Evidence map›Paper›PMID 26484113›Full record

ArticleGenomics data2014

Gene expression response to EWS-FLI1 in mouse embryonic cartilage.

Miwa Tanaka, Ken-Ichi Aisaki, Satoshi Kitajima, Katsuhide Igarashi, Jun Kanno, Takuro Nakamura

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Genomics data, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 40% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. Review
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

6 authors at 2 institutions in 1 country.

Miwa TanakaDivision of Carcinogenesis, The Cancer Institute, Japanese Foundation for Cancer Research, Tokyo, Japan.
Ken-Ichi AisakiDivision of Cellular and Molecular Toxicology, Biosafety Research Center, National Institute of Health Science, Tokyo, Japan.
Satoshi KitajimaDivision of Cellular and Molecular Toxicology, Biosafety Research Center, National Institute of Health Science, Tokyo, Japan.
Katsuhide IgarashiDivision of Cellular and Molecular Toxicology, Biosafety Research Center, National Institute of Health Science, Tokyo, Japan.
Jun KannoDivision of Cellular and Molecular Toxicology, Biosafety Research Center, National Institute of Health Science, Tokyo, Japan.
Takuro NakamuraDivision of Carcinogenesis, The Cancer Institute, Japanese Foundation for Cancer Research, Tokyo, Japan.
National Institute of Health Sciences · JPJapanese Foundation For Cancer Research · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ewing's sarcoma is a rare bone tumor that affects children and adolescents. We have recently succeeded to induce Ewing's sarcoma-like small round cell tumor in mice by expression of EWS-ETS fusion genes in murine embryonic osteochondrogenic progenitors. The Ewing's sarcoma precursors are enriched in embryonic superficial zone (eSZ) cells of long bone. To get insights into the mechanisms of Ewing's sarcoma development, gene expression profiles between EWS-FLI1-sensitive eSZ cells and EWS-FLI1-resistant embryonic growth plate (eGP) cells were compared using DNA microarrays. Gene expression of eSZ and eGP cells (total, 30 samples) was evaluated with or without EWS-FLI1 expression 0, 8 or 48 h after gene transduction. Our data provide useful information for gene expression responses to fusion oncogenes in human sarcoma.

Indexed as

cDNA microarraysEmbryonic cartilageEwing's sarcomaEWS–FLI1Gene expression profiling

Identifiers

PMID26484113
PMCPMC4535656
OpenAlexW1971327415

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.