| Literature DB >> 28818916 |
Mathias Uhlen1,2,3, Cheng Zhang4, Sunjae Lee4, Evelina Sjöstedt4,5, Linn Fagerberg4, Gholamreza Bidkhori4, Rui Benfeitas4, Muhammad Arif4, Zhengtao Liu4, Fredrik Edfors4, Kemal Sanli4, Kalle von Feilitzen4, Per Oksvold4, Emma Lundberg4, Sophia Hober3, Peter Nilsson4, Johanna Mattsson5, Jochen M Schwenk4, Hans Brunnström6, Bengt Glimelius5, Tobias Sjöblom5, Per-Henrik Edqvist5, Dijana Djureinovic5, Patrick Micke5, Cecilia Lindskog5, Adil Mardinoglu4,3,7, Fredrik Ponten5.
Abstract
Cancer is one of the leading causes of death, and there is great interest in understanding the underlying molecular mechanisms involved in the pathogenesis and progression of individual tumors. We used systems-level approaches to analyze the genome-wide transcriptome of the protein-coding genes of 17 major cancer types with respect to clinical outcome. A general pattern emerged: Shorter patient survival was associated with up-regulation of genes involved in cell growth and with down-regulation of genes involved in cellular differentiation. Using genome-scale metabolic models, we show that cancer patients have widespread metabolic heterogeneity, highlighting the need for precise and personalized medicine for cancer treatment. All data are presented in an interactive open-access database (www.proteinatlas.org/pathology) to allow genome-wide exploration of the impact of individual proteins on clinical outcomes.Entities:
Mesh:
Year: 2017 PMID: 28818916 DOI: 10.1126/science.aan2507
Source DB: PubMed Journal: Science ISSN: 0036-8075 Impact factor: 47.728