Sentences with phrase «decitabine in»

When the leaderless hives received decitabine in their nectar, the worker bees became much more likely to develop ovaries and lay eggs.

Not exact matches

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.

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

Glioblastoma cells do not naturally produce NY - ESO - 1, so the drug decitabine is given prior to injecting the NY - ESO - 1 targeting T cells in order to cause the tumor cells to express the NY - ESO - 1 target.

Atrial fibrillation is associated with hypermethylation in human left atrium, and treatment with decitabine reduces atrial tachyarrhythmias in spontaneously hypertensive rats.

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.

(A) Venn diagram depicting the overlap between transcription factors bound by H3K4me3 ChIP - seq in the combination group, as compared to the chidamide (CHID)- treated group and the decitabine (DECI)- treated group in KMT2D V5486 - mutated Jurkat cells.

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

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).

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.

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).

Azacytidine and Decitabine induce gene - specific and non-random DNA demethylation in human cancer cell lines