Evidence map›Paper›PMID 34885231›Full record

ArticleCancers2021

Receptor Activator of NF-κB (RANK) Confers Resistance to Chemotherapy in AML and Associates with Dismal Disease Course.

Kim L Clar, Lisa M Weber, Bastian J Schmied, Jonas S Heitmann, Maddalena Marconato, Claudia Tandler, Pascal Schneider, Helmut R Salih

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.3field-weighted citation impact, top 48% 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

4 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. 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

8 authors at 2 institutions in 2 countries.

Kim L ClarClinical Collaboration Unit Translational Immunology, German Cancer Consortium (DKTK) and German Cancer Research Center (DKFZ), Department of Internal Medicine, University Hospital Tuebingen, 72076 Tuebingen, Germany.ORCID 0000-0003-1454-9830
Lisa M WeberClinical Collaboration Unit Translational Immunology, German Cancer Consortium (DKTK) and German Cancer Research Center (DKFZ), Department of Internal Medicine, University Hospital Tuebingen, 72076 Tuebingen, Germany.ORCID 0000-0001-9514-5218
Bastian J SchmiedClinical Collaboration Unit Translational Immunology, German Cancer Consortium (DKTK) and German Cancer Research Center (DKFZ), Department of Internal Medicine, University Hospital Tuebingen, 72076 Tuebingen, Germany.
Jonas S HeitmannClinical Collaboration Unit Translational Immunology, German Cancer Consortium (DKTK) and German Cancer Research Center (DKFZ), Department of Internal Medicine, University Hospital Tuebingen, 72076 Tuebingen, Germany.
Maddalena MarconatoClinical Collaboration Unit Translational Immunology, German Cancer Consortium (DKTK) and German Cancer Research Center (DKFZ), Department of Internal Medicine, University Hospital Tuebingen, 72076 Tuebingen, Germany.
Claudia TandlerClinical Collaboration Unit Translational Immunology, German Cancer Consortium (DKTK) and German Cancer Research Center (DKFZ), Department of Internal Medicine, University Hospital Tuebingen, 72076 Tuebingen, Germany.
Pascal SchneiderDepartment of Biochemistry, University of Lausanne, 1066 Epalinges, Switzerland.
Helmut R SalihClinical Collaboration Unit Translational Immunology, German Cancer Consortium (DKTK) and German Cancer Research Center (DKFZ), Department of Internal Medicine, University Hospital Tuebingen, 72076 Tuebingen, Germany.ORCID 0000-0002-6719-1847
German Cancer Research Center · DEUniversity of Lausanne · CH

Funding

Deutsche Forschungsgemeinschaft SA1360/9-3Deutsche Krebshilfe 70113496Deutsche Krebshilfe 70113999Germany's Excellence Strategy EXC 2180/1, 390900677Swiss National Science Foundation 310030A 176256Wilhelm Sander-Stiftung 2017.100.2
6 · The paper itself

Abstract

Although treatment options of acute myeloid leukemia (AML) have improved over the recent years, prognosis remains poor. Better understanding of the molecular mechanisms influencing and predicting treatment efficacy may improve disease control and outcome. Here we studied the expression, prognostic relevance and functional role of the tumor necrosis factor receptor (TNFR) family member Receptor Activator of Nuclear Factor (NF)-κB (RANK) in AML. We conducted an experimental ex vivo study using leukemic cells of 54 AML patients. Substantial surface expression of RANK was detected on primary AML cells in 35% of the analyzed patients. We further found that RANK signaling induced the release of cytokines acting as growth and survival factors for the leukemic cells and mediated resistance of AML cells to treatment with doxorubicin and cytarabine, the most commonly used cytostatic compounds in AML treatment. In line, RANK expression correlated with a dismal disease course as revealed by reduced overall survival. Together, our results show that RANK plays a yet unrecognized role in AML pathophysiology and resistance to treatment, and identify RANK as "functional" prognostic marker in AML. Therapeutic modulation of RANK holds promise to improve treatment response in AML patients.

Indexed as

AMLchemotherapy resistancecytarabinedoxorubicinprognosisRANK

Identifiers

PMID34885231
PMCPMC8657109
OpenAlexW4200321642

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.