bay-11-7082 and Precursor-T-Cell-Lymphoblastic-Leukemia-Lymphoma

bay-11-7082 has been researched along with Precursor-T-Cell-Lymphoblastic-Leukemia-Lymphoma* in 2 studies

Other Studies

2 other study(ies) available for bay-11-7082 and Precursor-T-Cell-Lymphoblastic-Leukemia-Lymphoma

Article	Year
Rapid childhood T-ALL growth in xenograft models correlates with mature phenotype and NF-κB pathway activation but not with poor prognosis. Leukemia, 2015, Volume: 29, Issue:4 Topics: Adolescent; Animals; Antineoplastic Agents; Apoptosis; Cell Cycle; Child; Coculture Techniques; Gene Expression Regulation, Neoplastic; Graft Survival; Humans; Mice; Mice, SCID; NF-kappa B; Nitriles; Oncogene Proteins, Fusion; Phenotype; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma; Prognosis; Signal Transduction; Stromal Cells; Sulfones; T-Lymphocytes; Transplantation, Heterologous; Xenograft Model Antitumor Assays; Young Adult	2015
The synergistic repressive effect of NF-κB and JNK inhibitor on the clonogenic capacity of Jurkat leukemia cells. PloS one, 2014, Volume: 9, Issue:12 Deregulation of Nuclear Transcription Factor-κB (NF-κB) and Jun N-terminal kinase (JNK) signaling is commonly detected in leukemia, suggesting an important role for these two signaling pathways in the pathogenesis of leukemia. In this study, using Jurkat cells, an acute T-lymphoblastic leukemia (T-ALL) cell line, we evaluated the effects of an NF-κB inhibitor and a JNK inhibitor individually and in combination on the proliferation, survival and clonogenic capacity of leukemic cells. We found that leukemic stem/progenitor cells (LSPCs) were more sensitive to NF-κB inhibitor treatment than were healthy hematopoietic stem/progenitor cells (HSPCs), as shown by a reduction in the clonogenic capacity of the former. Inactivation of NF-κB leads to the activation of JNK signaling in both leukemic cells and healthy HSPCs. Interestingly, JNK inhibitor treatment enhanced the repressive effects of NF-κB inhibitor on LSPCs but prevented such repression in HSPCs. Our data suggest that JNK signaling stimulates proliferation/survival in LSPCs but is a death signal in HSPCs. The combination of NF-κB inhibitor and JNK inhibitor might provide a better treatment for T-ALL leukemia by synergistically killing LSPCs while simultaneously preventing the death of normal HPCs. Topics: Anthracenes; Cell Proliferation; Cell Survival; Cells, Cultured; Drug Synergism; Gene Expression Regulation, Neoplastic; Hematopoietic Stem Cells; Humans; Jurkat Cells; MAP Kinase Signaling System; NF-kappa B; Nitriles; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma; Sulfones	2014

Article

Year

Rapid childhood T-ALL growth in xenograft models correlates with mature phenotype and NF-κB pathway activation but not with poor prognosis.

Leukemia, 2015, Volume: 29, Issue:4

Topics: Adolescent; Animals; Antineoplastic Agents; Apoptosis; Cell Cycle; Child; Coculture Techniques; Gene Expression Regulation, Neoplastic; Graft Survival; Humans; Mice; Mice, SCID; NF-kappa B; Nitriles; Oncogene Proteins, Fusion; Phenotype; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma; Prognosis; Signal Transduction; Stromal Cells; Sulfones; T-Lymphocytes; Transplantation, Heterologous; Xenograft Model Antitumor Assays; Young Adult

2015

The synergistic repressive effect of NF-κB and JNK inhibitor on the clonogenic capacity of Jurkat leukemia cells.

PloS one, 2014, Volume: 9, Issue:12

Deregulation of Nuclear Transcription Factor-κB (NF-κB) and Jun N-terminal kinase (JNK) signaling is commonly detected in leukemia, suggesting an important role for these two signaling pathways in the pathogenesis of leukemia. In this study, using Jurkat cells, an acute T-lymphoblastic leukemia (T-ALL) cell line, we evaluated the effects of an NF-κB inhibitor and a JNK inhibitor individually and in combination on the proliferation, survival and clonogenic capacity of leukemic cells. We found that leukemic stem/progenitor cells (LSPCs) were more sensitive to NF-κB inhibitor treatment than were healthy hematopoietic stem/progenitor cells (HSPCs), as shown by a reduction in the clonogenic capacity of the former. Inactivation of NF-κB leads to the activation of JNK signaling in both leukemic cells and healthy HSPCs. Interestingly, JNK inhibitor treatment enhanced the repressive effects of NF-κB inhibitor on LSPCs but prevented such repression in HSPCs. Our data suggest that JNK signaling stimulates proliferation/survival in LSPCs but is a death signal in HSPCs. The combination of NF-κB inhibitor and JNK inhibitor might provide a better treatment for T-ALL leukemia by synergistically killing LSPCs while simultaneously preventing the death of normal HPCs.

Topics: Anthracenes; Cell Proliferation; Cell Survival; Cells, Cultured; Drug Synergism; Gene Expression Regulation, Neoplastic; Hematopoietic Stem Cells; Humans; Jurkat Cells; MAP Kinase Signaling System; NF-kappa B; Nitriles; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma; Sulfones

2014