Evidence map›Paper›PMID 34849464›Full record

ArticleiScience2021

Epithelial Wnt secretion drives the progression of inflammation-induced colon carcinoma in murine model.

Bahar Degirmenci, Cansu Dincer, Habibe Cansu Demirel, Linda Berkova, Andreas E Moor, Abdullah Kahraman, George Hausmann, Michel Aguet, Nurcan Tuncbag, Tomas Valenta and 1 more

Open access · goldAbstract read
In one paragraph

Article in iScience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

5 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Review
  3. The Roles of Secreted Wnt Ligands in Cancer.International journal of molecular sciences · 2023
    Review
  4. The role of Evi/Wntless in exporting Wnt proteins.Development (Cambridge, England) · 2023
    Review
  5. The emerging era of personalized medicine in advanced colorectal cancer.Journal of gastroenterology and hepatology · 2022
    Review
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

11 authors at 6 institutions in 3 countries.

Bahar DegirmenciDepartment of Molecular Life Sciences, University of Zurich, Winterthurerstrasse. 190, CH-8057 Zurich, Switzerland.
Cansu DincerGraduate School of Informatics, Department of Health Informatics, METU, Ankara, Turkey.
Habibe Cansu DemirelGraduate School of Informatics, Department of Health Informatics, METU, Ankara, Turkey.
Linda BerkovaInstitute of Molecular Genetics of the ASCR, v. v. i., Vídeňská 1083142 20, Prague 4, Czech Republic.
Andreas E MoorSwiss Institute for Experimental Cancer Research (ISREC), Ecole Polytechnique Fédérale de Lausanne (EPFL), School of Life Sciences, 1015 Lausanne, Switzerland.
Abdullah KahramanDepartment of Pathology and Molecular Pathology, University Hospital Zurich, Zurich, Switzerland.
George HausmannDepartment of Molecular Life Sciences, University of Zurich, Winterthurerstrasse. 190, CH-8057 Zurich, Switzerland.
Michel AguetSwiss Institute for Experimental Cancer Research (ISREC), Ecole Polytechnique Fédérale de Lausanne (EPFL), School of Life Sciences, 1015 Lausanne, Switzerland.
Nurcan TuncbagGraduate School of Informatics, Department of Health Informatics, METU, Ankara, Turkey.
Tomas ValentaDepartment of Molecular Life Sciences, University of Zurich, Winterthurerstrasse. 190, CH-8057 Zurich, Switzerland.
Konrad BaslerDepartment of Molecular Life Sciences, University of Zurich, Winterthurerstrasse. 190, CH-8057 Zurich, Switzerland.
University of Zurich · CHBilkent University · TRCzech Academy of Sciences, Institute of Molecular Genetics · CZÉcole Polytechnique Fédérale de Lausanne · CHETH Zurich · CHUniversity Hospital of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colon cancer is initiated by stem cells that escape the strict control. This process is often driven through aberrant activation of Wnt signaling by mutations in components acting downstream of the receptor complex that unfetter tumor cells from the need for Wnts. Here we describe a class of colon cancer that does not depend on mutated core components of the Wnt pathway. Genetically blocking Wnt secretion from epithelial cells of such tumors results in apoptosis, reduced expression of colon cancer markers, followed by enhanced tumor differentiation. In contrast to the normal colonic epithelium, such tumor cells autosecrete Wnts to maintain their uncontrolled proliferative behavior. In humans, we determined certain cases of colon cancers in which the Wnt pathway is hyperactive, but not through mutations in its core components. Our findings illuminate the path in therapy to find further subtypes of Wnt-dependent colon cancer that might be responsive to Wnt secretion inhibitors.

Indexed as

CancerCell biologyImmunologyMolecular physiologyOmics

Identifiers

PMID34849464
PMCPMC8607204
OpenAlexW3210070258

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.