Abstract
Aim: A gene set based systematic analysis strategy is used to investigate prostate tumors and its subclusters with focuses on similarities and differences of biological functions. Results: Dysregulation of methylation status, as well as RAS/RAF/ERK and PI3K-ATK signaling pathways, were found to be the most dramatic changes during prostate cancer tumorigenesis. Besides, neural and inflammation microenvironment is also significantly divergent between tumor and adjacent tissues. Insights of subclasses within prostate tumor cohorts revealed four different clusters with distinct gene expression patterns. We found that samples are mainly clustered by immune environments and proliferation traits. Conclusion: The findings of this article may help to advance the progress of identifying better diagnosis biomarkers and therapeutic targets.
Keywords:
immune environment; precision medicine; prostate cancer; signaling pathways; ssGSEA.
MeSH terms
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Agammaglobulinaemia Tyrosine Kinase / genetics
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Biomarkers, Tumor / genetics*
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Computational Biology / methods
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Extracellular Signal-Regulated MAP Kinases / genetics
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Gene Expression Profiling
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Humans
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Male
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Neoplasm Grading
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PTEN Phosphohydrolase / genetics
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Phosphatidylinositol 3-Kinases / genetics
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Prostatic Neoplasms / classification*
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Prostatic Neoplasms / enzymology
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Prostatic Neoplasms / genetics*
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Prostatic Neoplasms / pathology
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Proto-Oncogene Proteins B-raf / genetics
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Proto-Oncogene Proteins c-akt / genetics
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Proto-Oncogene Proteins c-raf / genetics
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Proto-Oncogene Proteins p21(ras) / genetics
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Sequence Analysis, RNA / methods
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Signal Transduction
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Survival Rate
Substances
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Biomarkers, Tumor
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KRAS protein, human
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Agammaglobulinaemia Tyrosine Kinase
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BTK protein, human
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Proto-Oncogene Proteins B-raf
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Proto-Oncogene Proteins c-akt
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Proto-Oncogene Proteins c-raf
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Raf1 protein, human
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Extracellular Signal-Regulated MAP Kinases
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PTEN Phosphohydrolase
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PTEN protein, human
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Proto-Oncogene Proteins p21(ras)