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 2013 Genentech USA, Inc. All rights reserved. Disclosure/Disclaimer The Molecular Basis of Gliomas slide presentation is not an independent educational.

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Nat. Rev. Urol. doi:10.1038/nrurol.2015.231 Figure 2 Cellular pathways affected in bladder cancer and targeting therapies Figure 2 | Cellular pathways affected in bladder cancer and targeting therapies. Multiple small-molecule inhibitors and antibodies against different receptors and pathways have been tested in preclinical and clinical studies. Agents targeting protein translation and cell metabolism affect the molecules at the end of signalling pathways and are not shown. Pathways and targets are located at various sites in and around the tumour cell (Figure 1). The percentage of bladder cancer samples harbouring mutations are shown for targets that have been screened by the TCGA.21 *Percentage depends on the RTK analysed. ‡Percentage harbouring a copy number variation. Abbreviations: ARF, tumour suppressor ARF; Akt, serine/threonine-protein kinases; B-raf, serine/threonine-protein kinase B-raf; BAX, apoptosis regulator BAX; E2F, transcription factors of the E2F family; MAPK, mitogen-activated protein kinases; MDM2, E3 ubiquitin-protein ligase Mdm2; MEK, dual specificity MAPK kinases 1 and 2; NF-κB, nuclear factor κB; p21, cyclin-dependent kinase inhibitor 1; p53, cellular tumour antigen p53; RPS6, 40S ribosomal protein S6; RTK, receptor tyrosine kinase; STAT, signal transducer and activator of transcription 1 and 3; TCGA, The Cancer Genome Atlas Research Network; VEGF, vascular endothelial growth factor. van Kessel, K. E. M. et al. (2015) Targeted therapies in bladder cancer: an overview of in vivo research Nat. Rev. Urol. doi:10.1038/nrurol.2015.231