Evidence map›Paper›PMID 24501428›Full record

ArticleMolecular cancer research : MCR2014

Contribution of tumor heterogeneity in a new animal model of CNS tumors.

Fuyi Chen, Albert J Becker, Joseph J LoTurco

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer research : MCR, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

18 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Rat and Mouse Brain Tumor Models for Experimental Neuro-Oncology Research.Journal of neuropathology and experimental neurology · 2022
    Review
  6. Review
  7. Article
  8. Frontiers in oncology · 2021
    Review
  9. Review
  10. Radiomic prediction models for the level of Ki-67 and p53 in glioma.The Journal of international medical research · 2020
    Article
  11. Article
  12. Article
  13. H3.3Cancer cell · 2017
    Article
  14. Epilepsy-Associated KCNQ2 Channels Regulate Multiple Intrinsic Properties of Layer 2/3 Pyramidal Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  15. Review
  16. Article
  17. Review
  18. Article
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 2 countries.

Fuyi ChenAuthors' Affiliations: Department of Physiology and Neurobiology, University of Connecticut, Storrs, Connecticut; and 2Department of Neuropathology, University of Bonn Medical Center, Bonn, Germany.
Albert J Becker
Joseph J LoTurco
University of Bonn · DE

Funding

MOLECULAR REGULATION OF NEOCORTICAL NEUROGENESISR01MH056524 · NIMH · UNIVERSITY OF CONNECTICUT STORRS · PI LOTURCO, JOSEPH J · 2003 to 2012
$3.3M
DYSLEXIA SUSCEPTIBILITY GENES AND MECHANISMS OF NEURONAL DEVELOPMENTR01HD055655 · NICHD · UNIVERSITY OF CONNECTICUT STORRS · PI LOTURCO, JOSEPH J · 2008 to 2012
$1.6M
NICHD NIH HHS R01 HD055655NICHD NIH HHS R01HD055655NIMH NIH HHS R01 MH056524NIMH NIH HHS R01MH056524
6 · The paper itself

Abstract

unlabelledThe etiology of central nervous system (CNS) tumor heterogeneity is unclear. To clarify this issue, a novel animal model was developed of glioma and atypical teratoid/rhabdoid-like tumor (ATRT) produced in rats by nonviral cellular transgenesis initiated in utero. This model system affords the opportunity for directed oncogene expression, clonal labeling, and addition of tumor-modifying transgenes. By directing HRasV12 and AKT transgene expression in different cell populations with promoters that are active ubiquitously (CAG promoter), astrocyte-selective (glial fibrillary acidic protein promoter), or oligodendrocyte-selective (myelin basic protein promoter) we generated glioblastoma multiforme and anaplastic oligoastrocytoma, respectively. Importantly, the glioblastoma multiforme and anaplastic oligoastrocytoma tumors were distinguishable at both the cellular and molecular level. Furthermore, proneural basic helix-loop-helix (bHLH) transcription factors, Ngn2 (NEUROG2) or NeuroD1, were expressed along with HRasV12 and AKT in neocortical radial glia, leading to the formation of highly lethal ATRT like tumors. This study establishes a unique model in which determinants of CNS tumor diversity can be parsed out and reveals that both mutation and expression of neurogenic bHLH transcription factors contribute to CNS tumor diversity. IMPLICATIONS: A novel CNS tumor model reveals that oncogenic events occurring in disparate cell types and/or molecular contexts lead to different tumor types; these findings shed light on the sources of brain tumor heterogeneity.

Indexed as

Disease Models, AnimalAnimalsBrain NeoplasmsCells, CulturedFemaleGlioblastomaMicePregnancyRatsRats, Wistar

Identifiers

PMID24501428
PMCPMC4024448
OpenAlexW2132778252

What OpenQuestion holds

Textmetadata
LicenceTDM
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.