Evidence map›Paper›PMID 27535218›Full record

ArticleLeukemia2017

Microenvironmental interactions between endothelial and lymphoma cells: a role for the canonical WNT pathway in Hodgkin lymphoma.

F Linke, M Harenberg, M M Nietert, S Zaunig, F von Bonin, A Arlt, M Szczepanowski, H A Weich, S Lutz, C Dullin and 11 more

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

26 citing papers in PubMed, 64 citations in OpenAlex.

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  15. Wnt Signaling in the Tumor Microenvironment.Advances in experimental medicine and biology · 2021
    Article
  16. RNA sequence analysis of dermal papilla cells' regeneration in 3D culture.Journal of cellular and molecular medicine · 2020
    Article
  17. Wnt Signaling in Leukemia and Its Bone Marrow Microenvironment.International journal of molecular sciences · 2020
    Review
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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

21 authors at 5 institutions in 2 countries.

F LinkeClinic of Hematology and Medical Oncology, University Medical Centre of the Georg-August University of Göttingen, Göttingen, Germany.
M HarenbergClinic of Hematology and Medical Oncology, University Medical Centre of the Georg-August University of Göttingen, Göttingen, Germany.
M M NietertDepartment of Medical Statistics, University Medical Centre of the Georg-August University of Göttingen, Göttingen, Germany.
S ZaunigClinic of Hematology and Medical Oncology, University Medical Centre of the Georg-August University of Göttingen, Göttingen, Germany.
F von BoninClinic of Hematology and Medical Oncology, University Medical Centre of the Georg-August University of Göttingen, Göttingen, Germany.
A ArltClinic of Hematology and Medical Oncology, University Medical Centre of the Georg-August University of Göttingen, Göttingen, Germany.
M SzczepanowskiSection Hematopathology, UKSH Campus Kiel, Kiel, Germany.
H A WeichDepartment of Chemical Biology, Helmholtz-Centre for Infection Research HZI, Braunschweig, Germany.
S LutzInstitute of Pharmacology, University Medical Centre of the Georg-August University of Göttingen, Göttingen, Germany.
C DullinInstitute of Diagnostic and Interventional Radiology, University Medical Centre of the Georg-August University of Göttingen, Göttingen, Germany.ORCID 0000-0003-4297-8077
P JanovskáFaculty of Science, Institute of Experimental Biology, Masaryk University, Brno, Czech Republic.
M KrafčíkováCentral European Institute of Technology, Masaryk University, Brno, Czech Republic.
L TrantírekCentral European Institute of Technology, Masaryk University, Brno, Czech Republic.
P OvesnáInstitute of Biostatistics and Analyses, Masaryk University, Brno, Czech Republic.
W KlapperSection Hematopathology, UKSH Campus Kiel, Kiel, Germany.
T BeissbarthDepartment of Medical Statistics, University Medical Centre of the Georg-August University of Göttingen, Göttingen, Germany.
F AlvesClinic of Hematology and Medical Oncology, University Medical Centre of the Georg-August University of Göttingen, Göttingen, Germany.
V BryjaFaculty of Science, Institute of Experimental Biology, Masaryk University, Brno, Czech Republic.
L TrümperClinic of Hematology and Medical Oncology, University Medical Centre of the Georg-August University of Göttingen, Göttingen, Germany.
J WiltingDepartment of Anatomy and Cell Biology, University Medical Centre of the Georg-August University of Göttingen, Göttingen, Germany.
D KubeClinic of Hematology and Medical Oncology, University Medical Centre of the Georg-August University of Göttingen, Göttingen, Germany.
University of Göttingen · DEMasaryk University · CZCentral European Institute of Technology · CZHelmholtz Centre for Infection Research · DEMax Planck Institute of Experimental Medicine · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The interaction between vascular endothelial cells (ECs) and cancer cells is of vital importance to understand tumor dissemination. A paradigmatic cancer to study cell-cell interactions is classical Hodgkin Lymphoma (cHL) owing to its complex microenvironment. The role of the interplay between cHL and ECs remains poorly understood. Here we identify canonical WNT pathway activity as important for the mutual interactions between cHL cells and ECs. We demonstrate that local canonical WNT signaling activates cHL cell chemotaxis toward ECs, adhesion to EC layers and cell invasion using not only the Wnt-inhibitor Dickkopf, tankyrases and casein kinase 1 inhibitors but also knockdown of the lymphocyte enhancer binding-factor 1 (LEF-1) and β-catenin in cHL cells. Furthermore, LEF-1- and β-catenin-regulated cHL secretome promoted EC migration, sprouting and vascular tube formation involving vascular endothelial growth factor A (VEGF-A). Importantly, high VEGFA expression is associated with a worse overall survival of cHL patients. These findings strongly support the concept that WNTs might function as a regulator of lymphoma dissemination by affecting cHL cell chemotaxis and promoting EC behavior and thus angiogenesis through paracrine interactions.

Indexed as

Cell CommunicationTumor MicroenvironmentWnt Signaling Pathwaybeta CateninCell AdhesionCell LineCell MovementChemokine CCL19ChemotaxisEndothelial CellsHodgkin DiseaseHumansLymphoid Enhancer-Binding Factor 1Neovascularization, PathologicVascular Endothelial Growth Factor Abeta CateninChemokine CCL19Lymphoid Enhancer-Binding Factor 1Vascular Endothelial Growth Factor A

Identifiers

PMID27535218
OpenAlexW2509240907

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.