Sentences with phrase «myeloma growth»

The researchers believe that these small changes could drive the key shifts in the bone marrow required to support myeloma growth.

Not exact matches

Uncontrolled growth of these cells leads to anemia, bone pain, kidney problems, Gaucher disease, and myeloma.

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.

«Taken together, these results support the hypothesis that multiple myeloma cells express bone - related genes in a Runx2 - dependent fashion that mimics bone marrow resident cells and likely contributes to tumor survival and growth in the bone microenvironment,» Yang and colleagues wrote in the paper.

Little research into multiple myeloma examines varying patient weight to see how cells encourage cancer growth.

«We know multiple myeloma cells will anchor into bone marrow, and fat cells in the bone marrow will support the growth and spread of the cancer.

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.

Multiple myeloma is a cancer of plasma cells in the blood that causes tumor growths in bone marrow.

Bradner and Mitsiades had reported in Cell in 2011 that the inhibitor blocks the Myc cancer gene and thereby slows the growth of multiple myeloma tumors in mice.

Here, we are focusing on the regulation of the cell cycle that seems to prevent clonal growth of premalignant stages compared to active myeloma.

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.

Your veterinarian will need to determine what type of growth it is, as well as rule out multiple myelomas.