Evidence map›Paper›PMID 32634176›Full record

ArticlePloS one2020

Targeted sequencing of genes associated with the mismatch repair pathway in patients with endometrial cancer.

Ashish Kumar Singh, Bente Talseth-Palmer, Mary McPhillips, Liss Anne Solberg Lavik, Alexandre Xavier, Finn Drabløs, Wenche Sjursen

Abstract read
In one paragraph

Article in PloS one, 2020. 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
–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

5 citing papers in PubMed.

  1. Article
  2. Review
  3. Case Report: Expansion of theFrontiers in oncology · 2025
    Article
  4. Article
  5. Article
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

7 authors.

Ashish Kumar SinghDepartment of Medical Genetics, St. Olavs Hospital, Trondheim, Norway.ORCID 0000-0002-3191-7677
Bente Talseth-PalmerDepartment of Medical Genetics, St. Olavs Hospital, Trondheim, Norway.
Mary McPhillipsNSW Health Pathology, Molecular Medicine, John Hunter Hospital, Newcastle, NSW, Australia.
Liss Anne Solberg LavikDepartment of Medical Genetics, St. Olavs Hospital, Trondheim, Norway.
Alexandre XavierSchool of Biomedical Science and Pharmacy, Faculty of Health and Medicine, University of Newcastle and Hunter Medical Research Institute, Newcastle, Australia.
Finn DrabløsDepartment of Clinical and Molecular Medicine, Faculty of Medicine and Health Sciences, NTNU-Norwegian University of Science and Technology, Trondheim, Norway.ORCID 0000-0001-5794-828X
Wenche SjursenDepartment of Medical Genetics, St. Olavs Hospital, Trondheim, Norway.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Germline variants inactivating the mismatch repair (MMR) genes MLH1, MSH2, MSH6 and PMS2 cause Lynch syndrome that implies an increased cancer risk, where colon and endometrial cancer are the most frequent. Identification of these pathogenic variants is important to identify endometrial cancer patients with inherited increased risk of new cancers, in order to offer them lifesaving surveillance. However, several other genes are also part of the MMR pathway. It is therefore relevant to search for variants in additional genes that may be associated with cancer risk by including all known genes involved in the MMR pathway. Next-generation sequencing was used to screen 22 genes involved in the MMR pathway in constitutional DNA extracted from full blood from 199 unselected endometrial cancer patients. Bioinformatic pipelines were developed for identification and functional annotation of variants, using several different software tools and custom programs. This facilitated identification of 22 exonic, 4 UTR and 9 intronic variants that could be classified according to pathogenicity. This study has identified several germline variants in genes of the MMR pathway that potentially may be associated with an increased risk for cancer, in particular endometrial cancer, and therefore are relevant for further investigation. We have also developed bioinformatics strategies to analyse targeted sequencing data, including low quality data and genomic regions outside of the protein coding exons of the relevant genes.

Indexed as

DNA Mismatch RepairColorectal Neoplasms, Hereditary NonpolyposisDNA Copy Number VariationsDNA, NeoplasmEndometrial NeoplasmsExonsFemaleHigh-Throughput Nucleotide SequencingHumansIntronsMismatch Repair Endonuclease PMS2MutL Protein Homolog 1MutS Homolog 2 ProteinRisk FactorsUntranslated RegionsDNA, NeoplasmMismatch Repair Endonuclease PMS2MLH1 protein, humanMSH2 protein, humanMutL Protein Homolog 1MutS Homolog 2 ProteinPMS2 protein, humanUntranslated Regions

Identifiers

PMID32634176
PMCPMC7340288

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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.