Evidence map›Paper›PMID 24862407›Full record

ArticleBrain pathology (Zurich, Switzerland)2015

Loss of Sparc in p53-null Astrocytes Promotes Macrophage Activation and Phagocytosis Resulting in Decreased Tumor Size and Tumor Cell Survival.

Stacey L Thomas, Chad R Schultz, Ezekiell Mouzon, William A Golembieski, Reima El Naili, Archanna Radakrishnan, Nancy Lemke, Laila M Poisson, Jorge A Gutiérrez, Sandra Cottingham and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Brain pathology (Zurich, Switzerland), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.7field-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

9 citing papers in PubMed, 15 citations in OpenAlex.

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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

11 authors at 2 institutions in 1 country.

Stacey L ThomasDepartment of Neurosurgery, Barbara Jane Levy Laboratory of Molecular Neuro-Oncology and Hermelin Brain Tumor Center, Henry Ford Hospital, Detroit, MI.
Chad R SchultzDepartment of Neurosurgery, Barbara Jane Levy Laboratory of Molecular Neuro-Oncology and Hermelin Brain Tumor Center, Henry Ford Hospital, Detroit, MI.
Ezekiell MouzonDepartment of Neurosurgery, Barbara Jane Levy Laboratory of Molecular Neuro-Oncology and Hermelin Brain Tumor Center, Henry Ford Hospital, Detroit, MI.
William A GolembieskiDepartment of Neurosurgery, Barbara Jane Levy Laboratory of Molecular Neuro-Oncology and Hermelin Brain Tumor Center, Henry Ford Hospital, Detroit, MI.
Reima El NailiDepartment of Neurosurgery, Barbara Jane Levy Laboratory of Molecular Neuro-Oncology and Hermelin Brain Tumor Center, Henry Ford Hospital, Detroit, MI.
Archanna RadakrishnanDepartment of Neurosurgery, Barbara Jane Levy Laboratory of Molecular Neuro-Oncology and Hermelin Brain Tumor Center, Henry Ford Hospital, Detroit, MI.
Nancy LemkeDepartment of Neurosurgery, Barbara Jane Levy Laboratory of Molecular Neuro-Oncology and Hermelin Brain Tumor Center, Henry Ford Hospital, Detroit, MI.
Laila M PoissonDepartment of Public Health Sciences, Henry Ford Hospital, Detroit, MI.
Jorge A GutiérrezDepartment of Pathology, Henry Ford Hospital, Detroit, MI.
Sandra CottinghamDepartment of Neuropathology and Clinical Neurosciences, Spectrum Health System, Grand Rapids, MI.
Sandra A RempelDepartment of Neurosurgery, Barbara Jane Levy Laboratory of Molecular Neuro-Oncology and Hermelin Brain Tumor Center, Henry Ford Hospital, Detroit, MI.
Henry Ford Hospital · USSpectrum Health · US

Funding

THE ROLE OF SPARC IN GLIOMA INVASIONR01CA086997 · NCI · HENRY FORD HEALTH SYSTEM · PI REMPEL, SANDRA ANN · 2001 to 2007
$1.8M
HSP27: A modulator and therapeutic target of SPARC-induced glioma invasion.R01CA138401 · NCI · HENRY FORD HEALTH SYSTEM · PI REMPEL, SANDRA ANN · 2011 to 2015
$1.5M
NCI NIH HHS CA138401NCI NIH HHS CA86997NCI NIH HHS R01 CA086997NCI NIH HHS R01 CA138401
6 · The paper itself

Abstract

Both the induction of SPARC expression and the loss of the p53 tumor suppressor gene are changes that occur early in glioma development. Both SPARC and p53 regulate glioma cell survival by inverse effects on apoptotic signaling. Therefore, during glioma formation, the upregulation of SPARC may cooperate with the loss of p53 to enhance cell survival. This study determined whether the loss of Sparc in astrocytes that are null for p53 would result in reduced cell survival and tumor formation and increased tumor immunogenicity in an in vivo xenograft brain tumor model. In vitro, the loss of Sparc in p53-null astrocytes resulted in an increase in cell proliferation, but a loss of tumorigenicity. At 7 days after intracranial implantation, Sparc-null tumors had decreased tumor cell survival, proliferation and reduced tumor size. The loss of Sparc promoted microglia/macrophage activation and phagocytosis of tumor cells. Our results indicate that the loss of p53 by deletion/mutation in the early stages of glioma formation may cooperate with the induction of SPARC to potentiate cancer cell survival and escape from immune surveillance.

Indexed as

AnimalsAstrocytesBrain NeoplasmsCell Line, TumorCell ProliferationCerebral CortexGenotypeGliomaHumansMacrophagesMiceMice, Inbred C57BLMice, KnockoutMice, NudeOsteonectinPhagocytosisOsteonectinSPARC protein, mouseTumor Suppressor Protein p53glioblastomagliomaimmunosuppressionmacrophagemicrogliap53p53-nullSPARCSparc-nullTP53xenograft

Identifiers

PMID24862407
PMCPMC4520390
OpenAlexW1794425699

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.