Evidence map›Paper›PMID 20805506›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2010

Identification of differential and functionally active miRNAs in both anaplastic lymphoma kinase (ALK)+ and ALK- anaplastic large-cell lymphoma.

Olaf Merkel, Frank Hamacher, Daniela Laimer, Eveline Sifft, Zlatko Trajanoski, Marcel Scheideler, Gerda Egger, Melanie R Hassler, Christiane Thallinger, Ana Schmatz and 3 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
5.4field-weighted citation impact, top 3% 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

67 citing papers in PubMed, 108 citations in OpenAlex.

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  9. Article
  10. Genome-Wide miRNA Expression Profiling of Molecular Subgroups of Peripheral T-cell Lymphoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021
    Article
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  18. Non-Coding RNA Networks in ALK-Positive Anaplastic-Large Cell Lymphoma.International journal of molecular sciences · 2019
    Review
  19. Article
  20. MiRNA Dysregulation in Childhood Hematological Cancer.International journal of molecular sciences · 2018
    Review

7 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

13 authors at 6 institutions in 3 countries.

Olaf MerkelLaboratory for Immunological and Molecular Cancer Research, Third Medical Department with Hematology, Paracelsus Medical University Salzburg, 5020 Salzburg, Austria. o.merkel@salk.at
Frank Hamacher
Daniela Laimer
Eveline Sifft
Zlatko Trajanoski
Marcel Scheideler
Gerda Egger
Melanie R Hassler
Christiane Thallinger
Ana Schmatz
Suzanne D Turner
Richard Greil
Lukas Kenner
Clinical Research Management · USParacelsus Medical University · ATAddenbrooke's Hospital · GBGraz University of Technology · ATInnsbruck Medical University · ATMedical University of Vienna · AT

Funding

Austrian Science Fund FWF V 102
6 · The paper itself

Abstract

Aberrant anaplastic lymphoma kinase (ALK) expression is a defining feature of many human cancers and was identified first in anaplastic large-cell lymphoma (ALCL), an aggressive non-Hodgkin T-cell lymphoma. Since that time, many studies have set out to identify the mechanisms used by aberrant ALK toward tumorigenesis. We have identified a distinct profile of micro-RNAs (miRNAs) that characterize ALCL; furthermore, this profile distinguishes ALK(+) from ALK(-) subtypes, and thus points toward potential mechanisms of tumorigenesis induced by aberrant ALK. Using a nucleophosmin-ALK transgenic mouse model as well as human primary ALCL tumor tissues and human ALCL-derived cell lines, we reveal a set of overlapping deregulated miRNAs that might be implicated in the development and progression of ALCL. Importantly, ALK(+) and ALK(-) ALCL could be distinguished by a distinct profile of "oncomirs": Five members of the miR-17-92 cluster were expressed more highly in ALK(+) ALCL, whereas miR-155 was expressed more than 10-fold higher in ALK(-) ALCL. Moreover, miR-101 was down-regulated in all ALCL model systems, but its forced expression attenuated cell proliferation only in ALK(+) and not in ALK(-) cell lines, perhaps suggesting different modes of ALK-dependent regulation of its target proteins. Furthermore, inhibition of mTOR, which is targeted by miR-101, led to reduced tumor growth in engrafted ALCL mouse models. In addition to future therapeutical and diagnostic applications, it will be of interest to study the physiological implications and prognostic value of the identified miRNA profiles.

Indexed as

Anaplastic Lymphoma KinaseAnimalsAntineoplastic AgentsBase SequenceCell Line, TumorCell ProliferationGene Expression ProfilingGene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticLymphoma, Large-Cell, AnaplasticMiceMice, TransgenicMicroRNAsMultigene FamilyProtein-Tyrosine KinasesReceptor Protein-Tyrosine KinasesALK protein, humanAlk protein, mouseAnaplastic Lymphoma KinaseAntineoplastic AgentsMicroRNAsProtein-Tyrosine KinasesReceptor Protein-Tyrosine KinasesSirolimustemsirolimus

Identifiers

PMID20805506
PMCPMC2941277
OpenAlexW2065800209

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.