We therefore speculated that the Aurora-A/STK15/BTAK gene, implicated in the regulation of centrosome duplication, may be associated with breast tumorigenesis.
We hypothesize that amplification of the STK15 gene may be a non-random genetic alteration in human gliomas playing a role in the genetic pathways of tumorigenesis.
These results suggest that Aurora2/BTAK/STK15 is an effective candidate to indicate not only disease activity but also tumorigenesis of non-Hodgkin's lymphoma.
These results show that STK15 is overexpressed in pancreatic tumors and carcinoma cell lines and suggest that overexpression of STK15 may play a role in pancreatic carcinogenesis.
Our results demonstrate that STK15/BTAK mRNA is over-expressed in the majority of breast cancers and its over-expression is significantly associated with CIN, implicating STK15/BTAK in carcinogenesis through induction of CIN.