Evidence map›Paper›PMID 21494621›Full record

ArticlePloS one2011

Inhibition of anaplastic lymphoma kinase (ALK) activity provides a therapeutic approach for CLTC-ALK-positive human diffuse large B cell lymphomas.

Leandro Cerchietti, Christine Damm-Welk, Inga Vater, Wolfram Klapper, Lana Harder, Christiane Pott, Shao Ning Yang, Alfred Reiter, Reiner Siebert, Ari Melnick and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 8% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. CD20-negative diffuse large B cell lymphoma: a comprehensive analysis of 695 cases.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. ALK: a tyrosine kinase target for cancer therapy.Cold Spring Harbor molecular case studies · 2017
    Review
  13. Review
  14. Current Progress in EBV-Associated B-Cell Lymphomas.Advances in experimental medicine and biology · 2017
    Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. ALK-driven tumors and targeted therapy: focus on crizotinib.Pharmacogenomics and personalized medicine · 2014
    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 4 institutions in 2 countries.

Leandro CerchiettiHematology and Oncology Division, Weill Cornell Medical College, Cornell University, New York, New York, United States of America. lec2010@med.cornell.edu
Christine Damm-Welk
Inga Vater
Wolfram Klapper
Lana Harder
Christiane Pott
Shao Ning Yang
Alfred Reiter
Reiner Siebert
Ari Melnick
Willi Woessmann
University Hospital Schleswig-Holstein · DECornell University · USUniversity of Giessen · DEUniversity of Lübeck · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

ALK positive diffuse large B-cell lymphomas (DLBCL) are a distinct lymphoma subtype associated with a poor outcome. Most of them feature a t(2;17) encoding a clathrin (CLTC)-ALK fusion protein. The contribution of deregulated ALK-activity in the pathogenesis and maintenance of these DLBCLs is not yet known. We established and characterized the first CLTC-ALK positive DLBCL cell line (LM1). LM1 formed tumors in NOD-SCID mice. The selective ALK inhibitor NVP-TAE684 inhibited growth of LM1 cells in vitro at nanomolar concentrations. NVP-TAE684 repressed ALK-activated signalling pathways and induced apoptosis of LM1 DLBCL cells. Inhibition of ALK-activity resulted in sustained tumor regression in the xenotransplant tumor model. These data indicate a role of CLTC-ALK in the maintenance of the malignant phenotype thereby providing a rationale therapeutic target for these otherwise refractory tumors.

Indexed as

Anaplastic Lymphoma KinaseAnimalsBase SequenceCell DeathCell Line, TumorCell ProliferationHumansImmunocompromised HostImmunophenotypingLymphoma, Large B-Cell, DiffuseMiceMice, SCIDMolecular Sequence DataOncogene Proteins, FusionProtein Kinase InhibitorsPyrimidinesALK protein, humanAlk protein, mouseAnaplastic Lymphoma KinaseNVP-TAE684Oncogene Proteins, Fusiononcoprotein CLTCL-ALKProtein Kinase InhibitorsPyrimidinesReceptor Protein-Tyrosine Kinases

Identifiers

PMID21494621
PMCPMC3072987
OpenAlexW2036895823

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.