Evidence map›Paper›PMID 33596640›Full record

ArticleHaematologica2022

The miR-200c/141-ZEB2-TGFβ axis is aberrant in human T-cell prolymphocytic leukemia.

Stefan J Erkeland, Christiaan J Stavast, Joyce Schilperoord-Vermeulen, Giada Dal Collo, Harmen J G Van de Werken, Leticia G Leon, Antoinette Van Hoven-Beijen, Iris Van Zuijen, Yvonne M Mueller, Eric M Bindels and 5 more

Open access · goldAbstract read
In one paragraph

Article in Haematologica, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.7field-weighted citation impact, top 35% 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

11 citing papers in PubMed, 10 citations in OpenAlex.

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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

15 authors at 2 institutions in 2 countries.

Stefan J ErkelandDepartment of Immunology, Erasmus University Medical Center, Rotterdam. s.erkeland@erasmusmc.nl.
Christiaan J StavastDepartment of Immunology, Erasmus University Medical Center, Rotterdam.
Joyce Schilperoord-VermeulenDepartment of Immunology, Erasmus University Medical Center, Rotterdam.
Giada Dal ColloDepartment of Immunology, Erasmus University Medical Center, Rotterdam.
Harmen J G Van de WerkenDepartment of Immunology, Erasmus University Medical Center, Rotterdam, the Netherlands; Cancer Computational Biology Center, Erasmus MC Cancer Institute, University Medical Center, Dr. Molewaterplein 40, 3015 GD, Rotterdam.
Leticia G LeonDepartment of Immunology, Erasmus University Medical Center, Rotterdam.
Antoinette Van Hoven-BeijenDepartment of Immunology, Erasmus University Medical Center, Rotterdam.
Iris Van ZuijenDepartment of Immunology, Erasmus University Medical Center, Rotterdam.
Yvonne M MuellerDepartment of Immunology, Erasmus University Medical Center, Rotterdam.
Eric M BindelsDepartment of Hematology, Erasmus University Medical Center, Rotterdam.
Dick De RidderBioinformatics Group, Wageningen University, Wageningen.
Mies C Kappers-KlunneDepartment of Hematology, Erasmus University Medical Center, Rotterdam.
Kirsten Van LomDepartment of Hematology, Erasmus University Medical Center, Rotterdam.
Vincent H J Van der VeldenDepartment of Immunology, Erasmus University Medical Center, Rotterdam.
Anton W LangerakDepartment of Immunology, Erasmus University Medical Center, Rotterdam. a.langerak@erasmusmc.nl.
Erasmus MC · NLWageningen University & Research · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

T-cell prolymphocytic leukemia (T-PLL) is mostly characterized by aberrant expansion of small- to medium-sized prolymphocytes with a mature post-thymic phenotype, high aggressiveness of the disease and poor prognosis. However, T-PLL is more heterogeneous with a wide range of clinical, morphological, and molecular features, which occasionally impedes the diagnosis. We hypothesized that T-PLL consists of phenotypic and/or genotypic subgroups that may explain the heterogeneity of the disease. Multi-dimensional immuno-phenotyping and gene expression profiling did not reveal clear T-PLL subgroups, and no clear T-cell receptor a or β CDR3 skewing was observed between different T-PLL cases. We revealed that the expression of microRNA (miRNA) is aberrant and often heterogeneous in T-PLL. We identified 35 miRNA that were aberrantly expressed in T-PLL with miR-200c/141 as the most differentially expressed cluster. High miR- 200c/141 and miR-181a/181b expression was significantly correlated with increased white blood cell counts and poor survival. Furthermore, we found that overexpression of miR-200c/141 correlated with downregulation of their targets ZEB2 and TGFβR3 and aberrant TGFβ1- induced phosphorylated SMAD2 (p-SMAD2) and p-SMAD3, indicating that the TGFβ pathway is affected in T-PLL. Our results thus highlight the potential role for aberrantly expressed oncogenic miRNA in T-PLL and pave the way for new therapeutic targets in this disease.

Indexed as

Leukemia, Prolymphocytic, T-CellMicroRNAsGene Expression ProfilingHumansLymphocytesTransforming Growth Factor betaZinc Finger E-box Binding Homeobox 2MicroRNAsMIRN200 microRNA, humanTransforming Growth Factor betaZEB2 protein, humanZinc Finger E-box Binding Homeobox 2

Identifiers

PMID33596640
PMCPMC8719092
OpenAlexW3132371426

What OpenQuestion holds

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Registered trials

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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.