Evidence map›Paper›PMID 31092812›Full record

ArticleOncogenesis2019

Transcriptional and functional consequences of TP53 splice mutations in colorectal cancer.

Jørgen Smeby, Anita Sveen, Ina A Eilertsen, Stine A Danielsen, Andreas M Hoff, Peter W Eide, Bjarne Johannessen, Merete Hektoen, Rolf I Skotheim, Marianne G Guren and 2 more

Open access · goldAbstract read
In one paragraph

Article in Oncogenesis, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
0.9field-weighted citation impact, top 31% 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

25 citing papers in PubMed, 33 citations in OpenAlex.

  1. International journal of molecular sciences · 2025
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  16. The Broad Spectrum ofHuman mutation · 2023
    Article
  17. Review
  18. Article
  19. Cancers · 2021
    Article
  20. 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

12 authors at 1 institution in 1 country.

Jørgen SmebyDepartment of Molecular Oncology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.
Anita SveenDepartment of Molecular Oncology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.
Ina A EilertsenDepartment of Molecular Oncology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.
Stine A DanielsenDepartment of Molecular Oncology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.
Andreas M HoffDepartment of Molecular Oncology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.
Peter W EideDepartment of Molecular Oncology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.
Bjarne JohannessenDepartment of Molecular Oncology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.
Merete HektoenDepartment of Molecular Oncology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.
Rolf I SkotheimDepartment of Molecular Oncology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.ORCID http://orcid.org/0000-0002-5609-4048
Marianne G GurenK.G. Jebsen Colorectal Cancer Research Centre, Division of Cancer Medicine, Oslo University Hospital, Oslo, Norway.
Arild NesbakkenK.G. Jebsen Colorectal Cancer Research Centre, Division of Cancer Medicine, Oslo University Hospital, Oslo, Norway.
Ragnhild A LotheDepartment of Molecular Oncology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway. ragnhild.a.lothe@rr-research.no.
Oslo University Hospital · NO

Funding

Kreftforeningen (Norwegian Cancer Society) 182759-2016Kreftforeningen (Norwegian Cancer Society) 6824048-2016Norges Forskningsråd (Research Council of Norway) 250993
6 · The paper itself

Abstract

TP53 mutations are common in colorectal cancer (CRC). Most TP53 sequencing studies have been restricted to coding regions, but recent studies have revealed that splice mutations can generate transcript variants with distinct tumorigenic and prognostic properties. Here, we performed unrestricted sequencing of all coding sequences and splice regions of TP53 in a single-hospital series of 401 primary CRCs. TP53 splice mutations were detected in 4% of the cases (N = 16), considerably more frequent than reported in major databases, and they were mutually exclusive to exon mutations. RNA sequencing revealed high-level expression of aberrant transcript variants in the majority of splice mutated tumors (75%). Most variants were predicted to produce truncated TP53 proteins, including one sample expressing the potentially oncogenic and druggable p53ψ isoform. Despite heterogeneous transcript structures, downstream transcriptional profiling revealed that TP53 splice mutations had similar effects on TP53 target gene expression and pathway activity as exonic mutations. Intriguingly, TP53 splice mutations were associated with worse 5-year relapse-free survival in stage II disease, compared to both TP53 wild-type and exon mutations (P = 0.007). These data highlight the importance of including splice regions when examining the biological and clinical consequences of TP53 mutations in CRC.

Identifiers

PMID31092812
PMCPMC6520361
OpenAlexW2945004393

What OpenQuestion holds

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LicenceCC BY
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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.