Evidence map›Paper›PMID 27268084›Full record

ArticleBlood2016

Dimethyl fumarate restores apoptosis sensitivity and inhibits tumor growth and metastasis in CTCL by targeting NF-κB.

Jan P Nicolay, Karin Müller-Decker, Anne Schroeder, Markus Brechmann, Markus Möbs, Cyrill Géraud, Chalid Assaf, Sergij Goerdt, Peter H Krammer, Karsten Gülow

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

64 citing papers in PubMed, 92 citations in OpenAlex.

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4 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 5 institutions in 2 countries.

Jan P NicolayDepartment of Dermatology, Venereology and Allergy, University Medical Center Mannheim, Ruprecht-Karls University of Heidelberg, Mannheim, Germany; Division of Immunogenetics, and.
Karin Müller-DeckerCore Facility Tumor Models, German Cancer Research Center, Heidelberg, Germany;
Anne SchroederDivision of Immunogenetics, and.
Markus BrechmannDivision of Immunogenetics, and.
Markus MöbsDepartment of Dermatology, Venereology and Allergy, and Institute of Pathology, University Medical Center Charité, Berlin, Germany; and.
Cyrill GéraudDepartment of Dermatology, Venereology and Allergy, University Medical Center Mannheim, Ruprecht-Karls University of Heidelberg, Mannheim, Germany;
Chalid AssafDepartment of Dermatology, Venereology and Allergy, and Department of Dermatology, Venereology and Allergy, HELIOS Klinikum, Krefeld, Germany.
Sergij GoerdtDepartment of Dermatology, Venereology and Allergy, University Medical Center Mannheim, Ruprecht-Karls University of Heidelberg, Mannheim, Germany;
Peter H KrammerDivision of Immunogenetics, and.
Karsten GülowDivision of Immunogenetics, and.
Immungenetics (Germany) · DEHeidelberg University · DEENT and Allergy · USHelios Klinikum Krefeld · DEUniversity Hospital Heidelberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite intensive efforts in recent years, a curative therapy for cutaneous T-cell lymphoma (CTCL) has not yet been developed. Therefore, the establishment of new therapeutic approaches with higher efficacy rates and milder side effects is strongly desired. A characteristic feature of the malignant T-cell population in CTCL is resistance toward cell death resulting from constitutive NF-κB activation. Therefore, NF-κB-dependent cell death resistance represents an interesting therapeutic target in CTCL because an NF-κB-directed therapy would leave bystander T cells widely unaffected. We investigated the effects of dimethyl fumarate (DMF) on CTCL cells in vitro and in vivo. DMF induced cell death in primary patient-derived CD4(+) cells and CTCL cell lines, but hardly in T cells from healthy donors. DMF-induced cell death was linked specifically to NF-κB inhibition. To study the impact of DMF in vivo, we developed 2 CTCL xenograft mouse models with different cutaneous localizations of the T-cell infiltrate. DMF treatment delayed the growth of CTCL tumors and prevented formation of distant metastases. In addition, DMF induced increased cell death in primary CTCL tumors and in liver metastases. In summary, DMF treatment represents a remarkable therapeutic option in CTCL because it restores CTCL apoptosis in vitro and in preclinical models in vivo and prevents spreading of the disease to distant sites. DMF treatment is of particular promise in CTCL because DMF is already in successful clinical use in the treatment of psoriasis and multiple sclerosis allowing fast translation into clinical studies in CTCL.

Indexed as

AnimalsApoptosisDimethyl FumarateHumansImmunosuppressive AgentsLymphoma, T-Cell, CutaneousMiceNeoplasm MetastasisNF-kappa BSignal TransductionSkinSkin NeoplasmsTumor Cells, CulturedDimethyl FumarateImmunosuppressive AgentsNF-kappa B

Identifiers

PMID27268084
PMCPMC5026464
OpenAlexW2417054233

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.