Early epigenetic changes and DNA damage do not predict clinical response in an overlapping schedule of 5-azacytidine and entinostat in patients with myeloid malignancies. - Wikidata - wikimedia - TriplyDB

Early epigenetic changes and DNA damage do not predict clinical response in an overlapping schedule of 5-azacytidine and entinostat in patients with myeloid malignancies.

Early epigenetic changes and DNA damage do not predict clinical response in an overlapping schedule of 5-azacytidine and entinostat in patients with myeloid malignancies.

http://www.wikidata.org/entity/Q37372837

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Epigenetic approaches in the treatment of myelodysplastic syndromes: clinical utility of azacitidine Targeting the epigenome in lung cancer: expanding approaches to epigenetic therapy Action mechanisms of histone deacetylase inhibitors in the treatment of hematological malignancies A clinical-molecular update on azanucleoside-based therapy for the treatment of hematologic cancers Targeting epigenetic pathways in acute myeloid leukemia and myelodysplastic syndrome: a systematic review of hypomethylating agents trials New ways to use DNA methyltransferase inhibitors for the treatment of myelodysplastic syndrome Epigenetic deregulation of microRNAs in rhabdomyosarcoma and neuroblastoma and translational perspectives Trials with 'epigenetic' drugs: an update New strategies in myelodysplastic syndromes: application of molecular diagnostics to clinical practice Predicting response to epigenetic therapy DNMT3A Mutations in Acute Myeloid Leukemia Hydralazine and magnesium valproate as epigenetic treatment for myelodysplastic syndrome. Preliminary results of a phase-II trial Equitoxic doses of 5-azacytidine and 5-aza-2'deoxycytidine induce diverse immediate and overlapping heritable changes in the transcriptome Established and emerging targeted therapies in the myelodysplastic syndromes.Dual epigenetic targeting with panobinostat and azacitidine in acute myeloid leukemia and high-risk myelodysplastic syndrome Comprehensive mapping of the effects of azacitidine on DNA methylation, repressive/permissive histone marks and gene expression in primary cells from patients with MDS and MDS-related disease.Phase 2 clinical trial of 5-azacitidine, valproic acid, and all-trans retinoic acid in patients with high-risk acute myeloid leukemia or myelodysplastic syndrome.The genetics of myelodysplastic syndrome: from clonal haematopoiesis to secondary leukaemia Epigenetic therapies in MDS and AML Enhancer of zeste homolog 2 (EZH2) in pediatric soft tissue sarcomas: first implications.Promoter hypermethylation in MLL-r infant acute lymphoblastic leukemia: biology and therapeutic targeting.Histone deacetylase inhibitor (HDACI) mechanisms of action: emerging insights.Histone gammaH2AX and poly(ADP-ribose) as clinical pharmacodynamic biomarkers.Targeting DNA methylation for epigenetic therapy.Azacitidine: a review of its use in the management of myelodysplastic syndromes/acute myeloid leukaemia.Leukaemogenesis: more than mutant genes Epigenetics in clinical practice: the examples of azacitidine and decitabine in myelodysplasia and acute myeloid leukemia.Clinical development of demethylating agents in hematology Histone deacetylase (HDAC) inhibitors in recent clinical trials for cancer therapy.DNA methylation changes following 5-azacitidine treatment in patients with myelodysplastic syndrome.Hypomethylating agents and other novel strategies in myelodysplastic syndromes.5-azacytidine as salvage treatment in relapsed myeloid tumors after allogeneic bone marrow transplantation.Myelodysplastic syndrome and histone deacetylase inhibitors: "to be or not to be acetylated"?Epigenetic priming of AML blasts for all-trans retinoic acid-induced differentiation by the HDAC class-I selective inhibitor entinostat.The interaction between epigenetics, nutrition and the development of cancer Phase 1 study of epigenetic priming with decitabine prior to standard induction chemotherapy for patients with AML.Novel agents for the treatment of childhood acute leukemia.5-aza-2'-deoxycytidine activates iron uptake and heme biosynthesis by increasing c-Myc nuclear localization and binding to the E-boxes of transferrin receptor 1 (TfR1) and ferrochelatase (Fech) genes.The DNA damage mark pH2AX differentiates the cytotoxic effects of small molecule HDAC inhibitors in ovarian cancer cells Pharmacokinetics and Pharmacodynamics with Extended Dosing of CC-486 in Patients with Hematologic Malignancies.

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Early epigenetic changes and DNA damage do not predict clinical response in an overlapping schedule of 5-azacytidine and entinostat in patients with myeloid malignancies.

http://www.wikidata.org/entity/Q37372837

description

article científic

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article scientifique

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artigo científico

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bilimsel makale

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scientific article published on 22 June 2009

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vedecký článok

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vetenskaplig artikel

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vědecký článek

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name

Early epigenetic changes and D ...... nts with myeloid malignancies.

@en

Early epigenetic changes and D ...... nts with myeloid malignancies.

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type

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Early epigenetic changes and D ...... nts with myeloid malignancies.

@en

Early epigenetic changes and D ...... nts with myeloid malignancies.

@nl

prefLabel

Early epigenetic changes and D ...... nts with myeloid malignancies.

@en

Early epigenetic changes and D ...... nts with myeloid malignancies.

@nl

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Early epigenetic changes and D ...... ents with myeloid malignancies

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Allen S Yang

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Anchalee Jiemjit

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Anthony Murgo

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Chris Nasrallah

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Elizabeth A Sugar

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Hetty E Carraway

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Ibitayo Owoeye

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Igor Espinoza-Delgado

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James G Herman

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Jonathan Licht

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P2860

Methylation-specific PCR: a novel PCR assay for methylation status of CpG islands

DNA damage activates ATM through intermolecular autophosphorylation and dimer dissociation

A gene hypermethylation profile of human cancer

Synergy of demethylation and histone deacetylase inhibition in the re-expression of genes silenced in cancer

A genomic screen for genes upregulated by demethylation and histone deacetylase inhibition in human colorectal cancer.

Results of a randomized study of 3 schedules of low-dose decitabine in higher-risk myelodysplastic syndrome and chronic myelomonocytic leukemia.

Further analysis of trials with azacitidine in patients with myelodysplastic syndrome: studies 8421, 8921, and 9221 by the Cancer and Leukemia Group B.

Phase I study of decitabine alone or in combination with valproic acid in acute myeloid leukemia.

Reactivating the expression of methylation silenced genes in human cancer.

A synthetic inhibitor of histone deacetylase, MS-27-275, with marked in vivo antitumor activity against human tumors.

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2764-2773

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10.1182/BLOOD-2009-02-203547

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Melanie J. McConnell

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