Evidence map›Paper›PMID 34572765›Full record

ArticleCancers2021

Histological and Somatic Mutational Profiles of Mismatch Repair Deficient Endometrial Tumours of Different Aetiologies.

Neil A J Ryan, Thomas D J Walker, James Bolton, Natalja Ter Haar, Tom Van Wezel, Mark A Glaire, David N Church, D Gareth Evans, Tjalling Bosse, Emma J Crosbie

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

7 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. A Focused Clinical Review of Lynch Syndrome.Cancer management and research · 2023
    Review
  5. Article
  6. Article
  7. 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

10 authors at 4 institutions in 2 countries.

Neil A J RyanDivision of Cancer Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester M13 9PL, UK.ORCID 0000-0003-3117-3257
Thomas D J WalkerDivision of Cancer Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester M13 9PL, UK.ORCID 0000-0003-4607-7321
James BoltonManchester Academic Health Science Centre, Department of Pathology, Manchester University NHS Foundation Trust, Manchester M13 9WL, UK.
Natalja Ter HaarDepartment of Pathology, Leiden University Medical Center, Albinusdreef 2, 2333 ZA Leiden, The Netherlands.
Tom Van WezelDepartment of Pathology, Leiden University Medical Center, Albinusdreef 2, 2333 ZA Leiden, The Netherlands.ORCID 0000-0001-5773-7730
Mark A GlaireTumour Genomics and Immunology Group, Wellcome Centre for Human Genetics, University of Oxford, Roosevelt Drive, Oxford OX3 7DQ, UK.
David N ChurchTumour Genomics and Immunology Group, Wellcome Centre for Human Genetics, University of Oxford, Roosevelt Drive, Oxford OX3 7DQ, UK.
D Gareth EvansDivision of Evolution and Genomic Medicine, Faculty of Biology, Medicine and Health, University of Manchester, Manchester M13 9WL, UK.ORCID 0000-0002-8482-5784
Tjalling BosseDepartment of Pathology, Leiden University Medical Center, Albinusdreef 2, 2333 ZA Leiden, The Netherlands.
Emma J CrosbieDivision of Cancer Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester M13 9PL, UK.ORCID 0000-0003-0284-8630
Leiden University Medical Center · NLManchester Academic Health Science Centre · GBCentre for Human Genetics · GBUniversity of Manchester · GB

Funding

Cancer Research UK 27963Medical Research Council MR/M018431/1
6 · The paper itself

Abstract

backgroundMismatch repair deficient (MMRd) tumours may arise from somatic events acquired during carcinogenesis or in the context of Lynch syndrome (LS), an inherited cancer predisposition condition caused by germline MMR pathogenic variants. Our aim was to explore whether sporadic and hereditary MMRd endometrial cancers (EC) display distinctive tumour biology.

methodsClinically annotated LS-EC were collected. Histological slide review was performed centrally by two specialist gynaecological pathologists. Mutational analysis was by a bespoke 75- gene next-generation sequencing panel. Comparisons were made with sporadic MMRd EC. Multiple correspondence analysis was used to explore similarities and differences between the cohorts.

resultsAfter exclusions, 135 LS-EC underwent independent histological review, and 64 underwent mutational analysis. Comparisons were made with 59 sporadic MMRd EC. Most tumours were of endometrioid histological subtype (92% LS-EC and 100% sporadic MMRd EC, respectively,

conclusionsWhilst MMRd EC of hereditary and sporadic aetiology may be difficult to distinguish by histology alone, differences in infiltrating immune cell counts and mutational profile may predict heterogenous responses to novel targeted therapies and warrant further study.

Indexed as

endometrial cancerlynch syndromemismatch repairsomatic mutation

Identifiers

PMID34572765
PMCPMC8469577
OpenAlexW3197463912

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.