Evidence map›Paper›PMID 26960970›Full record

ArticleFamilial cancer2016

CTNNB1-mutant colorectal carcinomas with immediate invasive growth: a model of interval cancers in Lynch syndrome.

Aysel Ahadova, Magnus von Knebel Doeberitz, Hendrik Bläker, Matthias Kloor

Registry-linked trialAbstract read
PubMed Publisher
In one paragraph

Article in Familial cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06708429 (Impact of Immune-surveillance on the Development of Colorectal Cancer in Patients With Lynch Syndrome), which is not on this map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
5.9field-weighted citation impact, top 3% 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.

NCT06708429 recruitingnot on this mapstarted 2023, after this paper: background citation

Impact of Immune-surveillance on the Development of Colorectal Cancer in Patients With Lynch Syndrome

TypeobservationalSponsorSan Raffaele UniversityRan2023 to 2034Enrolled300ConditionsLynch Syndrome, Lynch Syndrome I, Lynch Syndrome II, Lynch Syndrome I (Site-specific Colonic Cancer)ArmsLYNX EYE (Lynch syndrome X-Talk of Enteral mucosa with Immune System)
3 · Its place in the literature

Who cites it

50 citing papers in PubMed, 88 citations in OpenAlex.

  1. Review
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  3. Review
  4. Article
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  6. Therapeutic targeting of mismatch repair-deficient cancers.Nature reviews. Clinical oncology · 2025
    Review
  7. Review
  8. Article
  9. Article
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  11. Article
  12. Review
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  14. Review
  15. [Hereditary colorectal carcinogenesis].Pathologie (Heidelberg, Germany) · 2023
    Review
  16. Article
  17. Review
  18. Article
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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

4 authors at 4 institutions in 1 country.

Aysel AhadovaDepartment of Applied Tumor Biology, Institute of Pathology, University Hospital Heidelberg, Im Neuenheimer Feld 224, 69120, Heidelberg, Germany.
Magnus von Knebel DoeberitzDepartment of Applied Tumor Biology, Institute of Pathology, University Hospital Heidelberg, Im Neuenheimer Feld 224, 69120, Heidelberg, Germany.
Hendrik BläkerDepartment of General Pathology, University Hospital Charité, Charitéplatz 1, 10117, Berlin, Germany.
Matthias KloorDepartment of Applied Tumor Biology, Institute of Pathology, University Hospital Heidelberg, Im Neuenheimer Feld 224, 69120, Heidelberg, Germany. matthias.kloor@med.uni-heidelberg.de.
Charité - Universitätsmedizin Berlin · DEEuropean Molecular Biology Laboratory · DEGerman Cancer Research Center · DEHeidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The implementation of regular colonoscopy programs has significantly decreased the mortality associated with colorectal cancer (CRC) in Lynch syndrome patients. However, interval CRCs in Lynch syndrome that remain undetected by colonoscopy still represent a substantial problem in the management of the syndrome. One possible reason of interval cancers could be a non-polypous pathway of cancer development. To examine the possibility of a non-polypous pathway of CRC development in Lynch syndrome, we analyzed the histological appearance of 46 Lynch syndrome-associated CRCs and compared them to 34 sporadic microsatellite unstable cancers. We observed that 25 (62.5 %) out of 40 assessable Lynch syndrome-associated carcinomas lacked evidence of polypous growth, compared to 17 (50 %) out of 34 sporadic MSI-H cancers. We detected CTNNB1 mutations in 8 (17.4 %) out of 46 Lynch syndrome-associated cancers compared to 0 out of 34 sporadic MSI-H cancers (p = 0.01). The majority of CTNNB1-mutant cancers presented with a histological appearance suggesting immediate invasive growth. Our results suggest that a distinct subgroup of CRCs in Lynch syndrome may in fact emerge from a non-polypous precursor, thus potentially explaining the phenomenon of interval cancers. Such a non-polypous precursor may be the recently described mismatch repair-deficient crypt focus, which remains invisible for the examiner during colonoscopy. This calls for considering the implementation of active, primary preventive measures in the management of Lynch syndrome. Future studies on pathogenic pathways and precursor lesions in Lynch syndrome are strongly encouraged, and the clinical efficacy of new prevention approaches should be evaluated in prospective clinical trials.

Indexed as

beta CateninColorectal Neoplasms, Hereditary NonpolyposisHumansMicrosatellite InstabilityMutationbeta CateninCTNNB1 protein, humanInterval cancerLynch syndromeMicrosatellite instabilityMismatch repair deficiencyMismatch repair deficient crypt focusβ-catenin

Identifiers

PMID26960970
OpenAlexW2295960437

What OpenQuestion holds

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Read underepoch 390

Registered trials

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.