Monthly Archives: March 2012

IBVinfected ces. ttenution of the IBViuced II upregu tion t the mRN eve in pknockdown ces. H ces were trnsfected with either p MPK siRN or negtive contro siRN twice inh Masitinib interwere infected with IBVh fter the seco trnsfection. … Continue reading →

Esser S, Wolburg K, Wolburg H, Breier G, Kurzchalia T, Risau W. Vascular endothelial growth factor induces endothelial fenestrations in vitro. J Cell Biol 140: 94759, 1998. 11. Feng D, Nagy JA, Pyne K, Hammel I, Dvorak HF, Dvorak AM. … Continue reading →

that are sensitive to IGFR inhibitors rapidly upregulate signaling through the EGFR system as a means to resistance 38 , and the converse is also true 37 . For this reason, combining agents targeting both of these pathways would seem … Continue reading →

Jemmerson, X. Wang, Induction of apoptotic program in cell-free extracts: require- ment for dATP and cytochrome c , Cell 86 (1996)47?57. [29] S. Kamada, U. Kikkawa, Y. Tsujimoto, T. Hunter, Nuclear translocation of caspase-3 is dependent on its proteolytic activation … Continue reading →

lycol 1000 succinate (TPGS) in the micelle composition, the burst release of 17-AAG from the micelles was significantly reduced. These PEG-DSPE/TPGS mixed micelles have the potential to be further functionalized to achieve active targeting of 17-AAG to tumor cells. 2. … Continue reading →

lerability of EGFR antibodies and EGFR TKIs may still differ in sensitive patients, and/or in earlier lines of treatment. Similarly, the activity of VEGF/VEGFR-targeting agents on vasculature (and on tumour cells bearing VEGFR), may be affected by prior treatment with … Continue reading →

The presence of activating mutations in the tyrosine kinase domain of the human epidermal growth factor receptor (EGFR/HER/erbB) in nonsmall cell lung cancer (NSCLC) correlates with a clinical phenotype of adenocarcinoma in never or light smokers, and renders the tumor … Continue reading →