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FGFR follows a classic receptor tyrosine kinase signalling pathway and its deregulation at various points of its cascade could result in malignancy1. Chromosomal translocations can lead to an expression of fusion proteins with potent oncogenic function as seen in many hematological malignancies. FGFR3 translocation brings it under the influence of a strong IGH enhancer region results in overexpression often seen in multiple myeloma and has been associated with poor prognosis2. FGFR3 is reportedly one of the most commonly mutated genes in human urothelial cell carcinoma and has also been identified in a wide range of other cancers including cervical, prostate, lung and ovarian tumors3,4,5.
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