiegmann, Victoria Gonzalez, Glen M Boyle, Marianne B Powell, Pamela M Pollock and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Pigment cell & melanoma research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

37 citing papers in PubMed, 67 citations in OpenAlex.

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  17. Experimental and therapeutic medicine · 2016
    Article
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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

14 authors at 7 institutions in 2 countries.

Tamara TerzianDepartment of Dermatology and Charles C Gates Center for Regenerative Medicine and Stem Cell Biology, UC Denver, Aurora, CO 80045, USA.
Enrique C Torchia
Daisy Dai
Steven E Robinson
Kazutoshi Murao
Regan A Stiegmann
Victoria Gonzalez
Glen M Boyle
Marianne B Powell
Pamela M Pollock
Guillermina Lozano
William A Robinson
Dennis R Roop
Neil F Box
University of Colorado Denver · USGates (United States) · USThe Medical Center of Aurora · USQIMR Berghofer Medical Research Institute · AUStanford University · USThe University of Texas MD Anderson Cancer Center · USTranslational Genomics Research Institute · US

Funding

VITAMIN A, AND ITS PRECURSORS AND DERIVATIVES AS THERAPEUTIC MODALITIESP01CA027502 · NCI · UNIVERSITY OF ARIZONA · PI EINSPAHR, JANINE G · 1985 to 2015
$36.3M
TARGETING ONCOGENE EXPRESSION TO SKIN IN TRANSGENIC MICER01CA052607 · NCI · UNIVERSITY OF COLORADO DENVER · PI ROOP, DENNIS · 1990 to 2015
$6.5M
Transgenic and Gene Targeting CoreP30AR057212 · NIAMS · UNIVERSITY OF COLORADO DENVER · PI NORRIS, DAVID A. · 2009 to 2018
$6.2M
INDUCIBLE MOUSE MODELS FOR SKIN AND HEAD AND NECK CANCERU01CA105491 · NCI · UNIVERSITY OF COLORADO DENVER · PI ROOP, DENNIS · 2004 to 2009
$4.5M
Melanocyte Survival and Transformation: Hypoxia & P13 Kinase/Akt/mTOR SignalingR01CA120526 · NCI · STANFORD UNIVERSITY · PI POWELL, MARIANNE BROOME · 2007 to 2010
$1.1M
NCI NIH HHS CA105491NCI NIH HHS CA52607NCI NIH HHS P01 CA027502NCI NIH HHS P01CA27502NCI NIH HHS R01 CA052607NCI NIH HHS R01 CA120526NCI NIH HHS R01CA120526NCI NIH HHS U01 CA105491NIAMS NIH HHS P30 AR057212
6 · The paper itself

Abstract

p53 is the central member of a critical tumor suppressor pathway in virtually all tumor types, where it is silenced mainly by missense mutations. In melanoma, p53 predominantly remains wild type, thus its role has been neglected. To study the effect of p53 on melanocyte function and melanomagenesis, we crossed the ‘high-p53’Mdm4+/− mouse to the well-established TP-ras0/+ murine melanoma progression model. After treatment with the carcinogen dimethylbenzanthracene (DMBA), TP-ras0/+ mice on the Mdm4+/− background developed fewer tumors with a delay in the age of onset of melanomas compared to TP-ras0/+ mice. Furthermore, we observed a dramatic decrease in tumor growth, lack of metastasis with increased survival of TP-ras0/+: Mdm4+/− mice. Thus, p53 effectively prevented the conversion of small benign tumors to malignant and metastatic melanoma. p53 activation in cultured primary melanocyte and melanoma cell lines using Nutlin-3, a specific Mdm2 antagonist, supported these findings. Moreover, global gene expression and network analysis of Nutlin-3-treated primary human melanocytes indicated that cell cycle regulation through the p21WAF1/CIP1 signaling network may be the key anti-melanomagenic activity of p53.

Indexed as

Cell CycleDisease Progression9,10-Dimethyl-1,2-benzanthraceneAnimalsCell Line, TumorCell ProliferationCell SurvivalCellular SenescenceClone CellsDisease Models, AnimalHumansImidazolesMelanocytesMelanomaMiceMice, Inbred C57BL9,10-Dimethyl-1,2-benzanthraceneImidazolesMdm4 protein, mousenutlin 3PiperazinesProto-Oncogene ProteinsTumor Suppressor Protein p53Ubiquitin-Protein Ligases

Identifiers

PMID20849464
PMCPMC3137930
OpenAlexW2159633569

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.