The mitotic spindle checkpoint appeared generally upregulated, with overexpression of gene products of aurora kinase A (AURKA), aurora kinase B (AURKB), BUB1B, NUF2, MAD2L1, CCNB1, TPX2, ZWINT, ZWINT and CDC20. Although these genes may be upregulated simply due to increased proliferative capacity of carcinomas, aurora kinase A has been previously investigated in UCa, where it is commonly found to be amplified[13] and may be a potential novel therapeutic target[14], which validates our results. The gene discussed is CCNB1; the disease is carcinoma.