Evidence map›Paper›PMID 21102433›Full record

ArticleNature2010

Glioblastoma stem-like cells give rise to tumour endothelium.

Rong Wang, Kalyani Chadalavada, Jennifer Wilshire, Urszula Kowalik, Koos E Hovinga, Adam Geber, Boris Fligelman, Margaret Leversha, Cameron Brennan, Viviane Tabar

Abstract read
PubMed Publisher
In one paragraph

Article in Nature, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 646 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
646citing papers in PubMed, 2 pooled it
59.7field-weighted citation impact, top 1% 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

646 citing papers in PubMed, 2 syntheses or guidelines pooled it, 1,193 citations in OpenAlex.

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586 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 1 institution in 2 countries.

Rong WangDepartment of Neurosurgery, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA.
Kalyani Chadalavada
Jennifer Wilshire
Urszula Kowalik
Koos E Hovinga
Adam Geber
Boris Fligelman
Margaret Leversha
Cameron Brennan
Viviane Tabar
Memorial Sloan Kettering Cancer Center · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
6 · The paper itself

Abstract

Glioblastoma (GBM) is among the most aggressive of human cancers. A key feature of GBMs is the extensive network of abnormal vasculature characterized by glomeruloid structures and endothelial hyperplasia. Yet the mechanisms of angiogenesis and the origin of tumour endothelial cells remain poorly defined. Here we demonstrate that a subpopulation of endothelial cells within glioblastomas harbour the same somatic mutations identified within tumour cells, such as amplification of EGFR and chromosome 7. We additionally demonstrate that the stem-cell-like CD133(+) fraction includes a subset of vascular endothelial-cadherin (CD144)-expressing cells that show characteristics of endothelial progenitors capable of maturation into endothelial cells. Extensive in vitro and in vivo lineage analyses, including single cell clonal studies, further show that a subpopulation of the CD133(+) stem-like cell fraction is multipotent and capable of differentiation along tumour and endothelial lineages, possibly via an intermediate CD133(+)/CD144(+) progenitor cell. The findings are supported by genetic studies of specific exons selected from The Cancer Genome Atlas, quantitative FISH and comparative genomic hybridization data that demonstrate identical genomic profiles in the CD133(+) tumour cells, their endothelial progenitor derivatives and mature endothelium. Exposure to the clinical anti-angiogenesis agent bevacizumab or to a γ-secretase inhibitor as well as knockdown shRNA studies demonstrate that blocking VEGF or silencing VEGFR2 inhibits the maturation of tumour endothelial progenitors into endothelium but not the differentiation of CD133(+) cells into endothelial progenitors, whereas γ-secretase inhibition or NOTCH1 silencing blocks the transition into endothelial progenitors. These data may provide new perspectives on the mechanisms of failure of anti-angiogenesis inhibitors currently in use. The lineage plasticity and capacity to generate tumour vasculature of the putative cancer stem cells within glioblastoma are novel findings that provide new insight into the biology of gliomas and the definition of cancer stemness, as well as the mechanisms of tumour neo-angiogenesis.

Indexed as

Cell DifferentiationAC133 AntigenAmyloid Precursor Protein SecretasesAnimalsAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedAntigens, CDBevacizumabCadherin 5CadherinsCell LineageCell Line, TumorChromosome AberrationsCoculture TechniquesEndothelial CellsFemaleAC133 AntigenAmyloid Precursor Protein SecretasesAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedAntigens, CDBevacizumabCadherin 5CadherinsGlycoproteinsIntegrin beta4PeptidesPROM1 protein, humanProm1 protein, mouseReceptor, Notch1Vascular Endothelial Growth Factor A

Identifiers

PMID21102433
OpenAlexW2029470215

What OpenQuestion holds

Textmetadata
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.