Evidence map›Paper›PMID 30720096›Full record

ArticleMolecular medicine reports2019

Integrative analysis of cancer driver genes in prostate adenocarcinoma.

Xin Zhao, Yi Lei, Ge Li, Yong Cheng, Haifan Yang, Libo Xie, Hao Long, Rui Jiang

Open access · bronzeAbstract read
In one paragraph

Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

37 citing papers in PubMed, 54 citations in OpenAlex.

  1. Trial
  2. Clinical Context Shapes the Relationship between Genomic Alterations and Response to AR Inhibitors and Chemotherapy in Metastatic Prostate Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 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

8 authors at 1 institution in 1 country.

Xin ZhaoDepartment of Urology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, P.R. China.
Yi LeiDepartment of Endocrinology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, P.R. China.
Ge LiDepartment of Urology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, P.R. China.
Yong ChengDepartment of Urology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, P.R. China.
Haifan YangDepartment of Urology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, P.R. China.
Libo XieDepartment of Urology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, P.R. China.
Hao LongDepartment of Urology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, P.R. China.
Rui JiangDepartment of Urology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, P.R. China.
Affiliated Hospital of Southwest Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Large‑scale genomics studies have identified recurrently mutated genes in the ETS gene family, including fusions and copy number variations (CNVs), which are involved in the development of prostate adenocarcinoma (PRAD). However, the aetiology of PRAD remains to be fully elucidated. In the present study, 333 driver genes were identified using four computational tools: OncodriveFM, OncodriveCLUST, iCAGES and DrGaP. In addition, 32 driver pathways were identified using DrGaP. SPOP, TP53, SPTA1, AHNAK, HMCN1, ATM, FOXA1, CSMD3, LRP1B and FREM2 were the 10 most recurrently mutated genes in PRAD. ITGAL, TAGAP, SIGLEC10, RAC2 and ITGA4 were the five hub genes in the yellow module that were associated with the number of positive lymph nodes. Hierarchical clustering analysis of the 20 driver genes with the most frequent CNVs revealed three clusters of patients with PRAD. Cluster 3 tumours exhibited significantly higher numbers of positive lymph nodes, higher Gleason scores, more advanced cancer stages and poorer prognosis than cluster 1 and 2 tumours. A total of 48 genes were significantly associated with the number of positive lymph nodes, Gleason scores and pathologic stage in patients with PRAD. The identified set of cancer genes and pathways sheds light on the tumorigenesis of PRAD and creates avenues for the development of prognostic biomarkers and driver gene‑targeted therapies in PRAD.

Indexed as

Biomarkers, TumorComputational BiologyOncogenesAdenocarcinomaDNA Copy Number VariationsGene Expression ProfilingGene OntologyGene Regulatory NetworksHumansMaleMolecular Sequence AnnotationMutationProstatic NeoplasmsReproducibility of ResultsBiomarkers, Tumor

Identifiers

PMID30720096
PMCPMC6423600
OpenAlexW2912702154

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.