Analysis of the apoptotic and therapeutic activities of histone deacetylase inhibitors by using a mouse model of B cell lymphoma
about
New and emerging HDAC inhibitors for cancer treatmentRomidepsin in peripheral and cutaneous T-cell lymphoma: mechanistic implications from clinical and correlative dataIn Vitro and In Vivo Anti-tumoral Effects of the Flavonoid Apigenin in Malignant Mesothelioma.BET and HDAC inhibitors induce similar genes and biological effects and synergize to kill in Myc-induced murine lymphomaHistone deacetylase inhibitor (HDACI) mechanisms of action: emerging insights.An Integrated Genetic-Genomic Approach for the Identification of Novel Cancer Loci in Mice Sensitized to c-Myc-Induced Apoptosis.Histone Deacetylase Inhibitors: Advancing Therapeutic Strategies in Hematological and Solid Malignancies.Systematic analysis of time-series gene expression data on tumor cell-selective apoptotic responses to HDAC inhibitors.Targeting histone deacetyalses in the treatment of B- and T-cell malignancies.Maximal killing of lymphoma cells by DNA damage-inducing therapy requires not only the p53 targets Puma and Noxa, but also BimUtilization of the Eμ-Myc mouse to model heterogeneity of therapeutic response.Eradication of solid tumors using histone deacetylase inhibitors combined with immune-stimulating antibodies.Differentiation therapy for the treatment of t(8;21) acute myeloid leukemia using histone deacetylase inhibitorsA mammalian functional-genetic approach to characterizing cancer therapeutics.Myelodysplastic syndrome and histone deacetylase inhibitors: "to be or not to be acetylated"?The histone deacetylase inhibitor SAHA sensitizes acute myeloid leukemia cells to a combination of nucleoside analogs and the DNA-alkylating agent busulfan.Genome-wide functional genomic and transcriptomic analyses for genes regulating sensitivity to vorinostat.SAHA shows preferential cytotoxicity in mutant p53 cancer cells by destabilizing mutant p53 through inhibition of the HDAC6-Hsp90 chaperone axis.The histone deacetylase inhibitor entinostat (SNDX-275) induces apoptosis in Hodgkin lymphoma cells and synergizes with Bcl-2 family inhibitors.NKT cell-targeted vaccination plus anti-4-1BB antibody generates persistent CD8 T cell immunity against B cell lymphoma.Suppression of B-cell lymphomagenesis by the BH3-only proteins Bmf and Bad.Novel HDAC inhibitors exhibit pre-clinical efficacy in lymphoma models and point to the importance of CDKN1A expression levels in mediating their anti-tumor responseDevelopment of a castrate resistant transplant tumor model of prostate cancerDefective cell death signalling along the Bcl-2 regulated apoptosis pathway compromises Treg cell development and limits their functionality in miceBH3-only proteins in apoptosis at a glanceA genome scale RNAi screen identifies GLI1 as a novel gene regulating vorinostat sensitivity.The BCL-2 protein family, BH3-mimetics and cancer therapy.The histone deacetylase inhibitors LAQ824 and LBH589 do not require death receptor signaling or a functional apoptosome to mediate tumor cell death or therapeutic efficacy.Small molecule obatoclax (GX15-070) antagonizes MCL-1 and overcomes MCL-1-mediated resistance to apoptosis.Functional-genetic dissection of HDAC dependencies in mouse lymphoid and myeloid malignancies.Selective inhibition of HDAC8 decreases neuroblastoma growth in vitro and in vivo and enhances retinoic acid-mediated differentiation.Combination of glycolysis inhibition with chemotherapy results in an antitumor immune response.The mTORC1 inhibitor everolimus prevents and treats Eμ-Myc lymphoma by restoring oncogene-induced senescence.NKT cell adjuvant-based tumor vaccine for treatment of myc oncogene-driven mouse B-cell lymphoma.Combined inhibition of PI3K-related DNA damage response kinases and mTORC1 induces apoptosis in MYC-driven B-cell lymphomasDirect reprogramming of human fibroblasts into sweat gland-like cellsVorinostat synergistically potentiates MK-0457 lethality in chronic myelogenous leukemia cells sensitive and resistant to imatinib mesylate.Combination therapy of established cancer using a histone deacetylase inhibitor and a TRAIL receptor agonist.The SMAC mimetic, LCL-161, reduces survival in aggressive MYC-driven lymphoma while promoting susceptibility to endotoxic shock.MAPK pathway activation leads to Bim loss and histone deacetylase inhibitor resistance: rationale to combine romidepsin with an MEK inhibitor.
P2860
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P2860
Analysis of the apoptotic and therapeutic activities of histone deacetylase inhibitors by using a mouse model of B cell lymphoma
description
2007 nî lūn-bûn
@nan
2007年の論文
@ja
2007年論文
@yue
2007年論文
@zh-hant
2007年論文
@zh-hk
2007年論文
@zh-mo
2007年論文
@zh-tw
2007年论文
@wuu
2007年论文
@zh
2007年论文
@zh-cn
name
Analysis of the apoptotic and ...... mouse model of B cell lymphoma
@ast
Analysis of the apoptotic and ...... mouse model of B cell lymphoma
@en
type
label
Analysis of the apoptotic and ...... mouse model of B cell lymphoma
@ast
Analysis of the apoptotic and ...... mouse model of B cell lymphoma
@en
prefLabel
Analysis of the apoptotic and ...... mouse model of B cell lymphoma
@ast
Analysis of the apoptotic and ...... mouse model of B cell lymphoma
@en
P2093
P2860
P50
P356
P1476
Analysis of the apoptotic and ...... mouse model of B cell lymphoma
@en
P2093
A P Wiegmans
K F Whitecross
Paul A Marks
P2860
P304
P356
10.1073/PNAS.0702294104
P407
P577
2007-04-30T00:00:00Z