Bladder cancer (Homo sapiens)

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The urothelium covers the luminal surface of almost the entire urinary tract, extending from the renal pelvis, through the ureter and bladder, to the proximal urethra. The majority of urothelial carcinomas are bladder carcinomas, and urothelial carcinomas of the renal pelvis and ureter account for only approximately 7% of the total. Urothelial tumors arise and evolve through divergent phenotypic pathways. Some tumors progress from urothelial hyperplasia to low-grade non-invasive superficial papillary tumors. More aggressive variants arise either from flat, high-grade carcinoma in situ (CIS) and progress to invasive tumors, or they arise de novo as invasive tumors. Low-grade papillary tumors frequently show a constitutive activation of the receptor tyrosine kinase-Ras pathway, exhibiting activating mutations in the HRAS and fibroblast growth factor receptor 3 (FGFR3) genes. In contrast, CIS and invasive tumors frequently show alterations in the TP53 and RB genes and pathways. Invasion and metastases are promoted by several factors that alter the tumor microenvironment, including the aberrant expression of E-cadherins (E-cad), matrix metalloproteinases (MMPs), angiogenic factors such as vascular endothelial growth factor (VEGF). Phosphorylation sites were added based on information from PhosphoSitePlus (R), https://www.phosphosite.org. Proteins on this pathway have targeted assays available via the [CPTAC Assay Portal](https://assays.cancer.gov/available_assays?wp_id=WP2828).