Evidence map›Paper›PMID 32066735›Full record

ArticleNature communications2020

Inhibiting WNT and NOTCH in renal cancer stem cells and the implications for human patients.

Annika Fendler, Daniel Bauer, Jonas Busch, Klaus Jung, Annika Wulf-Goldenberg, Severine Kunz, Kun Song, Adam Myszczyszyn, Sefer Elezkurtaj, Bettina Erguen and 3 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers.

0numbers the graph read from it
0cells of the map it votes in
124citing papers in PubMed
12.6field-weighted citation impact, top 1% 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

124 citing papers in PubMed, 194 citations in OpenAlex.

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64 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 4 institutions in 2 countries.

Annika FendlerCancer Research Program, Max Delbrueck Center for Molecular Medicine (MDC) in the Helmholtz Association, Berlin, Germany.
Daniel BauerCancer Research Program, Max Delbrueck Center for Molecular Medicine (MDC) in the Helmholtz Association, Berlin, Germany.
Jonas BuschBerlin Institute of Health (BIH), Berlin, Germany.
Klaus JungDepartment of Urology, Charité-University Medicine, Berlin, Germany.ORCID http://orcid.org/0000-0001-9797-5362
Annika Wulf-GoldenbergExperimental Pharmacology and Oncology GmbH (EPO), Berlin, Germany.
Severine KunzElectron Microscopy Core Facility, Max Delbrueck Center for Molecular Medicine (MDC) in the Helmholtz Association, Berlin, Germany.ORCID http://orcid.org/0000-0002-0131-3506
Kun SongBerlin Institute for Medical Systems Biology (BIMSB), Max Delbrueck Center for Molecular Medicine (MDC) in the Helmholtz Association, Berlin, Germany.
Adam MyszczyszynCancer Research Program, Max Delbrueck Center for Molecular Medicine (MDC) in the Helmholtz Association, Berlin, Germany.
Sefer ElezkurtajDepartment of Pathology, Charité-University Medicine, Berlin, Germany.
Bettina ErguenDepartment of Urology, Charité-University Medicine, Berlin, Germany.ORCID http://orcid.org/0000-0003-1219-6517
Simone JungCancer Research Program, Max Delbrueck Center for Molecular Medicine (MDC) in the Helmholtz Association, Berlin, Germany.
Wei ChenBerlin Institute of Health (BIH), Berlin, Germany.ORCID http://orcid.org/0000-0003-3263-1627
Walter BirchmeierCancer Research Program, Max Delbrueck Center for Molecular Medicine (MDC) in the Helmholtz Association, Berlin, Germany. wbirch@mdc-berlin.de.
Max Delbrück Center · DECharité - Universitätsmedizin Berlin · DEBerlin Institute of Health at Charité - Universitätsmedizin Berlin · DEEcologic Institute · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Current treatments for clear cell renal cell cancer (ccRCC) are insufficient because two-thirds of patients with metastases progress within two years. Here we report the identification and characterization of a cancer stem cell (CSC) population in ccRCC. CSCs are quantitatively correlated with tumor aggressiveness and metastasis. Transcriptional profiling and single cell sequencing reveal that these CSCs exhibit an activation of WNT and NOTCH signaling. A significant obstacle to the development of rational treatments has been the discrepancy between model systems and the in vivo situation of patients. To address this, we use CSCs to establish non-adherent sphere cultures, 3D tumor organoids, and xenografts. Treatment with WNT and NOTCH inhibitors blocks the proliferation and self-renewal of CSCs in sphere cultures and organoids, and impairs tumor growth in patient-derived xenografts in mice. These findings suggest that our approach is a promising route towards the development of personalized treatments for individual patients.

Indexed as

AdultAgedAged, 80 and overAnimalsAntineoplastic AgentsBridged Bicyclo Compounds, HeterocyclicCarcinoma, Renal CellCell Line, TumorCell ProliferationFemaleHeterocyclic Compounds, 3-RingHumansKidneyKidney NeoplasmsMaleMiceAntineoplastic AgentsBridged Bicyclo Compounds, HeterocyclicHeterocyclic Compounds, 3-RingICG 001PyrimidinonesReceptors, NotchRNA, Small InterferingWnt ProteinsXAV939

Identifiers

PMID32066735
PMCPMC7026425
OpenAlexW3005687797

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.