fenretinide and Bronchial-Diseases

fenretinide has been researched along with Bronchial-Diseases* in 1 studies

Other Studies

1 other study(ies) available for fenretinide and Bronchial-Diseases

Article	Year
Involvement of mitochondrial and Akt signaling pathways in augmented apoptosis induced by a combination of low doses of celecoxib and N-(4-hydroxyphenyl) retinamide in premalignant human bronchial epithelial cells. Cancer research, 2006, Oct-01, Volume: 66, Issue:19 Celecoxib is being evaluated as a chemopreventive agent. However, its mechanism of action is not clear because high doses were used for in vitro studies to obtain antitumor effects. We found that celecoxib inhibited the growth of premalignant and malignant human bronchial epithelial cells with IC(50) values between 8.9 and 32.7 micromol/L, irrespective of cyclooxygenase-2 (COX-2) expression. Normal human bronchial epithelial cells were less sensitive to celecoxib. Because these concentrations were higher than those attainable in vivo ( Topics: Anticarcinogenic Agents; Apoptosis; Bronchi; Bronchial Diseases; Celecoxib; Cell Line, Tumor; Cells, Cultured; Cyclooxygenase 2 Inhibitors; Drug Screening Assays, Antitumor; Drug Synergism; Epithelial Cells; Fenretinide; Humans; Lung Neoplasms; Mitochondria; Phosphorylation; Precancerous Conditions; Protein Processing, Post-Translational; Proto-Oncogene Proteins c-akt; Pyrazoles; Recombinant Fusion Proteins; Sulfonamides	2006

Article

Year

Involvement of mitochondrial and Akt signaling pathways in augmented apoptosis induced by a combination of low doses of celecoxib and N-(4-hydroxyphenyl) retinamide in premalignant human bronchial epithelial cells.

Cancer research, 2006, Oct-01, Volume: 66, Issue:19

Celecoxib is being evaluated as a chemopreventive agent. However, its mechanism of action is not clear because high doses were used for in vitro studies to obtain antitumor effects. We found that celecoxib inhibited the growth of premalignant and malignant human bronchial epithelial cells with IC(50) values between 8.9 and 32.7 micromol/L, irrespective of cyclooxygenase-2 (COX-2) expression. Normal human bronchial epithelial cells were less sensitive to celecoxib. Because these concentrations were higher than those attainable in vivo (

Topics: Anticarcinogenic Agents; Apoptosis; Bronchi; Bronchial Diseases; Celecoxib; Cell Line, Tumor; Cells, Cultured; Cyclooxygenase 2 Inhibitors; Drug Screening Assays, Antitumor; Drug Synergism; Epithelial Cells; Fenretinide; Humans; Lung Neoplasms; Mitochondria; Phosphorylation; Precancerous Conditions; Protein Processing, Post-Translational; Proto-Oncogene Proteins c-akt; Pyrazoles; Recombinant Fusion Proteins; Sulfonamides

2006