Evidence map›Paper›PMID 16763206›Full record

ArticleBlood2006

Autocrine release of interleukin-9 promotes Jak3-dependent survival of ALK+ anaplastic large-cell lymphoma cells.

Lin Qiu, Raymond Lai, Quan Lin, Esther Lau, David M Thomazy, Daniel Calame, Richard J Ford, Larry W Kwak, Robert A Kirken, Hesham M Amin

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

56 citing papers in PubMed, 80 citations in OpenAlex.

  1. Review
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  3. Article
  4. Review
  5. Article
  6. Article
  7. The World according to IL-9.Journal of immunology (Baltimore, Md. : 1950) · 2023
    Article
  8. The Dichotomy of Interleukin-9 Function in the Tumor Microenvironment.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2023
    Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Review
  19. Targeting the IL-9 pathway in cancer immunotherapy.Human vaccines & immunotherapeutics · 2020
    Review
  20. The Role of Interleukin-9 in Cancer.Pathology oncology research : POR · 2020
    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

10 authors at 2 institutions in 2 countries.

Lin QiuDepartment of Hematopathology, Box 72, University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Blvd, Houston, TX 77030, USA.
Raymond Lai
Quan Lin
Esther Lau
David M Thomazy
Daniel Calame
Richard J Ford
Larry W Kwak
Robert A Kirken
Hesham M Amin
University of Alberta · CAThe University of Texas at El Paso · US

Funding

TOXICOLOGY PROJECTG12RR008124 · NCRR · UNIVERSITY OF TEXAS EL PASO · PI WALSH, ELIZABETH J · 1992 to 2011
$20.8M
T-cell growth factor pathways and immune modulationR01AI053566 · NIAID · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI KIRKEN, ROBERT · 2003 to 2007
$1.2M
Role of Jak3 in Anaplastic Large Cell LymphomaK08CA114395 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI AMIN, HESHAM M · 2006 to 2008
$408k
NCI NIH HHS K08 CA114395NCI NIH HHS K08CA114395NCRR NIH HHS SG12RR008124NIAID NIH HHS AI053566
6 · The paper itself

Abstract

The aberrant fusion protein NPM-ALK plays an important pathogenetic role in ALK+ anaplastic large-cell lymphoma (ALCL). We previously demonstrated that Jak3 potentiates the activity of NPM-ALK. Jak3 activation is restricted to interleukins that recruit the common gamma chain (gammac) receptor, including IL-9. NPM-ALK was previously shown to promote widespread lymphomas in IL-9 transgenic mice by unknown mechanisms. We hypothesized that IL-9 plays an important role in ALK+ ALCL via Jak3 activation. Our studies demonstrate the expression of IL-9Ralpha and IL-9 in 3 ALK+ ALCL-cell lines and 75% and 83% of primary tumors, respectively. IL-9 was detected in serum-free culture medium harvested from ALK+ ALCL-cell lines, supporting autocrine release of IL-9. Treatment of these cells with an anti-IL-9-neutralizing antibody decreased pJak3 and its kinase activity, along with pStat3 and ALK kinase activity. These effects were associated with decreased cell proliferation and colony formation in soft agar and cell-cycle arrest. Evidence suggests that cell-cycle arrest can be attributed to up-regulation of p21 and down-regulation of Pim-1. Our results illustrate that IL-9/Jak3 signaling plays a significant role in the pathogenesis of ALK+ ALCL and that it represents a potential therapeutic target for treating patients with ALK+ ALCL.

Indexed as

Gene Expression Regulation, NeoplasticAnaplastic Lymphoma KinaseAnimalsCarcinomaCell SurvivalG1 PhaseHumansInterleukin-9Janus Kinase 3Lymphoma, Large B-Cell, DiffuseMiceMice, TransgenicProtein-Tyrosine KinasesReceptor Protein-Tyrosine KinasesALK protein, humanAlk protein, mouseAnaplastic Lymphoma KinaseInterleukin-9JAK3 protein, humanJak3 protein, mouseJanus Kinase 3Protein-Tyrosine KinasesReceptor Protein-Tyrosine Kinases

Identifiers

PMID16763206
PMCPMC1895569
OpenAlexW1968969270

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.