Sentences with phrase «lymphoma cells through»

Not exact matches

Like a free pass, its presence on the surface of lymphoma cells facilitates their migration through the vessel walls between adjacent endothelial cells.

In a xenograft KMT2D - mutated T - lymphoma model, dual treatment with chidamide and decitabine significantly retarded tumor growth and induced cell apoptosis through modulation of the KMT2D / H3K4me axis.

Inhibition of histone deacetylase overcomes rapamycin - mediated resistance in diffuse large B - cell lymphoma by inhibiting Akt signaling through mTORC2.

It is well known that HDAC inhibitors are potent anticancer drugs in hematopoietic malignancies, including lymphoma.19 — 21 The aim of using HDAC inhibitors is to restore normal histone modification patterns through inhibition of various components of the epigenetic machinery.22, 23 In B - cell lymphoma, HDAC inhibitors can rescue deficits in histone acetylation induced by EP300 / CREBBP mutations, 24 rendering tumor cells more sensitive to suberoylanilide hydroxamic acid.25 This can explain why chidamide also has favorable efficacy on PTCL - NOS patients bearing EP300 / CREBBP mutations.

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, we have access to new agent trials through the Therapeutic Advances in Childhood Leukemia and Lymphoma (TACL) consortium, and we offer CAR T - cell therapy for eligible children with relapsed or refractory acute lymphoblastic leukemia (ALL).

Dr. Choy's professional interests include lymphoma, transitional cell carcinoma, localized tumor treatment with electrochemotherapy and translational cancer research through cooperative clinical trials and research projects with both local and national institutions including the Fred Hutchinson Cancer Research Center to improve patient care in both animals and their owners.

Canine Epidermotropic Lymphoma spreads through cells in the immune system.