ArticleOncotarget2018
Integrative landscape of dysregulated signaling pathways of clinically distinct pancreatic cancer subtypes.
Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Metabolic pathway signatures define prognostic subtypes of lung adenocarcinoma.Discover oncology · 2026Article
- Article
- Mutational landscape of cancer-driver genes across human cancers.Scientific reports · 2023Article
- Prognostic biomarkers of pancreatic cancer identified based on a competing endogenous RNA regulatory network.Translational cancer research · 2022Article
- Integrated molecular characterisation of the MAPK pathways in human cancers reveals pharmacologically vulnerable mutations and gene dependencies.Communications biology · 2021Article
- Identification of Novel Metabolism-Associated Subtypes for Pancreatic Cancer to Establish an Eighteen-Gene Risk Prediction Model.Frontiers in cell and developmental biology · 2021Article
- Proteogenomic analysis of pancreatic cancer subtypes.PloS one · 2021Article
- Machine Learning and Network Analyses Reveal Disease Subtypes of Pancreatic Cancer and their Molecular Characteristics.Scientific reports · 2020Article
- Systems Biology Approach to Identify Novel Genomic Determinants for Pancreatic Cancer Pathogenesis.Scientific reports · 2019Article
- Metabolic gene alterations impact the clinical aggressiveness and drug responses of 32 human cancers.Communications biology · 2019Article
- Targeting AKT/PKB to improve treatment outcomes for solid tumors.Mutation researchReview
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Despite modern therapeutic advances, the survival prospects of pancreatic cancer patients have remained poor. Besides being highly metastatic, pancreatic cancer is challenging to treat because it is caused by a heterogeneous array of somatic mutations that impact a variety of signaling pathways and cellular regulatory systems. Here we use publicly available transcriptomic, copy number alteration and mutation profiling datasets from pancreatic cancer patients together with data on disease outcomes to show that the three major pancreatic cancer subtypes each display distinctive aberrations in cell signaling and metabolic pathways. Importantly, patients afflicted with these different pancreatic cancer subtypes also exhibit distinctive survival profiles. Within these patients, we find that dysregulation of the phosphoinositide 3-kinase and mitogen-activated protein kinase pathways, and p53 mediated disruptions of cell cycle processes are apparently drivers of disease. Further, we identify for the first time the molecular perturbations of signalling networks that are likely the primary causes of oncogenesis in each of the three pancreatic cancer subtypes.
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Registered trials
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