Evidence map›Paper›PMID 26446363›Full record

ArticleJournal of human genetics2016

Co-occurrence of nonsense mutations in MSH6 and MSH2 in Lynch syndrome families evidencing that not all truncating mutations are equal.

Carla Pinto, Manuela Pinheiro, Ana Peixoto, Catarina Santos, Isabel Veiga, Patrícia Rocha, Pedro Pinto, Paula Lopes, Manuela Baptista, Rui Henrique and 1 more

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Journal of human genetics, 2016. 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
0.7field-weighted citation impact, top 28% 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, 9 citations in OpenAlex.

  1. Characterisation of a Portuguese origin founder missense variant in MSH6.European journal of human genetics : EJHG · 2026
    Article
  2. Coexisting germline variants ofInternational cancer conference journal · 2025
    Article
  3. 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

11 authors at 3 institutions in 1 country.

Carla PintoDepartment of Genetics, Portuguese Oncology Institute, Porto, Portugal.
Manuela PinheiroDepartment of Genetics, Portuguese Oncology Institute, Porto, Portugal.
Ana PeixotoDepartment of Genetics, Portuguese Oncology Institute, Porto, Portugal.
Catarina SantosDepartment of Genetics, Portuguese Oncology Institute, Porto, Portugal.
Isabel VeigaDepartment of Genetics, Portuguese Oncology Institute, Porto, Portugal.
Patrícia RochaDepartment of Genetics, Portuguese Oncology Institute, Porto, Portugal.
Pedro PintoDepartment of Genetics, Portuguese Oncology Institute, Porto, Portugal.
Paula LopesDepartment of Pathology, Portuguese Oncology Institute, Porto, Portugal.
Manuela BaptistaDepartment of Surgery, São João Hospital, Porto, Portugal.
Rui HenriqueDepartment of Pathology, Portuguese Oncology Institute, Porto, Portugal.
Manuel R TeixeiraDepartment of Genetics, Portuguese Oncology Institute, Porto, Portugal.
Instituto Português de Oncologia Francisco Gentil · PTUniversidade do Porto · PTHospital de São João · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The majority of pathogenic mismatch repair (MMR) gene mutations detected in Lynch syndrome patients are truncating (frameshift or nonsense). However, the classification of terminal truncating mutations is sometimes difficult and predictive testing based on non-deleterious variants can have very serious consequences. Here, we report eight probands that have two germline nonsense mutations, namely MSH6 c.1030C>T, p.(Gln344Ter) and MSH2 c.2785C>T, p.(Arg929Ter), and one additional patient who presented only the MSH2 mutation previously reported as deleterious. The novel MSH6 truncating mutation was classified as deleterious, as it is predicted to encode a protein with loss of 1017 amino acid residues. The MSH2 mutation, which is expected to encode a protein lacking six amino acid residues, was considered a variant of unknown significance. Five tumors of the eight double-mutant individuals had normal MSH2 expression, whereas MSH6 immunoexpression was lost in all evaluable cases. None of the variants were detected in normal controls or associated with other MMR germline mutations in our series. This study emphasizes that not all truncating mutations are equal and that one must be cautious in the interpretation of the presumed deleterious effect of terminal frameshift or nonsense mutations.

Indexed as

Codon, NonsenseColorectal Neoplasms, Hereditary NonpolyposisDNA-Binding ProteinsFamilyHaplotypesHumansMutS Homolog 2 ProteinPhenotypeCodon, NonsenseDNA-Binding ProteinsG-T mismatch-binding proteinMSH2 protein, humanMutS Homolog 2 Protein

Identifiers

PMID26446363
OpenAlexW2203714801

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.