Evidence map›Paper›PMID 34234399›Full record

ArticleCancer informatics2021

Re-Evaluate Fusion Genes in Prostate Cancer.

Ting Wei, Ji Lu, Tao Ma, Haojie Huang, Jean-Pierre Kocher, Liguo Wang

Open access · goldAbstract read
In one paragraph

Article in Cancer informatics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 17% 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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Contemporary review of prognostic markers of prostate cancer from a pathologist perspective.Biomedical papers of the Medical Faculty of the University Palacky, Olomouc, Czechoslovakia · 2025
    Review
  4. Article
  5. Article
  6. Article
  7. 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

6 authors at 2 institutions in 2 countries.

Ting WeiDivision of Computational Biology, College of Medicine and Science, Mayo Clinic, Rochester, MN, USA.
Ji LuDepartment of Urology, The First Hospital of Jilin University, Changchun, People's Republic of China.
Tao MaDivision of Computational Biology, College of Medicine and Science, Mayo Clinic, Rochester, MN, USA.
Haojie HuangDepartment of Biochemistry and Molecular Biology, College of Medicine and Science, Mayo Clinic, Rochester, MN, USA.
Jean-Pierre KocherDivision of Computational Biology, College of Medicine and Science, Mayo Clinic, Rochester, MN, USA.
Liguo WangDivision of Computational Biology, College of Medicine and Science, Mayo Clinic, Rochester, MN, USA.ORCID https://orcid.org/0000-0003-2072-4826
Mayo Clinic · USJilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThousands of gene fusions have been reported in prostate cancer, but their authenticity, incidence, and tumor specificity have not been thoroughly evaluated, nor have their genomic characteristics been carefully explored.

methodsWe developed FusionVet to dedicatedly validate known fusion genes using RNA-seq alignments. Using FusionVet, we re-assessed 2727 gene fusions reported from 36 studies using the RNA-seq data generated by The Cancer Genome Atlas (TCGA). We also explored their genomic characteristics and interrogated the transcriptomic and DNA methylomic consequences of the E26 transformation-specific (ETS) fusions.

resultsWe found that nearly two-thirds of reported fusions are intra-chromosomal, and 80% of them were formed between 2 protein-coding genes. Although most (76%) genes were fused to only 1 partner, we observed many fusion hub genes that have multiple fusion partners, including ETS family genes, androgen receptor signaling pathway genes, tumor suppressor genes, and proto-oncogenes. More than 90% of the reported fusions cannot be validated by TCGA RNA-seq data. For those fusions that can be validated, 5% were detected from tumor and normal samples with similar frequencies, and only 4% (120 fusions) were tumor-specific. The occurrences of

conclusionsMost of the reported fusion genes cannot be validated by TCGA samples. The ETS family and androgen response genes were significantly enriched in prostate cancer-specific fusion genes. Transcription activity was significantly repressed, and the DNA methylation was significantly increased in samples carrying

Indexed as

fusion genegene fusionmeta-analysisProstate cancerTMPRSS2-ERG

Identifiers

PMID34234399
PMCPMC8226361
OpenAlexW3177170937

What OpenQuestion holds

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LicenceCC BY-NC
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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.