Evidence map›Paper›PMID 33097916›Full record

ReviewNature reviews. Cancer2021

Mutations and mechanisms of WNT pathway tumour suppressors in cancer.

Jeroen M Bugter, Nicola Fenderico, Madelon M Maurice

Erratum issuedAbstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Cancer, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 283 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
283citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

283 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Host andGut microbes · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors.

Jeroen M BugterOncode Institute and Department of Cell Biology, Center for Molecular Medicine, University Medical Center Utrecht, Utrecht, Netherlands.ORCID http://orcid.org/0000-0001-9920-2937
Nicola FendericoOncode Institute and Department of Cell Biology, Center for Molecular Medicine, University Medical Center Utrecht, Utrecht, Netherlands.ORCID http://orcid.org/0000-0003-3599-7931
Madelon M MauriceOncode Institute and Department of Cell Biology, Center for Molecular Medicine, University Medical Center Utrecht, Utrecht, Netherlands. m.m.maurice@umcutrecht.nl.ORCID http://orcid.org/0000-0001-6885-5361

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mutation-induced activation of WNT-β-catenin signalling is a frequent driver event in human cancer. Sustained WNT-β-catenin pathway activation endows cancer cells with sustained self-renewing growth properties and is associated with therapy resistance. In healthy adult stem cells, WNT pathway activity is carefully controlled by core pathway tumour suppressors as well as negative feedback regulators. Gene inactivation experiments in mouse models unequivocally demonstrated the relevance of WNT tumour suppressor loss-of-function mutations for cancer growth. However, in human cancer, a far more complex picture has emerged in which missense or truncating mutations mediate stable expression of mutant proteins, with distinct functional and phenotypic ramifications. Herein, we review recent advances and challenges in our understanding of how different mutational subsets of WNT tumour suppressor genes link to distinct cancer types, clinical outcomes and treatment strategies.

Indexed as

Molecular Targeted TherapyMutationAnimalsAntineoplastic AgentsHumansNeoplasmsTumor Suppressor ProteinsWnt ProteinsWnt Signaling PathwayAntineoplastic AgentsTumor Suppressor ProteinsWnt Proteins

Identifiers

What OpenQuestion holds

Textmetadata
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.