laq824 and Blast-Crisis

laq824 has been researched along with Blast-Crisis* in 1 studies

Other Studies

1 other study(ies) available for laq824 and Blast-Crisis

Article	Year
Histone deacetylase inhibitor LAQ824 both lowers expression and promotes proteasomal degradation of Bcr-Abl and induces apoptosis of imatinib mesylate-sensitive or -refractory chronic myelogenous leukemia-blast crisis cells. Cancer research, 2003, Aug-15, Volume: 63, Issue:16 Treatment with LAQ824 (Novartis Pharmaceutical, Inc.), a cinnamyl hydroxamic acid analogue inhibitor of histone deacetylases, depleted the mRNA and protein expression of Bcr-Abl in human chronic myeloid leukemia blast crisis (CML-BC) cells. Exposure to LAQ824 induced the expression of the cell cycle-dependent kinase inhibitors p21 and p27 and caused cell cycle G(1)-phase accumulation and apoptosis of CML-BC cells. LAQ824 also induced acetylation of heat shock protein 90. This inhibited the chaperone association of Bcr-Abl with heat shock protein 90, thereby promoting the proteasomal degradation of Bcr-Abl. Cotreatment with LAQ824 increased imatinib mesylate-induced apoptosis of CML-BC cells. Additionally, LAQ824 down-regulated the levels of mutant Bcr-Abl possessing the T315I point mutation, as well as induced apoptosis of imatinib-refractory primary CML-BC cells. Therefore, LAQ824 may be a promising therapeutic agent in the treatment of imatinib-sensitive or -refractory human leukemia. Topics: Acetylation; Antineoplastic Agents; Apoptosis; Benzamides; Blast Crisis; Cyclin-Dependent Kinase Inhibitor p21; Cyclins; Cysteine Endopeptidases; Drug Resistance, Neoplasm; Enzyme Inhibitors; Fusion Proteins, bcr-abl; G1 Phase; Histone Deacetylase Inhibitors; Humans; Hydroxamic Acids; Imatinib Mesylate; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Microfilament Proteins; Multienzyme Complexes; Muscle Proteins; Piperazines; Promoter Regions, Genetic; Proteasome Endopeptidase Complex; Pyridones; Pyrimidines; Tumor Cells, Cultured	2003

Article

Year

Histone deacetylase inhibitor LAQ824 both lowers expression and promotes proteasomal degradation of Bcr-Abl and induces apoptosis of imatinib mesylate-sensitive or -refractory chronic myelogenous leukemia-blast crisis cells.

Cancer research, 2003, Aug-15, Volume: 63, Issue:16

Treatment with LAQ824 (Novartis Pharmaceutical, Inc.), a cinnamyl hydroxamic acid analogue inhibitor of histone deacetylases, depleted the mRNA and protein expression of Bcr-Abl in human chronic myeloid leukemia blast crisis (CML-BC) cells. Exposure to LAQ824 induced the expression of the cell cycle-dependent kinase inhibitors p21 and p27 and caused cell cycle G(1)-phase accumulation and apoptosis of CML-BC cells. LAQ824 also induced acetylation of heat shock protein 90. This inhibited the chaperone association of Bcr-Abl with heat shock protein 90, thereby promoting the proteasomal degradation of Bcr-Abl. Cotreatment with LAQ824 increased imatinib mesylate-induced apoptosis of CML-BC cells. Additionally, LAQ824 down-regulated the levels of mutant Bcr-Abl possessing the T315I point mutation, as well as induced apoptosis of imatinib-refractory primary CML-BC cells. Therefore, LAQ824 may be a promising therapeutic agent in the treatment of imatinib-sensitive or -refractory human leukemia.

Topics: Acetylation; Antineoplastic Agents; Apoptosis; Benzamides; Blast Crisis; Cyclin-Dependent Kinase Inhibitor p21; Cyclins; Cysteine Endopeptidases; Drug Resistance, Neoplasm; Enzyme Inhibitors; Fusion Proteins, bcr-abl; G1 Phase; Histone Deacetylase Inhibitors; Humans; Hydroxamic Acids; Imatinib Mesylate; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Microfilament Proteins; Multienzyme Complexes; Muscle Proteins; Piperazines; Promoter Regions, Genetic; Proteasome Endopeptidase Complex; Pyridones; Pyrimidines; Tumor Cells, Cultured

2003