Showing papers by "Salomon M. Stemmer published in 2004"
TL;DR: Oral CF101 has been shown to inhibit colon, prostate, melanoma, pancreatic and hepatocellular cancer growth in experimental animal models, via down-regulation of the Wnt and NF-κB signal transduction pathways.
Abstract: 13082 Background: The A3 adenosine Gi protein-coupled receptor is highly expressed in malignant compared to normal cells. Activating the A3 adenosine receptor (A3AR) with the highly selective non-c...
3 citations
TL;DR: This data indicates that targeting the A3 adenosine receptor (A3AR) with the highly selective agonist CF101 induces growth inhibition of colon carcinoma and other tumor cell types via down-regulation of PKB/Akt and NF-kB.
Abstract: 3173 Background: The A3 adenosine Gi protein-coupled receptor is highly expressed in tumor as compared to normal cells. Targeting the A3 adenosine receptor (A3AR) with the highly selective agonist CF101 induces growth inhibition of colon carcinoma and other tumor cell types via down-regulation of PKB/Akt and NF-kB. High expression level of these two signaling proteins is associated with the development of chemo-resistance in various tumor cell types, thus it prompted us to explore whether CF101 would enhance the anti-tumor effect of chemotherapy. Methods: HCT-116 human colon and Bx-PC3 human pancreatic carcinoma cell lines were used. Cells were cultured for 48h in the presence of 5-FU (0.625 μM), oxaliplatin (0.5 μM) or gemcitabine (0.02 mM) and CF101 (10nM) was introduced for an additional 24h. Proliferation assay (MTT) and protein expression profile were conducted at 72h. In vivo studies included nude mice that were inoculated with the tumor cells. Treatment with chemotherapy alone or in combination wit...
1 citations