作者: Irina V. Lebedeva , Devanand Sarkar , Zao-Zhong Su , Rahul V. Gopalkrishnan , Mohammad Athar
DOI: 10.1158/0008-5472.CAN-05-3510
关键词:
摘要: Pancreatic cancer is genetically complex, and without effective therapy. Mutations in the Kirsten-ras (K-ras) oncogene occur early frequently (∼90%) during pancreatic development progression. In this context, K-ras represents a potential molecular target for therapy of highly aggressive cancer. We now show that bipartite adenovirus expressing novel cancer-specific apoptosis-inducing cytokine gene, mda-7/interleukin-24 (IL-24), AS but not either gene alone, promotes growth suppression, induction apoptosis, suppression tumor mediated by mutant cells. Equally, combination an mda-7/IL-24 pharmacologic genetic agents simultaneously blocking or downstream extracellular regulated kinase 1/2 signaling also similar inhibitory effects on survival carcinoma This activity correlates with reversal translational block mRNA cells limits message association polysomes, thereby impeding translation into protein. Our study provides support “dual targeted therapy” involving inhibition selective expression effectively treating invariably fatal (Cancer Res 2006; 66(4): 2403-13)