Evidence map›Paper›PMID 12538861›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2003

Oncogenic targeting of an activated tyrosine kinase to the Golgi apparatus in a glioblastoma.

Alan Charest, Vicky Kheifets, Julie Park, Keara Lane, Kevin McMahon, Cathy L Nutt, David Housman

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
0.8field-weighted citation impact, top 32% 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

41 citing papers in PubMed, 88 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Importance ofCancer drug resistance (Alhambra, Calif.) · 2023
    Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Rare but Recurrent ROS1 Fusions Resulting From Chromosome 6q22 Microdeletions are Targetable Oncogenes in Glioma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2018
    Article
  17. Article
  18. Recent Advances in Targeting ROS1 in Lung Cancer.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2017
    Review
  19. Article
  20. Testing for ROS1 in non-small cell lung cancer: a review with recommendations.Virchows Archiv : an international journal of pathology · 2016
    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

7 authors at 3 institutions in 1 country.

Alan CharestCenter for Cancer Research, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139, USA. charest@mit.edu
Vicky Kheifets
Julie Park
Keara Lane
Kevin McMahon
Cathy L Nutt
David Housman
Massachusetts Institute of Technology · USCenter for Cancer Research · USMassachusetts General Hospital · US

Funding

USE OF RETROVIRUS PROMOTER TRAP VECTORS TO IDENTIFY ONCOGENES AND ANTI-ONCOGENESP01CA042063 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI JACKS, TYLER E. · 1986 to 2021
$30.5M
NCI NIH HHS 2-P01-CA42063-16NCI NIH HHS P01 CA042063
6 · The paper itself

Abstract

Activating oncogenic mutations of receptor tyrosine kinases (RTKs) have been reported in several types of cancers. In many cases, genomic rearrangements lead to the fusion of unrelated genes to the DNA coding for the kinase domain of RTKs. All RTK-derived fusion proteins reported so far display oligomerization sequences within the 5' fusion partners that are responsible for oncogenic activation. Here, we report a mechanism by which an altered RTK gains oncogenic potential in a glioblastoma cell line. A microdeletion on 6q21 results in the fusion of FIG, a gene coding for a Golgi apparatus-associated protein, to the kinase domain of the protooncogene c-ROS. The fused protein product FIG-ROS is a potent oncogene, and its transforming potential resides in its ability to interact with and become localized to the Golgi apparatus. Thus we have found a RTK fusion protein whose subcellular location leads to constitutive kinase activation and results in oncogenic transformation.

Indexed as

AnimalsBlotting, WesternCell LineCell Transformation, NeoplasticChromosomes, Human, Pair 6Fluorescent Antibody Technique, IndirectGlioblastomaGolgi ApparatusHumansMiceMice, NudeMicroscopy, FluorescenceMutationOncogene Proteins, FusionPeptidesPhosphorylationOncogene Proteins, FusionPeptidesProtein IsoformsProtein-Tyrosine KinasesProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesROS1 protein, humanRos1 protein, mouseRos1 protein, rat

Identifiers

PMID12538861
PMCPMC298701
OpenAlexW1972731187

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.