Evidence map›Paper›PMID 29955133›Full record

ArticleBritish journal of cancer2018

Integrative analysis of oncogenic fusion genes and their functional impact in colorectal cancer.

Yuri Choi, Chae Hwa Kwon, Seon Jin Lee, Joonghoon Park, Jong-Yeon Shin, Do Youn Park

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2018. 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
3.8field-weighted citation impact, top 6% 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, 40 citations in OpenAlex.

  1. Whole transcriptome analysis identifiesCancer pathogenesis and therapy · 2025
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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 2 institutions in 1 country.

Yuri ChoiDepartment of Pathology, Pusan National University School of Medicine, and Biomedical Research Institute, Pusan National University Hospital, Gudeok-ro 179, Seo-Gu, Busan, 49241, Republic of Korea.
Chae Hwa KwonDepartment of Pathology, Pusan National University School of Medicine, and Biomedical Research Institute, Pusan National University Hospital, Gudeok-ro 179, Seo-Gu, Busan, 49241, Republic of Korea.
Seon Jin LeeDepartment of Pathology, Pusan National University School of Medicine, and Biomedical Research Institute, Pusan National University Hospital, Gudeok-ro 179, Seo-Gu, Busan, 49241, Republic of Korea.
Joonghoon ParkGraduate School of International Agricultural Technology and Institute of Green-Bio Science and Technology, Seoul National University, Pyeongchang-gun, Gangwon-do, 232-916, Republic of Korea.
Jong-Yeon ShinGenomic Medicine Institute (GMI), Medical Research Center, Seoul National University, Seoul, 159-781, Republic of Korea.
Do Youn ParkDepartment of Pathology, Pusan National University School of Medicine, and Biomedical Research Institute, Pusan National University Hospital, Gudeok-ro 179, Seo-Gu, Busan, 49241, Republic of Korea. pdy220@pusan.ac.kr.
Pusan National University Hospital · KRSeoul National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundFusion genes are good candidates of molecular targets for cancer therapy. However, there is insufficient research on the clinical implications and functional characteristics of fusion genes in colorectal cancer (CRC).

methodsIn this study, we analysed RNA sequencing data of CRC patients (147 tumour and 47 matched normal tissues) to identify oncogenic fusion genes and evaluated their role in CRC.

resultsWe validated 24 fusion genes, including novel fusions, by three algorithms and Sanger sequencing. Fusions from most patients were mutually exclusive CRC oncogenes and included tumour suppressor gene mutations. Eleven fusion genes from 13 patients (8.8%) were determined as oncogenic fusion genes by analysing their gene expression and function. To investigate their oncogenic impact, we performed proliferation and migration assays of CRC cell lines expressing fusion genes of GTF3A-CDK8, NAGLU- IKZF3, RNF121- FOLR2, and STRN-ALK. Overexpression of these fusion genes increased cell proliferation except GTF3A-CDK8. In addition, overexpression of NAGLU-IKZF3 enhanced migration of CRC cells. We demonstrated that NAGLU-IKZF3, RNF121-FOLR2, and STRN-ALK had tumourigenic effects in CRC.

conclusionIn summary, we identified and characterised oncogenic fusion genes and their function in CRC, and implicated NAGLU-IKZF3 and RNF121-FOLR2 as novel molecular targets for personalised medicine development.

Indexed as

AcetylglucosaminidaseAnaplastic Lymphoma KinaseCalmodulin-Binding ProteinsCell MovementCell ProliferationColorectal NeoplasmsCyclin-Dependent Kinase 8Disease-Free SurvivalFemaleFolate Receptor 2Gene Expression Regulation, NeoplasticHigh-Throughput Nucleotide SequencingHumansIkaros Transcription FactorKaplan-Meier EstimateMaleAcetylglucosaminidaseALK protein, humanalpha-N-acetyl-D-glucosaminidaseAnaplastic Lymphoma KinaseCalmodulin-Binding ProteinsCDK8 protein, humanCyclin-Dependent Kinase 8Folate Receptor 2FOLR2 protein, humanIkaros Transcription FactorIKZF3 protein, humanMembrane ProteinsNerve Tissue ProteinsOncogene Proteins, Fusionring finger protein 121, humanSTRN protein, humanTranscription Factor TFIIIA

Identifiers

PMID29955133
PMCPMC6048111
OpenAlexW2809946219

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.