dehydroxymethylepoxyquinomicin and Leukemia--Lymphocytic--Chronic--B-Cell

dehydroxymethylepoxyquinomicin has been researched along with Leukemia--Lymphocytic--Chronic--B-Cell* in 2 studies

Other Studies

2 other study(ies) available for dehydroxymethylepoxyquinomicin and Leukemia--Lymphocytic--Chronic--B-Cell

ArticleYear
Microenvironmental stromal cells abrogate NF-κB inhibitor-induced apoptosis in chronic lymphocytic leukemia.
    Haematologica, 2018, Volume: 103, Issue:1

    Nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB) is known to play an important role in the pathogenesis of chronic lymphocytic leukemia (CLL). Several NF-κB inhibitors were shown to successfully induce apoptosis of CLL cells

    Topics: Antineoplastic Agents; Apoptosis; Benzamides; Biomarkers; Cell Line, Tumor; Cell Survival; Coculture Techniques; Cyclohexanones; Humans; Leukemia, Lymphocytic, Chronic, B-Cell; Mesenchymal Stem Cells; NF-kappa B; RNA, Small Interfering; Signal Transduction; Tumor Microenvironment

2018
DHMEQ, a new NF-kappaB inhibitor, induces apoptosis and enhances fludarabine effects on chronic lymphocytic leukemia cells.
    Leukemia, 2006, Volume: 20, Issue:5

    Chronic lymphocytic leukemia (CLL) is a low-grade lymphoid malignancy incurable with conventional modalities of chemotherapy. Strong and constitutive nuclear factor kappa B (NF-kappaB) activation is a characteristic of CLL cells. We examined the effects of a new NF-kappaB inhibitor, dehydroxymethylepoxyquinomicin (DHMEQ), on CLL cells. Dehydroxymethylepoxyquinomicin completely abrogated constitutive NF-kappaB activity and induced apoptosis of CLL cells. Apoptosis induced by DHMEQ was accompanied by downregulation of NF-kappaB-dependent antiapoptotic genes: c-IAP, Bfl-1, Bcl-X(L) and c-FLIP. Dehydroxymethylepoxyquinomicin also inhibited NF-kappaB induced by CD40 and enhanced fludarabine-mediated apoptosis of CLL cells. Results of this study suggest that inhibition of constitutive and inducible NF-kappaB by DHMEQ in combination with fludarabine is a promising strategy for the treatment of CLL.

    Topics: Aged; Aged, 80 and over; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; bcl-X Protein; Benzamides; CASP8 and FADD-Like Apoptosis Regulating Protein; Caspases; CD40 Antigens; Cell Line, Tumor; Cell Survival; Cyclohexanones; Down-Regulation; Drug Synergism; Female; Humans; Inhibitor of Apoptosis Proteins; Intracellular Signaling Peptides and Proteins; Leukemia, Lymphocytic, Chronic, B-Cell; Male; Middle Aged; Minor Histocompatibility Antigens; NF-kappa B; Proto-Oncogene Proteins c-bcl-2; Tumor Cells, Cultured; Vidarabine

2006