Connectivity mapping identifies HDAC inhibitors for the treatment of t(4;11)-positive infant acute lymphoblastic leukemia.
about
Systematic chemical and molecular profiling of MLL-rearranged infant acute lymphoblastic leukemia reveals efficacy of romidepsinChromatin modifications as therapeutic targets in MLL-rearranged leukemia.Genetic methylation and lymphoid malignancies: biomarkers of tumor progression and targeted therapy.Novel agents for the treatment of childhood acute leukemia.Epigenetic reprogramming reverses the relapse-specific gene expression signature and restores chemosensitivity in childhood B-lymphoblastic leukemia.Disease-drug pairs revealed by computational genomic connectivity mapping on GBA1 deficient, Gaucher disease mice.Collaborative Efforts Driving Progress in Pediatric Acute Myeloid Leukemia.Treatment of infant leukemias: challenge and promise.The genomic landscape of breast cancer as a therapeutic roadmapMLL-Rearranged Leukemias-An Update on Science and Clinical Approaches.c-Myc suppresses miR-451⊣YWTAZ/AKT axis via recruiting HDAC3 in acute myeloid leukemia.The evolution of clinical trials for infant acute lymphoblastic leukemia.SIAH proteins: critical roles in leukemogenesis.In focus: MLL-rearranged leukemia.RUNX1 meets MLL: epigenetic regulation of hematopoiesis by two leukemia genes.Epigenetic regulation of cell signaling pathways in acute lymphoblastic leukemia.Histone deacetylases and their inhibitors in cancer, neurological diseases and immune disorders.Novel methods and approaches to acute lymphoblastic leukemia drug discovery.The HDAC inhibitor panobinostat (LBH589) exerts in vivo anti-leukaemic activity against MLL-rearranged acute lymphoblastic leukaemia and involves the RNF20/RNF40/WAC-H2B ubiquitination axis.How do tumor cells respond to HDAC inhibition?Selective Inhibition of HDAC1 and HDAC2 as a Potential Therapeutic Option for B-ALL.The development of targeted new agents to improve the outcome for children with leukemia.Gene expression signature-based approach identifies a pro-resolving mechanism of action for histone deacetylase inhibitors.AF4 and AF4-MLL mediate transcriptional elongation of 5-lipoxygenase mRNA by 1, 25-dihydroxyvitamin D3Inhibition of class I HDACs abrogates the dominant effect of MLL-AF4 by activation of wild-type MLL.Entinostat prevents leukemia maintenance in a collaborating oncogene-dependent model of cytogenetically normal acute myeloid leukemia.The histone deacetylase inhibitor givinostat (ITF2357) exhibits potent anti-tumor activity against CRLF2-rearranged BCP-ALL.Outcome of relapsed infant acute lymphoblastic leukemia treated on the interfant-99 protocol.Childhood relapsed acute lymphoblastic leukemia: Biology and recent treatment progress.
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P2860
Connectivity mapping identifies HDAC inhibitors for the treatment of t(4;11)-positive infant acute lymphoblastic leukemia.
description
2011 nî lūn-bûn
@nan
2011年の論文
@ja
2011年学术文章
@wuu
2011年学术文章
@zh
2011年学术文章
@zh-cn
2011年学术文章
@zh-hans
2011年学术文章
@zh-my
2011年学术文章
@zh-sg
2011年學術文章
@yue
2011年學術文章
@zh-hant
name
Connectivity mapping identifies HDAC inhibitors for the treatment of t
@nl
Connectivity mapping identifie ...... acute lymphoblastic leukemia.
@en
type
label
Connectivity mapping identifies HDAC inhibitors for the treatment of t
@nl
Connectivity mapping identifie ...... acute lymphoblastic leukemia.
@en
prefLabel
Connectivity mapping identifies HDAC inhibitors for the treatment of t
@nl
Connectivity mapping identifie ...... acute lymphoblastic leukemia.
@en
P2093
P2860
P356
P1433
P1476
Connectivity mapping identifie ...... acute lymphoblastic leukemia.
@en
P2093
D J P M Stumpel
O Williams
P Schneider
P2860
P2888
P304
P356
10.1038/LEU.2011.278
P577
2011-10-21T00:00:00Z
P6179
1045480274