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PLoS One. 2015 Jan 8;10(1):e0116404. doi: 10.1371/journal.pone.0116404. eCollection 2015.

Protein interactome of muscle invasive bladder cancer.

Author information

Charité-Universitätsmedizin Berlin, Med. Klinik IV, Berlin, Germany; Mosaiques diagnostics GmbH, Hannover, Germany.
emergentec biodevelopment GmbH, Vienna, Austria.
BHF Glasgow Cardiovascular Research Centre, University of Glasgow, Glasgow, United Kingdom.
Department of Urology and Urological Oncology, Hannover Medical School, Hannover, Germany.
Biomedical Research Foundation Academy of Athens, Biotechnology Division, Athens, Greece.
Institut National de la Santé et de la Recherche Médicale (INSERM), U1048, Institute of Cardiovascular and Metabolic Diseases, Toulouse, France; Université de Toulouse III Paul Sabatier, Toulouse, France.
Mosaiques diagnostics GmbH, Hannover, Germany; BHF Glasgow Cardiovascular Research Centre, University of Glasgow, Glasgow, United Kingdom.
Institute for Molecular Cardiovascular Research (IMCAR), Aachen, Germany.


Muscle invasive bladder carcinoma is a complex, multifactorial disease caused by disruptions and alterations of several molecular pathways that result in heterogeneous phenotypes and variable disease outcome. Combining this disparate knowledge may offer insights for deciphering relevant molecular processes regarding targeted therapeutic approaches guided by molecular signatures allowing improved phenotype profiling. The aim of the study is to characterize muscle invasive bladder carcinoma on a molecular level by incorporating scientific literature screening and signatures from omics profiling. Public domain omics signatures together with molecular features associated with muscle invasive bladder cancer were derived from literature mining to provide 286 unique protein-coding genes. These were integrated in a protein-interaction network to obtain a molecular functional map of the phenotype. This feature map educated on three novel disease-associated pathways with plausible involvement in bladder cancer, namely Regulation of actin cytoskeleton, Neurotrophin signalling pathway and Endocytosis. Systematic integration approaches allow to study the molecular context of individual features reported as associated with a clinical phenotype and could potentially help to improve the molecular mechanistic description of the disorder.

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