Linked Life Data

20004792

Source:http://linkedlifedata.com/resource/pubmed/id/20004792

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2009-12-16
pubmed:abstractText
The implication of DNA hypermethylation in the pathogenesis of myelodysplastic syndromes (MDS) provides a rationale for using hypomethylating agents such as azacitidine. Growing evidence suggests that azacitidine may reverse epigenetic gene silencing at specific genomic targets. AZA-001 established azacitidine as the first agent to provide a significant overall survival benefit in MDS patients. These data confirmed that azacitidine has a progressively cumulative effect on the MDS clone and support the value of maintenance therapy. Prolonged survival was independent of achieving complete response. Azacitidine in combination with histone deacetylase inhibitors might offer better efficacy by modulating the methylation and acetylation states of silenced genes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1873-5835
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
33 Suppl 2
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
S18-21
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Hypomethylating agents in myelodysplastic syndromes changing the inevitable: the value of azacitidine as maintenance therapy, effects on transfusion and combination with other agents.
pubmed:affiliation
Division of Hematology/Oncology, Tisch Cancer Institute, Mount Sinai School of Medicine, New York, NY 10029, USA. lewis.silverman@mssm.edu
pubmed:publicationType
Journal Article