ArticleMolecular medicine (Cambridge, Mass.)
Peeling off the hidden genetic heterogeneities of cancers based on disease-relevant functional modules.
Article in Molecular medicine (Cambridge, Mass.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 11 citations in OpenAlex.
- Pathway-based analysis of the hidden genetic heterogeneities in cancers.Genomics, proteomics & bioinformatics · 2014Article
- Unravelling the hidden heterogeneities of diffuse large B-cell lymphoma based on coupled two-way clustering.BMC genomics · 2007Article
- Meta-analysis of several gene lists for distinct types of cancer: a simple way to reveal common prognostic markers.BMC bioinformatics · 2007Article
- GO-2D: identifying 2-dimensional cellular-localized functional modules in Gene Ontology.BMC genomics · 2007Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
Discovering molecular heterogeneities in phenotypically defined disease is of critical importance both for understanding pathogenic mechanisms of complex diseases and for finding efficient treatments. Recently, it has been recognized that cellular phenotypes are determined by the concerted actions of many functionally related genes in modular fashions. The underlying modular mechanisms should help the understanding of hidden genetic heterogeneities of complex diseases. We defined a putative disease module to be the functional gene groups in terms of both biological process and cellular localization, which are significantly enriched with genes highly variably expressed across the disease samples. As a validation, we used two large cancer datasets to evaluate the ability of the modules for correctly partitioning samples. Then, we sought the subtypes of complex diffuse large B-cell lymphoma (DLBCL) using a public dataset. Finally, the clinical significance of the identified subtypes was verified by survival analysis. In two validation datasets, we achieved highly accurate partitions that best fit the clinical cancer phenotypes. Then, for the notoriously heterogeneous DLBCL, we demonstrated that two partitioned subtypes using an identified module ("cellular response to stress") had very different 5-year overall rates (65% vs. 14%) and were highly significantly (P < 0.007) correlated with the clinical survival rate. Finally, we built a multivariate Cox proportional-hazard prediction model that included 4 genes as risk predictors for survival over DLBCL. The proposed modular approach is a promising computational strategy for peeling off genetic heterogeneities and understanding the modular mechanisms of human diseases such as cancers.
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