Evidence map›Paper›PMID 32009247›Full record

ArticleThe EMBO journal2020

Stable expansion of high-grade serous ovarian cancer organoids requires a low-Wnt environment.

Karen Hoffmann, Hilmar Berger, Hagen Kulbe, Sukanija Thillainadarasan, Hans-Joachim Mollenkopf, Tomasz Zemojtel, Eliane Taube, Silvia Darb-Esfahani, Mandy Mangler, Jalid Sehouli and 4 more

Open access · hybridAbstract read
In one paragraph

Article in The EMBO journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed
41.4field-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

82 citing papers in PubMed, 249 citations in OpenAlex.

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22 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

14 authors at 3 institutions in 1 country.

Karen HoffmannDepartment of Molecular Biology, Max Planck Institute for Infection Biology, Berlin, Germany.
Hilmar BergerDepartment of Molecular Biology, Max Planck Institute for Infection Biology, Berlin, Germany.
Hagen KulbeDepartment of Gynecology, Charité University Medicine, Campus Virchow-Klinikum, Berlin, Germany.
Sukanija ThillainadarasanDepartment of Molecular Biology, Max Planck Institute for Infection Biology, Berlin, Germany.
Hans-Joachim MollenkopfDepartment of Molecular Biology, Max Planck Institute for Infection Biology, Berlin, Germany.
Tomasz ZemojtelBIH Genomics Core Unit, Charité University Medicine, Campus Virchow-Klinikum, Berlin, Germany.
Eliane TaubeDepartment of Pathology, Charité University Medicine, Campus Charité, Berlin, Germany.
Silvia Darb-EsfahaniDepartment of Pathology, Charité University Medicine, Campus Charité, Berlin, Germany.
Mandy ManglerDepartment of Gynecology, Vivantes Auguste-Viktoria-Klinikum, Berlin, Germany.
Jalid SehouliDepartment of Gynecology, Charité University Medicine, Campus Virchow-Klinikum, Berlin, Germany.
Radoslav ChekerovDepartment of Gynecology, Charité University Medicine, Campus Virchow-Klinikum, Berlin, Germany.
Elena I BraicuDepartment of Gynecology, Charité University Medicine, Campus Virchow-Klinikum, Berlin, Germany.
Thomas F MeyerDepartment of Molecular Biology, Max Planck Institute for Infection Biology, Berlin, Germany.ORCID 0000-0002-6120-8679
Mirjana KesslerDepartment of Molecular Biology, Max Planck Institute for Infection Biology, Berlin, Germany.ORCID 0000-0002-9879-1052
Charité - Universitätsmedizin Berlin · DEMax Planck Institute for Infection Biology · DEAuguste-Viktoria-Klinik · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

High-grade serous ovarian cancer (HGSOC) likely originates from the fallopian tube (FT) epithelium. Here, we established 15 organoid lines from HGSOC primary tumor deposits that closely match the mutational profile and phenotype of the parental tumor. We found that Wnt pathway activation leads to growth arrest of these cancer organoids. Moreover, active BMP signaling is almost always required for the generation of HGSOC organoids, while healthy fallopian tube organoids depend on BMP suppression by Noggin. Fallopian tube organoids modified by stable shRNA knockdown of p53, PTEN, and retinoblastoma protein (RB) also require a low-Wnt environment for long-term growth, while fallopian tube organoid medium triggers growth arrest. Thus, early changes in the stem cell niche environment are needed to support outgrowth of these genetically altered cells. Indeed, comparative analysis of gene expression pattern and phenotypes of normal vs. loss-of-function organoids confirmed that depletion of tumor suppressors triggers changes in the regulation of stemness and differentiation.

Indexed as

CarcinogenesisCell DifferentiationDisease ProgressionEpitheliumFallopian TubesFemaleGene Knockdown TechniquesHumansOrganoidsOvarian NeoplasmsPhenotypeStem Cell NicheTumor Suppressor ProteinsWnt Signaling PathwayTumor Suppressor ProteinsBMP signalingpatient-derived HGSOC organoidsstemnesstumor suppressor knockdownWnt signaling

Identifiers

PMID32009247
PMCPMC7073464
OpenAlexW3003894034

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.