Evidence map›Paper›PMID 22249260›Full record

ArticleOncogene2012

Aberrant activation of ALK kinase by a novel truncated form ALK protein in neuroblastoma.

J Okubo, J Takita, Y Chen, K Oki, R Nishimura, M Kato, M Sanada, M Hiwatari, Y Hayashi, T Igarashi and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

33 citing papers in PubMed, 58 citations in OpenAlex.

  1. Trial
  2. Review
  3. Lung adenocarcinoma withTranslational lung cancer research · 2025
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Targeting anaplastic lymphoma kinase in neuroblastoma.APMIS : acta pathologica, microbiologica, et immunologica Scandinavica · 2019
    Review
  18. Article
  19. Review
  20. 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

11 authors at 2 institutions in 1 country.

J OkuboDepartment of Pediatrics, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
J Takita
Y Chen
K Oki
R Nishimura
M Kato
M Sanada
M Hiwatari
Y Hayashi
T Igarashi
S Ogawa
The University of Tokyo · JPGunma Children's Medical Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Anaplastic lymphoma kinase (ALK) was originally identified from a rare subtype of non-Hodgkin's lymphomas carrying t(2;5)(p23;q35) translocation, where ALK was constitutively activated as a result of a fusion with nucleophosmin (NPM). Aberrant ALK fusion proteins were also generated in inflammatory fibrosarcoma and a subset of non-small-cell lung cancers, and these proteins are implicated in their pathogenesis. Recently, ALK has been demonstrated to be constitutively activated by gene mutations and/or amplifications in sporadic as well as familial cases of neuroblastoma. Here we describe another mechanism of aberrant ALK activation observed in a neuroblastoma-derived cell line (NB-1), in which a short-form ALK protein (ALK(del2-3)) having a truncated extracellular domain is overexpressed because of amplification of an abnormal ALK gene that lacks exons 2 and 3. ALK(del2-3) was autophosphorylated in NB-1 cells as well as in ALK(del2-3)-transduced cells and exhibited enhanced in vitro kinase activity compared with the wild-type kinase. ALK(del2-3)-transduced NIH3T3 cells exhibited increased colony-forming capacity in soft agar and tumorigenicity in nude mice. RNAi-mediated ALK knockdown resulted in the growth suppression of ALK(del2-3)-expressing cells, arguing for the oncogenic role of this mutant. Our findings provide a novel insight into the mechanism of deregulation of the ALK kinase and its roles in neuroblastoma pathogenesis.

Indexed as

Anaplastic Lymphoma KinaseAnimalsCell Line, TumorCell ProliferationCell Transformation, NeoplasticEndoplasmic ReticulumEnzyme ActivationGene OrderHumansMiceNeuroblastomaNIH 3T3 CellsPyrimidinesReceptor Protein-Tyrosine KinasesSequence DeletionALK protein, humanAlk protein, mouseAnaplastic Lymphoma KinaseNVP-TAE684PyrimidinesReceptor Protein-Tyrosine Kinases

Identifiers

PMID22249260
OpenAlexW2015926937

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.