Evidence map›Paper›PMID 26455317›Full record

ArticleOncogene2016

Modeling the initiation of Ewing sarcoma tumorigenesis in differentiating human embryonic stem cells.

D J Gordon, M Motwani, D Pellman

Open access · bronzeAbstract read
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

17 citing papers in PubMed, 25 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

3 authors at 1 institution in 1 country.

D J GordonDepartment of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
M MotwaniDepartment of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
D PellmanDepartment of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
Dana-Farber Cancer Institute · US

Funding

Polyploidy, aneuploidy and genome stabilityR01GM083299 · NIGMS · DANA-FARBER CANCER INST · PI PELLMAN, DAVID S · 2007 to 2015
$2.9M
Trisomy 8 in Hematopoiesis and Myeloid LeukemiaK08CA160346 · NCI · UNIVERSITY OF IOWA · PI GORDON, DAVID J · 2011 to 2015
$839k
Howard Hughes Medical InstituteNCI NIH HHS K08 CA160346NIGMS NIH HHS R01 GM083299
6 · The paper itself

Abstract

Oncogenic transformation in Ewing sarcoma tumors is driven by the fusion oncogene EWS-FLI1. However, despite the well-established role of EWS-FLI1 in tumor initiation, the development of models of Ewing sarcoma in human cells with defined genetic elements has been challenging. Here, we report a novel approach to model the initiation of Ewing sarcoma tumorigenesis that exploits the developmental and pluripotent potential of human embryonic stem cells. The inducible expression of EWS-FLI1 in embryoid bodies, or collections of differentiating stem cells, generates cells with properties of Ewing sarcoma tumors, including characteristics of transformation. These cell lines exhibit anchorage-independent growth, a lack of contact inhibition and a strong Ewing sarcoma gene expression signature. Furthermore, these cells also demonstrate a requirement for the persistent expression of EWS-FLI1 for cell survival and growth, which is a hallmark of Ewing sarcoma tumors.

Indexed as

CarcinogenesisCell DifferentiationCell Line, TumorEmbryoid BodiesEmbryonic Stem CellsHumansOligonucleotide Array Sequence AnalysisOncogene Proteins, FusionProto-Oncogene Protein c-fli-1RNA-Binding Protein EWSSarcoma, EwingEWS-FLI fusion proteinOncogene Proteins, FusionProto-Oncogene Protein c-fli-1RNA-Binding Protein EWS

Identifiers

PMID26455317
PMCPMC4829493
OpenAlexW2219603515

What OpenQuestion holds

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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.