“…Increased Src activity has been found, for example, in human mammary carcinomas, colon cancer and pancreatic cancer (Jacobs and Rubsamen, 1983;Rosen et al, 1986;Ottenhoff-Kalff et al, 1992;Talamonti et al, 1993;Termuhlen et al, 1993;Maa et al, 1995;Verbeek et al, 1996;Mao et al, 1997;Egan et al, 1999;Hakak and Martin, 1999;Harris et al, 1999;Shimakage et al, 2000). The increased Src kinase activity in these tumors has been proposed to be due to tyrosine phosphatase-mediated dephosphorylation of the carboxy-terminal negative regulatory element, an increase in Src protein levels and/or altered protein stability, an increase in upstream receptor tyrosine kinase activity, or loss of key regulatory proteins (Maa et al, 1995;Mao et al, 1997;Egan et al, 1999;Hakak and Martin, 1999;Harris et al, 1999;Shimakage et al, 2000;Masaki et al, 2003). A few human colon cancers exhibit Src activating mutations (Irby et al, 1999).…”