Evidence map›Paper›PMID 25230976›Full record

ArticleGenes, chromosomes & cancer2014

Comprehensive exploration of novel chimeric transcripts in clear cell renal cell carcinomas using whole transcriptome analysis.

Masahiro Gotoh, Hitoshi Ichikawa, Eri Arai, Suenori Chiku, Hiromi Sakamoto, Hiroyuki Fujimoto, Masaki Hiramoto, Takao Nammo, Kazuki Yasuda, Teruhiko Yoshida and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Genes, chromosomes & cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

16 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Tex264 Binding to SNX27 Regulates ItgBioMed research international · 2022
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  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Shift work, DNA methylation and epigenetic age.International journal of epidemiology · 2019
    Article
  12. Article
  13. Review
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  15. Transposon mutagenesis identifies chromatin modifiers cooperating withProceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  16. 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 4 institutions in 2 countries.

Masahiro GotohDivision of Molecular Pathology, National Cancer Center Research Institute, Tokyo, Japan.
Hitoshi Ichikawa
Eri Arai
Suenori Chiku
Hiromi Sakamoto
Hiroyuki Fujimoto
Masaki Hiramoto
Takao Nammo
Kazuki Yasuda
Teruhiko Yoshida
Yae Kanai
National Cancer Centre Japan · JPNational Center for Global Health and Medicine · JPMizuho (Japan) · JPTokyo National Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aim of this study was to clarify the participation of expression of chimeric transcripts in renal carcinogenesis. Whole transcriptome analysis (RNA sequencing) and exploration of candidate chimeric transcripts using the deFuse program were performed on 68 specimens of cancerous tissue (T) and 11 specimens of non-cancerous renal cortex tissue (N) obtained from 68 patients with clear cell renal cell carcinomas (RCCs) in an initial cohort. As positive controls, two RCCs associated with Xp11.2 translocation were analyzed. After verification by reverse transcription (RT)-PCR and Sanger sequencing, 26 novel chimeric transcripts were identified in 17 (25%) of the 68 clear cell RCCs. Genomic breakpoints were determined in five of the chimeric transcripts. Quantitative RT-PCR analysis revealed that the mRNA expression levels for the MMACHC, PTER, EPC2, ATXN7, FHIT, KIFAP3, CPEB1, MINPP1, TEX264, FAM107A, UPF3A, CDC16, MCCC1, CPSF3, and ASAP2 genes, being partner genes involved in the chimeric transcripts in the initial cohort, were significantly reduced in 26 T samples relative to the corresponding 26 N samples in the second cohort. Moreover, the mRNA expression levels for the above partner genes in T samples were significantly correlated with tumor aggressiveness and poorer patient outcome, indicating that reduced expression of these genes may participate in malignant progression of RCCs. As is the case when their levels of expression are reduced, these partner genes also may not fully function when involved in chimeric transcripts. These data suggest that generation of chimeric transcripts may participate in renal carcinogenesis by inducing dysfunction of tumor-related genes.

Indexed as

Gene Expression ProfilingAdultAgedAged, 80 and overCarcinoma, Renal CellCohort StudiesFemaleGene FusionHumansKidney NeoplasmsMaleMiddle AgedOncogene Proteins, FusionRNA, MessengerOncogene Proteins, FusionRNA, Messenger

Identifiers

PMID25230976
PMCPMC4304365
OpenAlexW1572901993

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

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.