Evidence map›Paper›PMID 26429724›Full record

ArticleClinical & experimental metastasis2015

GNL3 and SKA3 are novel prostate cancer metastasis susceptibility genes.

Minnkyong Lee, Kendra A Williams, Ying Hu, Jonathan Andreas, Shashank J Patel, Suiyuan Zhang, Nigel P S Crawford

Abstract read
PubMed Publisher
In one paragraph

Article in Clinical & experimental metastasis, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing 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

34 citing papers in PubMed, 50 citations in OpenAlex.

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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 1 country.

Minnkyong LeeGenetics and Molecular Biology Branch, National Human Genome Research Institute, NIH, Bethesda, MD, 20892, USA.
Kendra A WilliamsGenetics and Molecular Biology Branch, National Human Genome Research Institute, NIH, Bethesda, MD, 20892, USA.
Ying HuCenter for Biomedical Informatics and Information Technology, National Cancer Institute, NIH, Rockville, MD, 20850, USA.
Jonathan AndreasGenetics and Molecular Biology Branch, National Human Genome Research Institute, NIH, Bethesda, MD, 20892, USA.
Shashank J PatelGenetics and Molecular Biology Branch, National Human Genome Research Institute, NIH, Bethesda, MD, 20892, USA.
Suiyuan ZhangComputational and Statistical Genomics Branch, National Human Genome Research Institute, NIH, Bethesda, MD, 20892, USA.
Nigel P S CrawfordGenetics and Molecular Biology Branch, National Human Genome Research Institute, NIH, Bethesda, MD, 20892, USA. crawforn@mail.nih.gov.
National Human Genome Research Institute · USNational Cancer Institute · US

Funding

Germline modifiers of tumor progression and metastasis in prostate cancerZIAHG200366 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI CRAWFORD, NIGEL · 2010 to 2016
$5.0M
Intramural NIH HHS
6 · The paper itself

Abstract

Prostate cancer (PC) is very common in developed countries. However, the molecular determinants of PC metastasis are unclear. Previously, we reported that germline variation influences metastasis in the C57BL/6-Tg(TRAMP)8247Ng/J (TRAMP) mouse model of PC. These mice develop prostate tumors similar to a subset of poor outcome, treatment-associated human PC tumors. Here, we used TRAMP mice to nominate candidate genes and validate their role in aggressive human PC in PC datasets and cell lines. Candidate metastasis susceptibility genes were identified through quantitative trait locus (QTL) mapping in 201 (TRAMP × PWK/PhJ) F2 males. Two metastasis-associated QTLs were identified; one on chromosome 12 (LOD = 5.86), and one on chromosome 14 (LOD = 4.41). Correlation analysis using microarray data from (TRAMP × PWK/PhJ) F2 prostate tumors identified 35 metastasis-associated transcripts within the two loci. The role of these genes in susceptibility to aggressive human PC was determined through in silico analysis using multiple datasets. First, analysis of candidate gene expression in two human PC datasets demonstrated that five candidate genes were associated with an increased risk of aggressive disease and lower disease-free survival. Second, four of these genes (GNL3, MAT1A, SKA3, and ZMYM5) harbored SNPs associated with aggressive tumorigenesis in the PLCO/CGEMS GWAS of 1172 PC patients. Finally, over-expression of GNL3 and SKA3 in the PC-3 human PC cell line decreased in vitro cell migration and invasion. This novel approach demonstrates how mouse models can be used to identify metastasis susceptibility genes, and gives new insight into the molecular mechanisms of fatal PC.

Indexed as

Genetic Predisposition to DiseaseAnimalsCell Cycle ProteinsCell Line, TumorCell MovementDisease Models, AnimalGenome-Wide Association StudyGTP-Binding ProteinsHumansMaleMiceMice, Inbred C57BLMicrotubule-Associated ProteinsNeoplasm InvasivenessNeoplasm MetastasisNuclear ProteinsCell Cycle ProteinsGNL3 protein, humanGTP-Binding ProteinsMicrotubule-Associated ProteinsNuclear ProteinsSka3 protein, humanGenetic susceptibilityMetastasisMouse modelsProstate cancerTRAMP

Identifiers

PMID26429724
OpenAlexW1883415090

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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.