The researchers also tested a Runx2 knock - down variant of a human multiple
myeloma cell line and found that it produced significantly less tumor growth in immunodeficient mice than the original human multiple myeloma cells.
sorafenib induces cell death in human
myeloma cell lines in a laboratory environment by preventing a certain kind of protein - level activity, an effect that also was achieved when the myeloma cells had developed a resistance to
Not exact matches
They fused mouse B
cells — antibody - producing
cells of the immune system — with human
myeloma (also known as B
cell cancer)
cell lines in a new technique called hybridoma technology.
This is in accordance with previous reports that decitabine and 5 - azacytidine produce a marked synergistic effect in combination with suberoylanilide hydroxamic acid and romidepsin in T - lymphoma
cell lines by modulating
cell cycle arrest and apoptosis.26, 27 As a mechanism of action, KMT2D mutations of B - lymphoma
cells promote malignant outgrowth by perturbing methylation of H3K4 that affect the JAK - STAT, Toll - like receptor, or B -
cell receptor pathway.28, 29 Here our study indicated that dual treatment with chidamide and decitabine enhanced the interaction of KMT2D with the transcription factor PU.1, thereby inactivating the H3K4me - associated signaling pathway MAPK, which is constitutively activated in T -
cell lymphoma.13, 30,31 The transcription factor PU.1 is involved in the development of all hematopoietic lineages32 and regulates lymphoid
cell growth and transformation.33 Aberrant PU.1 expression promotes acute myeloid leukemia and is related to the pathogenesis of multiple
myeloma via the MAPK pathway.34, 35 On the other hand, PU.1 is also shown to interact with chromatin remodeler and DNA methyltransferease to control hematopoiesis and suppress leukemia.36 Our data thus suggested that the combined action of chidamide and decitabine may interfere with the differentiation and / or viability of PTCL - NOS through a PU.1 - dependent gene expression program.
ONC201 demonstrated (GI50 1 - 8 µM) dose - and time - dependent efficacy in acute myeloid leukemia (AML), acute lymphoblastic leukemia (ALL), chronic myelogenous leukemia (CML), chronic lymphocytic leukemia (CLL), diffuse large B -
cell lymphoma (DLBCL), mantle
cell lymphoma (MCL), Burkitt's lymphoma, anaplastic large
cell lymphoma (ALCL), cutaneous T -
cell lymphoma (CTCL), Hodgkin's lymphoma (nodular sclerosis) and multiple
myeloma (MM)
cell lines including
cells resistant to standard of care (dexamethasone in MM) and primary samples.