Evidence map›Paper›PMID 17047730›Full record

ArticleNeuron glia biology2004

Overexpression of c-MYC promotes an undifferentiated phenotype in cultured astrocytes and allows elevated Ras and Akt signaling to induce gliomas from GFAP-expressing cells in mice.

Andrew B Lassman, Chengkai Dai, Gregory N Fuller, Andrew J Vickers, Eric C Holland

Open access · greenAbstract read
In one paragraph

Article in Neuron glia biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.1field-weighted citation impact, top 20% 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

29 citing papers in PubMed, 62 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. IRES inhibition induces terminal differentiation and synchronized death in triple-negative breast cancer and glioblastoma cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  8. miRNA-regulated cancer stem cells: understanding the property and the role of miRNA in carcinogenesis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review: insights gained from modelling high-grade glioma in the mouse.Neuropathology and applied neurobiology · 2012
    Review
  15. Article
  16. Myc proteins in brain tumor development and maintenance.Upsala journal of medical sciences · 2012
    Article
  17. Article
  18. Review
  19. Article
  20. 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

5 authors at 3 institutions in 1 country.

Andrew B LassmanDepartment of Neurology, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, NY 10021, USA.
Chengkai Dai
Gregory N Fuller
Andrew J Vickers
Eric C Holland
Memorial Sloan Kettering Cancer Center · USMassachusetts Institute of Technology · USThe University of Texas MD Anderson Cancer Center · US

Funding

CLINICAL SCHOLARS BIOMEDICAL RESEARCH TRAINING PROGRAMT32CA009512 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Ping Chi · 1985 to 2026
$6.3M
NCI NIH HHS T32 CA009512
6 · The paper itself

Abstract

The c-MYC protooncogene is overexpressed in the most malignant primary brain tumor, glioblastoma multiforme (GBM), and has been correlated with the undifferentiated character of several cell types. However, the role of Myc activity in the generation of GBMs is not known. In this report, we show that gene transfer of c-MYC to GFAP-expressing astrocytes in vitro promotes the outgrowth of GFAP-negative, nestin-expressing cells with progenitor-like morphology, growth characteristics and gene-expression pattern. In addition, gene transfer of c-MYC to GFAP-expressing astrocytes in vivo induces GBMs when co-expressed with activated Ras and Akt. Without c-MYC, Ras+Akt induces GBMs from nestin-expressing CNS progenitors but is insufficient in GFAP-expressing differentiated astrocytes. The ability of Myc activity to enhance the oncogenic effects of Ras+Akt appears to be limited to GFAP-expressing astrocytes because nestin-expressing progenitors show no increase in GBM formation with the addition of MYC to Ras+Akt. These studies indicate that one role of MYC activity in the formation of gliomas might be to either promote or reinforce an undifferentiated phenotype required for glioma cells to respond to the oncogenic effects of elevated Ras and Akt activity.

Identifiers

PMID17047730
PMCPMC1615889
OpenAlexW2007382415

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.