Evidence map›Paper›PMID 27345406›Full record

ArticleOncogene2017

Differential propagation of stroma and cancer stem cells dictates tumorigenesis and multipotency.

J Behnan, B Stangeland, S A M Hosainey, M Joel, T K Olsen, F Micci, J C Glover, P Isakson, J E Brinchmann

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.3field-weighted citation impact, top 6% 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

45 citing papers in PubMed, 62 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

9 authors at 3 institutions in 2 countries.

J BehnanNorwegian Center for Stem Cell Research, Department of Immunology, Oslo University Hospital, Oslo, Norway.
B StangelandNorwegian Center for Stem Cell Research, Department of Immunology, Oslo University Hospital, Oslo, Norway.
S A M HosaineyDepartment of Neurosurgery, St. Olavs University Hospital, Trondheim, Norway.
M JoelDepartment of Radiation Biology, Institute for Cancer Research, Norwegian Radium Hospital, Oslo University Hospital, Oslo, Norway.
T K OlsenSection for Cancer Cytogenetics, Institute for Cancer Genetics and Informatics, Norwegian Radium Hospital, Oslo University Hospital, Oslo, Norway.
F MicciSection for Cancer Cytogenetics, Institute for Cancer Genetics and Informatics, Norwegian Radium Hospital, Oslo University Hospital, Oslo, Norway.
J C GloverNorwegian Center for Stem Cell Research, Department of Immunology, Oslo University Hospital, Oslo, Norway.
P IsaksonDepartment of Clinical Immunology and Transfusion Medicine, Sahlgrenska University Hospital, Gothenburg, Sweden.
J E BrinchmannNorwegian Center for Stem Cell Research, Department of Immunology, Oslo University Hospital, Oslo, Norway.
Oslo University Hospital · NOSahlgrenska University Hospital · SEUniversity of Oslo · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma Multiforme (GBM) is characterized by high cancer cell heterogeneity and the presence of a complex tumor microenvironment. Those factors are a key obstacle for the treatment of this tumor type. To model the disease in mice, the current strategy is to grow GBM cells in serum-free non-adherent condition, which maintains their tumor-initiating potential. However, the so-generated tumors are histologically different from the one of origin. In this work, we performed high-throughput marker expression analysis and investigated the tumorigenicity of GBM cells enriched under different culture conditions. We identified a marker panel that distinguished tumorigenic sphere cultures from non-tumorigenic serum cultures (high CD56, SOX2, SOX9, and low CD105, CD248, αSMA). Contrary to previous work, we found that 'mixed cell cultures' grown in serum conditions are tumorigenic and express cancer stem cell (CSC) markers. As well, 1% serum plus bFGF and TGF-α preserved the tumorigenicity of sphere cultures and induced epithelial-to-mesenchymal transition gene expression. Furthermore, we identified 12 genes that could replace the 840 genes of The Cancer Genome Atlas (TCGA) used for GBM-subtyping. Our data suggest that the tumorigenicity of GBM cultures depend on cell culture strategies that retain CSCs in culture rather than the presence of serum in the cell culture medium.

Indexed as

AnimalsCarcinogenesisCell Culture TechniquesCell Line, TumorHumansMesenchymal Stem CellsMiceNeoplastic Stem Cells

Identifiers

PMID27345406
PMCPMC5290038
OpenAlexW2470252718

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.