Evidence map›Paper›PMID 19275511›Full record

ReviewExpert review of anticancer therapy2009

Anaplastic lymphoma kinase: role in cancer pathogenesis and small-molecule inhibitor development for therapy.

Thomas R Webb, Jake Slavish, Rani E George, A Thomas Look, Liquan Xue, Qin Jiang, Xiaoli Cui, Walter B Rentrop, Stephan W Morris

Open access · greenAbstract readReview
In one paragraph

Review in Expert review of anticancer therapy, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed
13.5field-weighted citation impact, top 1% 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

89 citing papers in PubMed, 230 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Update of Diagnosis and Targeted Therapy for ALKCurrent treatment options in oncology · 2023
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. Molecular targeted therapy for anticancer treatment.Experimental & molecular medicine · 2022
    Review

29 more citing papers are in PubMed but not listed here.

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

9 authors at 2 institutions in 1 country.

Thomas R WebbDepartment of Chemical Biology and Therapeutics, St Jude Children's Research Hospital, 332 North Lauderdale Street, Mail Stop 1000, Memphis, TN 38105, USA.
Jake Slavish
Rani E George
A Thomas Look
Liquan Xue
Qin Jiang
Xiaoli Cui
Walter B Rentrop
Stephan W Morris
St. Jude Children's Research Hospital · USDana-Farber Cancer Institute · US

Funding

Viral Vector Technology (VVTSR)P30CA021765 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI CHARLES ROBERTS · 1985 to 2026
$166.9M
NPM-ALK AND ALK IN LYMPHOMA AND NORMAL DEVELOPMENTR01CA069129 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI MORRIS, STEPHAN W · 1996 to 2006
$2.0M
NCI NIH HHS CA21765NCI NIH HHS P30 CA021765NCI NIH HHS R01 CA069129NCI NIH HHS R01 CA69129
6 · The paper itself

Abstract

Anaplastic lymphoma kinase (ALK), a receptor tyrosine kinase in the insulin receptor superfamily, was initially identified in constitutively activated oncogenic fusion forms - the most common being nucleophosmin-ALK - in anaplastic large-cell lymphomas, and subsequent studies have identified ALK fusions in diffuse large B-cell lymphomas, systemic histiocytosis, inflammatory myofibroblastic tumors, esophageal squamous cell carcinomas and non-small-cell lung carcinomas. More recently, genomic DNA amplification and protein overexpression, as well as activating point mutations, of ALK have been described in neuroblastomas. In addition to those cancers for which a causative role for aberrant ALK activity is well validated, more circumstantial links implicate the full-length, normal ALK receptor in the genesis of other malignancies - including glioblastoma and breast cancer - via a mechanism of receptor activation involving autocrine and/or paracrine growth loops with the reported ALK ligands, pleiotrophin and midkine. This review summarizes normal ALK biology, the confirmed and putative roles of ALK in the development of human cancers and efforts to target ALK using small-molecule kinase inhibitors.

Indexed as

Anaplastic Lymphoma KinaseAnimalsAntineoplastic AgentsCarrier ProteinsCytokinesEnzyme InhibitorsHumansMidkineNeoplasmsNuclear ProteinsNucleophosminProtein-Tyrosine KinasesReceptor Protein-Tyrosine KinasesALK protein, humanAnaplastic Lymphoma KinaseAntineoplastic AgentsCarrier ProteinsCytokinesEnzyme InhibitorsMidkineNPM1 protein, humanNuclear ProteinsNucleophosminpleiotrophinProtein-Tyrosine KinasesReceptor Protein-Tyrosine Kinases

Identifiers

PMID19275511
PMCPMC2780428
OpenAlexW2031196045

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.