Sentences with phrase «myeloma cells produce»

Healthy plasma cells produce antibodies that fight infection in the body, but myeloma cells produce high levels of abnormal antibodies that, when the cancer cells accumulate, they crowd out production of other important blood cells, both red and white.

In mice, the Runx2 knock - in myeloma cells produced greater tumor growth and a wider spread of disease compared with the original myeloma cells; conversely, the Runx2 knock - down cells had less tumor growth and disease spread.

Not exact matches

What they produce more of, however, are fatty acids, and it is likely that myeloma cells can feed on these fatty acids.

Fat cells cultured from the body mass index of a morbidly obese patient cause multiple myeloma cells to anchor to a much greater extent than normal cells and produce a significantly larger number of blood vessels to sustain the cancer cells.

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.

In multiple myeloma, normal plasma cells transform into malignant myeloma cells and produce large quantities of toxic abnormal immunoglobulin called monoclonal protein that can damage multiple organs.

Multiple myeloma is preceded by a blood disorder called monoclonal gammopathy of undetermined significance (MGUS) in which abnormal plasma cells produce many copies of an antibody protein.

The monoclonal protein produced by the myeloma cells interferes with normal blood cell production.

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.

Multiple myeloma is a rare, malignant plasma cell cancer affecting the bone marrow and other blood producing organs.