Evidence map›Paper›PMID 24608966›Full record

ArticlePloS one2014

High frequency of fusion transcripts involving TCF7L2 in colorectal cancer: novel fusion partner and splice variants.

Torfinn Nome, Andreas M Hoff, Anne Cathrine Bakken, Torleiv O Rognum, Arild Nesbakken, Rolf I Skotheim

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

15 citing papers in PubMed, 28 citations in OpenAlex.

  1. TargetedCell reports methods · 2023
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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

6 authors at 3 institutions in 1 country.

Torfinn NomeDepartment of Cancer Prevention, Institute for Cancer Research, Norwegian Radium Hospital - Oslo University Hospital, Oslo, Norway; Centre for Cancer Biomedicine, Faculty of Medicine, University of Oslo, Oslo, Norway.
Andreas M HoffDepartment of Cancer Prevention, Institute for Cancer Research, Norwegian Radium Hospital - Oslo University Hospital, Oslo, Norway; Centre for Cancer Biomedicine, Faculty of Medicine, University of Oslo, Oslo, Norway.
Anne Cathrine BakkenDepartment of Cancer Prevention, Institute for Cancer Research, Norwegian Radium Hospital - Oslo University Hospital, Oslo, Norway; Centre for Cancer Biomedicine, Faculty of Medicine, University of Oslo, Oslo, Norway.
Torleiv O RognumUniversity of Oslo, Oslo, Norway; Department of forensic pathology and clinical forensic medicine, Division for forensic medicine, The Norwegian Institute of Public Health, Oslo, Norway.
Arild NesbakkenCentre for Cancer Biomedicine, Faculty of Medicine, University of Oslo, Oslo, Norway; Department of Gastrointestinal Surgery, Oslo University Hospital-Aker, Oslo, Norway.
Rolf I SkotheimDepartment of Cancer Prevention, Institute for Cancer Research, Norwegian Radium Hospital - Oslo University Hospital, Oslo, Norway; Centre for Cancer Biomedicine, Faculty of Medicine, University of Oslo, Oslo, Norway.
University of Oslo · NOOslo University Hospital · NONorwegian Institute of Public Health · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

VTI1A-TCF7L2 was reported as a recurrent fusion gene in colorectal cancer (CRC), found to be expressed in three out of 97 primary cancers, and one cell line, NCI-H508, where a genomic deletion joins the two genes [1]. To investigate this fusion further, we analyzed high-throughput DNA and RNA sequencing data from seven CRC cell lines, and identified the gene RP11-57H14.3 (ENSG00000225292) as a novel fusion partner for TCF7L2. The fusion was discovered from both genome and transcriptome data in the HCT116 cell line. By triplicate nested RT-PCR, we tested both the novel fusion transcript and VTI1A-TCF7L2 for expression in a series of 106 CRC tissues, 21 CRC cell lines, 14 normal colonic mucosa, and 20 normal tissues from miscellaneous anatomical sites. Altogether, 42% and 45% of the CRC samples expressed VTI1A-TCF7L2 and TCF7L2-RP11-57H14.3 fusion transcripts, respectively. The fusion transcripts were both seen in 29% of the normal colonic mucosa samples, and in 25% and 75% of the tested normal tissues from other organs, revealing that the TCF7L2 fusion transcripts are neither specific to cancer nor to the colon and rectum. Seven different splice variants were detected for the VTI1A-TCF7L2 fusion, of which three are novel. Four different splice variants were detected for the TCF7L2-RP11-57H14.3 fusion. In conclusion, we have identified novel variants of VTI1A-TCF7L2 fusion transcripts, including a novel fusion partner gene, RP11-57H14.3, and demonstrated detectable levels in a large fraction of CRC samples, as well as in normal colonic mucosa and other tissue types. We suggest that the fusion transcripts observed in a high frequency of samples are transcription induced chimeras that are expressed at low levels in most samples. The similar fusion transcripts induced by genomic rearrangements observed in individual cancer cell lines may yet have oncogenic potential as suggested in the original study by Bass et al.

Indexed as

Base SequenceColorectal NeoplasmsExonsGene RearrangementGenetic LociGenome, HumanHCT116 CellsHumansMolecular Sequence DataOncogene Proteins, FusionReproducibility of ResultsRNA, MessengerRNA Splice SitesRNA SplicingTranscription Factor 7-Like 2 ProteinOncogene Proteins, FusionRNA, MessengerRNA Splice SitesTranscription Factor 7-Like 2 Protein

Identifiers

PMID24608966
PMCPMC3946716
OpenAlexW1980719375

What OpenQuestion holds

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LicenceCC BY
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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.