Evidence map›Paper›PMID 28148265›Full record

ReviewMolecular cancer2017

Cancer stem cell niche models and contribution by mesenchymal stroma/stem cells.

Catharina Melzer, Juliane von der Ohe, Hendrik Lehnert, Hendrik Ungefroren, Ralf Hass

Abstract readReview
In one paragraph

Review in Molecular cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed
–field-weighted citation impact
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

86 citing papers in PubMed.

  1. Head and neck squamous cell carcinoma: current and emerging therapeutic strategies.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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  5. Circular RNAs: key regulators in cancer stem cell dynamics.Molecular genetics and genomics : MGG · 2026
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26 more citing papers are in PubMed but not listed here.

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

5 authors.

Catharina MelzerBiochemistry and Tumor Biology Lab, Department of Obstetrics and Gynecology, Hannover Medical School, Medical University Hannover, Carl-Neuberg-Str. 1, D - 30625, Hannover, Germany.
Juliane von der OheBiochemistry and Tumor Biology Lab, Department of Obstetrics and Gynecology, Hannover Medical School, Medical University Hannover, Carl-Neuberg-Str. 1, D - 30625, Hannover, Germany.
Hendrik LehnertFirst Department of Medicine, University Hospital Schleswig-Holstein (UKSH), Campus Lübeck, Lübeck, Germany.
Hendrik UngefrorenFirst Department of Medicine, University Hospital Schleswig-Holstein (UKSH), Campus Lübeck, Lübeck, Germany.
Ralf HassBiochemistry and Tumor Biology Lab, Department of Obstetrics and Gynecology, Hannover Medical School, Medical University Hannover, Carl-Neuberg-Str. 1, D - 30625, Hannover, Germany. hass.ralf@mh-hannover.de.ORCID 0000-0002-2481-7547

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe initiation and progression of malignant tumors is driven by distinct subsets of tumor-initiating or cancer stem-like cells (CSCs) which develop therapy/apoptosis resistance and self-renewal capacity. In order to be able to eradicate these CSCs with novel classes of anti-cancer therapeutics, a better understanding of their biology and clinically-relevant traits is mandatory. MAIN BODY: Several requirements and functions of a CSC niche physiology are combined with current concepts for CSC generation such as development in a hierarchical tumor model, by stochastic processes, or via a retrodifferentiation program. Moreover, progressive adaptation of endothelial cells and recruited immune and stromal cells to the tumor site substantially contribute to generate a tumor growth-permissive environment resembling a CSC niche. Particular emphasis is put on the pivotal role of multipotent mesenchymal stroma/stem cells (MSCs) in supporting CSC development by various kinds of interaction and cell fusion to form hybrid tumor cells.

conclusionA better knowledge of CSC niche physiology may increase the chances that cancer stemness-depleting interventions ultimately result in arrest of tumor growth and metastasis.

Indexed as

Cell CommunicationModels, BiologicalStem Cell NicheAnimalsAutophagyCell DifferentiationCell Self RenewalEnergy MetabolismHumansHypoxiaMesenchymal Stem CellsNeoplastic Stem CellsCancer stem cellsMSCRetrodifferentiationTumor cell interactionTumor microenvironment

Identifiers

PMID28148265
PMCPMC5286787

What OpenQuestion holds

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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.