Activation of Raf-1 in Human Pancreatic Adenocarcinoma

摘要: Abstract Point mutations in the Ras oncogene cause to remain its active GTP-bound state sending signals downstream continuously. Since 75 90% of all human pancreatic ductal adenocarcinomas harbor activating at codon 12 K-ras it was our belief that Raf-1–;MEK–;MAPK will be activated majority cancers. The aim this study confirm activation Raf-1 mutant cancer. Additionally, we sought determine if differed and nonmutant Futhermore, were interested determining cancer led subsequent effectors such as MAP kinase. presence 14 adenocarcinoma cell lines determined by use allele-specific PCR restriction fragment length polymorphism analysis. expression quiescent cells immunoblotting using a rabbit anti-human polyclonal antibody enhanced chemiluminescence. kinase activity measuring incorporation phosphate into Myelin Basic Protein. Seven noted have while seven did not. There no difference 74 kDa-activated form vs lines. However, there significant increase compared with (P= 0.026). We conclude is expressed regardless status. signaling differs those without mutations.