«But our findings show that obesity can now be defined as a risk factor for developing multiple
myeloma through this condition,» said the study's first author, Su - Hsin Chang, PhD, an assistant professor of surgery in the Division of Public Health Sciences at Washington University.
Not exact matches
The antihelmintic flubendazole inhibits microtubule function
through a mechanism distinct from Vinca alkaloids and displays preclinical activity in leukemia and
myeloma.
This enhances the immune response
through multiple mechanisms: by attaching to the
myeloma cells, it marks them for destruction, and by attaching to the NK cells, it primes the immune cells to search for and attack the
myeloma cells.
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.
In addition, a growing number of immunotherapy clinical trials are in place to test this groundbreaking approach on other cancers like lymphoma, multiple
myeloma, and for solid tumors,
through trials in glioblastoma, mesothelioma, and ovarian and pancreatic cancer.