Official websites use. Share sensitive information only on official, secure websites. Email: maxim. Pichler uk-augsburg. Bladder cancer BLCA accounts for the 10th most common cancer globally, with more than , newly diagnosed cases and over , annual deaths worldwide [ 1 , 2 ].
Male gender increases the risk for BLCA , making it the 6 th most common cancer among all cancer types worldwide [ 1 , 2 ]. Nevertheless, the biological females are diagnosed at more advanced and deadlier stages of BLCA [ 2 ]. With the emergence of knowledge about genetic alterations in BLCA, the association of these alterations with different subtypes has been unveiled [ 1 ]. Figure generated in Biorender. In Cappellen et al. Later, Tomlinson et al. Apart from mutation or overexpression, FGFR3 can also be activated in BLCA through chromosomal rearrangements that generate constitutively activated fusion genes [ 10 ].
In , during a Cancer Genome Atlas project study, a comprehensive genetic analysis of urothelial carcinomas discovered FGFR3 alterations as one of the genetic hallmarks of urothelial bladder carcinoma [ 11 ].
Komura et al. MIBC in which the subtyping was not originally described [ 17 ]. For example, the class I, differentiated vs. Moreover, Komura et al. Interestingly, these hotspots do not involve the tyrosine kinase domain but induce a conformational change that leads to constitutive protein activity and triggers its downstream signaling output [ 7 , 19 , 20 ].
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These findings are, in principle, consistent with previous reports [ 23 ]. Querying BLCA samples in 19 studies. Based on the query, the figure was generated in cBioPortal and modified for clarity. Unlike the Western population, FGFR3 mutations within the kinase domain, specifically KE and TP, were more prevalent yet showed no conclusive changes in clinical outcomes [ 17 ].
