Sentences with phrase «of decitabine»

Both in vitro and in vivo, the combination of decitabine and chidamide induced apoptosis of Jurkat cells bearing the KMT2D mutant.

It is a continuation of previous research, published in 2011, that focused on the effect of decitabine on glioblastoma human cell cultures.

Not exact matches

Dr. Rassool says that a clinical trial is planned to test whether low doses of a DNMT inhibitor, decitabine, and an investigational PARP inhibitor, talazoparib, can be safely combined and whether this therapy shows efficacy for AML patients, especially those who can not receive intensive chemotherapy, whose leukemia is resistant to treatment, or who have experienced a relapse after treatment.

DMNT inhibitors, such as 5 - azacytidine and decitabine, boost the interactions of PARP inhibitors to block these proteins even further, causing cancer cell death, the researchers found.

New findings published in the Proceedings of the National Academy of Sciences showed in lab studies that supplementing an epigenetic cancer drug called decitabine with vitamin C enhanced the drug's ability to impede cancer cell growth and trigger cellular self - destruction in cancer cell lines.

Decitabine is approved by the U.S. Food and Drug Administration to treat myelodysplastic syndromes and leukemia, and for use in clinical trials for several types of solid - tumour cancers including colorectal.

Dr. De Carvalho says: «Another important implication of our finding is that since decitabine induces an anti-viral response, which is highly immunogenic, it may be useful to combine this agent with immune therapy to further advance personalized cancer medicine by boosting an individual's natural defenses to fight disease.

A study led by UCLA's Drs. Robert Prins and Linda Liau, both UCLA Jonsson Comprehensive Cancer Center members, looked at the impact of a combined treatment using a chemotherapy drug called decitabine and genetically modified immune cells or T cell immunotherapy.

A new study demonstrates that it is possible to vaccinate patients with MDS against a decitabine - induced antigen and that the level of induced expression is sufficient to trigger cytotoxicity in patient - derived vaccine - induced T cells.

In vitro, Jurkat cells bearing the KMT2D V5486M or EP300 H1377R mutant were treated with different concentrations of chidamide and / or the hypomethylating agent decitabine for 48 h.

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.

HDAC inhibitors and decitabine are highly synergistic and associated with unique gene - expression and epigenetic profiles in models of DLBCL

The tumors formed in mice co-treated with chidamide and decitabine were significantly smaller than those that formed in untreated animals or those treated with the single agents, starting from 15 days of treatment (Figure 4C, left panel), as visualized by 18F - fluorodeoxyglucose small - animal positron emission tomography — computed tomography at 21 days of treatment (Figure 4C, right panel).

The group of promoters, whose H3K4me3 levels were affected by combined chidamide and decitabine treatment, but not by either chidamide or decitabine treatment alone, was enriched with binding site motifs for PU.1, a transcription factor that activates gene expression during myeloid and B - cell lymphoid cell development15, 16 (Figure 5C).

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.

Mechanistically, decitabine acted synergistically with chidamide to enhance the interaction of KMT2D with transcription factor PU.1, regulated H3K4me - associated signaling pathways, and sensitized T - lymphoma cells to chidamide.

Chip - seq and RNA sequencing data of KMT2D - mutated T - lymphoma cells treated with chidamide and / or decitabine.

Accordingly, p - ERK upregulation was observed not only in tumor samples of PTCL - NOS patients with KMT2D mutations, but also in those of xenografted T - lymphoma mice bearing KMT2D V5486M mutants, the latter being inhibited by combined treatment with chidamide and decitabine (Figure 5F, G).