Evidence map›Paper›PMID 25364760›Full record

ReviewFrontiers in cell and developmental biology2014

PrP(C) from stem cells to cancer.

Séverine Martin-Lannerée, Théo Z Hirsch, Julia Hernandez-Rapp, Sophie Halliez, Jean-Luc Vilotte, Jean-Marie Launay, Sophie Mouillet-Richard

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cell and developmental biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 11% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

  1. Pooled it
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    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

7 authors at 5 institutions in 3 countries.

Séverine Martin-LanneréeToxicology, Pharmacology and Cellular Signaling, INSERM UMR-S1124 Paris, France ; Toxicology, Pharmacology and Cellular Signaling, Université Paris Descartes, Sorbonne Paris Cité, UMR-S1124 Paris, France.
Théo Z HirschToxicology, Pharmacology and Cellular Signaling, INSERM UMR-S1124 Paris, France ; Toxicology, Pharmacology and Cellular Signaling, Université Paris Descartes, Sorbonne Paris Cité, UMR-S1124 Paris, France.
Julia Hernandez-RappToxicology, Pharmacology and Cellular Signaling, INSERM UMR-S1124 Paris, France ; Toxicology, Pharmacology and Cellular Signaling, Université Paris Descartes, Sorbonne Paris Cité, UMR-S1124 Paris, France ; Université Paris Sud 11, ED419 Biosigne Orsay, France.
Sophie HalliezU892 Virologie et Immunologie Moléculaires, INRA Jouy-en-Josas, France.
Jean-Luc VilotteUMR1313 Génétique Animale et Biologie Intégrative, INRA Jouy-en-Josas, France.
Jean-Marie LaunayAP-HP Service de Biochimie, Fondation FondaMental, INSERM U942 Hôpital Lariboisière Paris, France ; Pharma Research Department, F. Hoffmann-La-Roche Ltd. Basel, Switzerland.
Sophie Mouillet-RichardToxicology, Pharmacology and Cellular Signaling, INSERM UMR-S1124 Paris, France ; Toxicology, Pharmacology and Cellular Signaling, Université Paris Descartes, Sorbonne Paris Cité, UMR-S1124 Paris, France.
Délégation Paris 5 · FRGénétique Animale et Biologie Intégrative · FRInserm · FRInstitut National de la Recherche Agronomique · MAUniversité Paris-Sud · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The cellular prion protein PrP(C) was initially discovered as the normal counterpart of the pathological scrapie prion protein PrP(Sc), the main component of the infectious agent of Transmissible Spongiform Encephalopathies. While clues as to the physiological function of this ubiquitous protein were greatly anticipated from the development of knockout animals, PrP-null mice turned out to be viable and to develop without major phenotypic abnormalities. Notwithstanding, the discovery that hematopoietic stem cells from PrP-null mice have impaired long-term repopulating potential has set the stage for investigating into the role of PrP(C) in stem cell biology. A wealth of data have now exemplified that PrP(C) is expressed in distinct types of stem cells and regulates their self-renewal as well as their differentiation potential. A role for PrP(C) in the fate restriction of embryonic stem cells has further been proposed. Paralleling these observations, an overexpression of PrP(C) has been documented in various types of tumors. In line with the contribution of PrP(C) to stemness and to the proliferation of cancer cells, PrP(C) was recently found to be enriched in subpopulations of tumor-initiating cells. In the present review, we summarize the current knowledge of the role played by PrP(C) in stem cell biology and discuss how the subversion of its function may contribute to cancer progression.

Indexed as

cancercell fate specificationcellular prion proteinprion infectionself-renewalstem cell

Identifiers

PMID25364760
PMCPMC4207012
OpenAlexW2088630336

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.