Evidence map›Paper›PMID 26628996›Full record

ArticleInternational journal of clinical and experimental medicine2015

High frequency of the SDK1:AMACR fusion transcript in Chinese prostate cancer.

Yanling Zhang, Xue-Ying Mao, Xiaoyan Liu, Rong-Rong Song, Daniel Berney, Yong-Jie Lu, Guoping Ren

Abstract read
In one paragraph

Article in International journal of clinical and experimental medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

9 citing papers in PubMed, 16 citations in OpenAlex.

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  6. Structure and Functions of Sidekicks.Frontiers in molecular neuroscience · 2020
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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

7 authors at 2 institutions in 2 countries.

Yanling ZhangDepartment of Pathology, The First Affiliated Hospital, Zhejiang University Medical College Hangzhou, China ; Department of Gynecology and Obstetrics, Sir Run Run Shaw Hospital, Zhejiang University Medical College Hangzhou, China.
Xue-Ying MaoCentre for Molecular Oncology, Barts Cancer Institute, Queen Mary University of London UK.
Xiaoyan LiuDepartment of Pathology, The First Affiliated Hospital, Zhejiang University Medical College Hangzhou, China.
Rong-Rong SongDepartment of Pathology, The First Affiliated Hospital, Zhejiang University Medical College Hangzhou, China.
Daniel BerneyCentre for Molecular Oncology, Barts Cancer Institute, Queen Mary University of London UK.
Yong-Jie LuCentre for Molecular Oncology, Barts Cancer Institute, Queen Mary University of London UK.
Guoping RenDepartment of Pathology, The First Affiliated Hospital, Zhejiang University Medical College Hangzhou, China.
First Affiliated Hospital Zhejiang University · CNQueen Mary University of London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chromosomal rearrangements and fusion genes play important roles in tumor development and progression. Four high-frequency prostate cancer (CaP) specific fusion genes, SDK1:AMACR, RAD50:PDLIM4, CTAGE5:KHDRBS3 and USP9Y:TTTY15 have been reported in Chinese CaP samples through a transcriptome sequencing study. We previously reported that USP9Y:TTTY15 is a transcription-mediated chimeric RNA, which is expressed in both tumor and non-malignant samples, and here we attempted to confirm the existence of the other three fusion genes SDK1:AMACR, RAD50:PDLIM and CTAGE5:KHDRBS3. We detected SDK1:AMACR fusion transcript in 23 of 100 Chinese CaP samples, but did not detect RAD50:PDLIM4 and CTAGE5:KHDRBS3 transcripts in any of those samples. SDK1:AMACR fusion transcript is Chinese CaP specific, which was neither detected in non-malignant prostate tissues adjacent to cancer from Chinese patient nor in CaP samples from UK patients. However, we did not detect genomic rearrangement of SDK1 gene by fluorescence in situ hybridization analysis, indicating that SDK1:AMACR is also a transcription-mediated chimeric RNA. Quantitative analysis demonstrated that high level AMACR expression was associated with SDK1:AMACR fusion status (P=0.004), suggesting that SDK1:AMACR fusion transcript may promote prostate carcinogenesis through increasing AMACR expression. However, the fusion status was not significantly correlated with any poor disease progression clinical features. The identification of the SDK1:AMACR fusion transcript in CaP cases from China but not from UK further supports our previous observation that different genetic alterations contribute to CaP in China and Western countries, although many genetic changes are also shared. Further studies are required to establish if CaPs with SDK1:AMACR represent a distinct subtype.

Indexed as

chimeric RNAChinese CaPchromosomal rearrangementsSDK1:AMACR

Identifiers

PMID26628996
PMCPMC4658885
OpenAlexW2410091873

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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.