Identifying colon cancer risk modules with better classification performance based on human signaling network
Genomics, ISSN: 0888-7543, Vol: 104, Issue: 4, Page: 242-248
2014
- 8Citations
- 13Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations8
- Citation Indexes8
- CrossRef5
- Captures13
- Readers13
- 13
Article Description
Identifying differences between normal and tumor samples from a modular perspective may help to improve our understanding of the mechanisms responsible for colon cancer. Many cancer studies have shown that signaling transduction and biological pathways are disturbed in disease states, and expression profiles can distinguish variations in diseases. In this study, we integrated a weighted human signaling network and gene expression profiles to select risk modules associated with tumor conditions. Risk modules as classification features by our method had a better classification performance than other methods, and one risk module for colon cancer had a good classification performance for distinguishing between normal/tumor samples and between tumor stages. All genes in the module were annotated to the biological process of positive regulation of cell proliferation, and were highly associated with colon cancer. These results suggested that these genes might be the potential risk genes for colon cancer.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S088875431300205X; http://dx.doi.org/10.1016/j.ygeno.2013.11.002; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84908239492&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/24239682; https://linkinghub.elsevier.com/retrieve/pii/S088875431300205X; https://dx.doi.org/10.1016/j.ygeno.2013.11.002
Elsevier BV
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