Sentences with phrase «myeloid lymphoma»

The biotech received Food and Drug Administration (FDA) approval for its drug to treat the rare blood cancer acute myeloid lymphoma (AML), which will be marketed as Idhifa, on Tuesday.

Not exact matches

A National Cancer Institute long - termstudy, involving25, 619 industrial workers in 10 factories that produced or used formaldehyde, found an increased risk of death due to leukemia, particularly myeloid leukemia, and higher rates of nasal - pharynx cancer.Further examination of the same workers, with ten more years of data, continued to show a possible link to leukemia, as well as lymphoma and multiple myeloma, amongthosewiththe highest exposures.

Dr Matt Kaiser, Head of Research at Leukemia & Lymphoma Research, said: «Unfortunately there have been no significant improvements in survival rates for acute myeloid leukemia in the last two decades.

The findings of multiple in vivo preclinical studies published online in Blood Advances, a Journal of the American Society of Hematology (ASH), indicate that this therapy could potentially treat multiple cancers, including non-Hodgkin lymphoma (NHL), multiple myeloma (MM), and acute myeloid leukemia (AML).

Dr Xu showed that for BET inhibitors to successfully kill lymphoma and myeloid leukemia cells the presence of a protein called BIM, which brings on apoptosis, was critical.

About one - half (45 %) of patients were enrolled in lymphoma trials, one - quarter (24 %) in chronic myeloid leukemia (CML) trials or multiple myeloma trials (22 %), and 2 % of patients were enrolled in trials of acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS).

Mutations in IDH1 and IDH2 occur in myeloid malignancies, T - cell lymphomas, and certain solid tumors.

The study will enroll patients with acute myeloid leukemia (AML) and is supported by a $ 3.5 million investment from The Leukemia & Lymphoma Society (LLS) Therapy Acceleration Program ®.

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.

Tags: Acute Lymphoblastic Leukemia, acute myeloid leukemia, Brian Till, Cecilia Yeung, Clinical Research, Hyundai Hope on Wheels, immunotherapy, non-hodgkin lymphoma, Oliver Press, Ovarian Cancer, Pediatric Oncology, Philip D Greenberg, Transplant and Immunotherapy

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