Decitabine and suberoylanilide hydroxamic acid (SAHA) inhibit growth of ovarian cancer cell lines and xenografts while inducing expression of imprinted tumor suppressor genes, apoptosis, G2/M arrest, and autophagy.
about
Therapeutic interactions of autophagy with radiation and temozolomide in glioblastoma: evidence and issues to resolveGenetic and epigenetic heterogeneity of epithelial ovarian cancer and the clinical implications for molecular targeted therapyDNA demethylation and invasive cancer: implications for therapeuticsUme6 transcription factor is part of a signaling cascade that regulates autophagy.Oncogenic potential of yin yang 1 mediated through control of imprinted genesDecitabine and vorinostat cooperate to sensitize colon carcinoma cells to Fas ligand-induced apoptosis in vitro and tumor suppression in vivoProlonged treatment with DNMT inhibitors induces distinct effects in promoters and gene-bodiesPeg3 mutational effects on reproduction and placenta-specific gene familiesSuberoylanilide hydroxamic acid increases anti-cancer effect of tumor necrosis factor-α through up-regulation of TNF receptor 1 in lung cancer cellsHistones and their modifications in ovarian cancer - drivers of disease and therapeutic targets.ARHI (DIRAS3) induces autophagy in ovarian cancer cells by downregulating the epidermal growth factor receptor, inhibiting PI3K and Ras/MAP signaling and activating the FOXo3a-mediated induction of Rab7Regulation and function of the peg3 imprinted domain.Augmenting antitumor immune responses with epigenetic modifying agents.Suberoylanilide hydroxamic acid treatment reveals crosstalks among proteome, ubiquitylome and acetylome in non-small cell lung cancer A549 cell lineDecitabine inhibits the cell growth of cholangiocarcinoma in cultured cell lines and mouse xenografts.HDAC Family Members Intertwined in the Regulation of Autophagy: A Druggable Vulnerability in Aggressive Tumor Entities.In vivo efficacy of the histone deacetylase inhibitor suberoylanilide hydroxamic acid in combination with radiotherapy in a malignant rhabdoid tumor mouse model.Vorinostat approved in Japan for treatment of cutaneous T-cell lymphomas: status and prospects.Phylogenetic and Epigenetic Footprinting of the Putative Enhancers of the Peg3 Domain.A unique histone deacetylase inhibitor alters microRNA expression and signal transduction in chemoresistant ovarian cancer cellsSex and Tissue Specificity of Peg3 Promoters.Autophagy and lysosomal related protein expression patterns in human glioblastoma.Quantitative Analysis of Global Proteome and Lysine Acetylome Reveal the Differential Impacts of VPA and SAHA on HL60 CellsEnhanced inhibition of clonogenic survival of human medulloblastoma cells by multimodal treatment with ionizing irradiation, epigenetic modifiers, and differentiation-inducing drugsExpression and epigenetic regulation of angiogenesis-related factors during dormancy and recurrent growth of ovarian carcinomaHistone deacetylase inhibition blunts ischemia/reperfusion injury by inducing cardiomyocyte autophagy.Targeting the epigenome in ovarian cancer.Specific changes in the expression of imprinted genes in prostate cancer--implications for cancer progression and epigenetic regulation.Immunotherapy of cancer: reprogramming tumor-immune crosstalk.Involvement of autophagy in cervical, endometrial and ovarian cancer.The protein restriction mimetic Resveratrol is an autophagy inducer stronger than amino acid starvation in ovarian cancer cells.Histone Deacetylase Inhibitors as Anticancer Drugs.Ribosomal S6 kinase 4 (RSK4) expression in ovarian tumors and its regulation by antineoplastic drugs in ovarian cancer cell lines.Effects of suberoylanilide hydroxamic acid (SAHA) combined with paclitaxel (PTX) on paclitaxel-resistant ovarian cancer cells and insights into the underlying mechanisms.Histone Deacetylase (HDAC) Inhibition Induces IκB Kinase (IKK)-dependent Interleukin-8/CXCL8 Expression in Ovarian Cancer Cells.Combined treatment with low concentrations of decitabine and SAHA causes cell death in leukemic cell lines but not in normal peripheral blood lymphocytesBasic nuclear processes affected by histone acetyltransferases and histone deacetylase inhibitors.Inhibitory effects of epigenetic modulators and differentiation inducers on human medulloblastoma cell lines.Effect of ARHI on lung cancer cell proliferation, apoptosis and invasion in vitro.Effects of ARHI on cell cycle progression and apoptosis levels of breast cancer cells.
P2860
Q26764947-C4F0ECD3-2614-4473-8DED-E267A9560E42Q26769604-9C01C79C-B364-4795-A541-9070307B581BQ27011914-65B6D23A-98FC-4926-AD6D-6DA48C370FC1Q27932364-387685C9-F506-4C3A-8D1D-BEB442FB9B91Q28257555-94D5B1F4-1F02-4409-ABDC-B66072B68A29Q28263221-15DD8141-F717-4A89-98E1-6A3D74D23EA4Q28535153-DC84E147-374C-4E03-845B-888FE9BD769EQ28593550-2F6DAD5C-13AC-4E0E-B24A-84A2120B9885Q33566645-A7AF79AE-5824-4B12-8215-4556D178C11FQ33741828-A8484441-B7B2-4E2E-84A4-FD0B82C08286Q33858449-570A4E89-EAF9-4009-AAF6-781708BDC7ACQ34335413-B9BE7785-166D-411C-9F47-77C3687DB647Q35048054-712132E9-6C52-477B-BD9B-EB77E729D63DQ35232590-AB769C9D-95F4-42CE-BB43-11F3FA7874D3Q35311768-C2A36919-9BEF-4BCE-A965-24D0CED3C6BFQ35824343-6638B9E2-49F8-4C0E-A858-FBFA83879BC3Q35927871-EB62223A-E568-406B-8D09-D34ED53C651EQ35939690-F79B4675-9B06-4288-9372-458E9B5342EDQ35996810-105EC1B1-DC1A-4C56-A9CF-C52BCB356C30Q36129967-6BE45F13-2B03-470B-90DA-B427B6577702Q36154951-1333980B-3CD1-4164-95B0-E397BF0D97AFQ36214533-B8439045-4010-4B76-BE83-9F466C0AE51AQ36517161-6DCA6774-6F98-44DA-8E54-3A121F62F2CBQ37018003-401D7FDF-7D16-4B0E-9A8C-28ABCF40EB57Q37600920-07516001-B05F-4AB1-BAC4-63863085D6E9Q37700043-1BB78431-7C45-4192-B50F-6B35FDDD94D0Q37984122-5DD0B563-6EC8-4EDF-9B14-82F1244C3CAFQ37988364-4C9630B6-B7C0-409D-83EE-113D9EDD294CQ38055479-31A914EF-2E4F-40D3-80F0-22144AB8B207Q38152325-8F4C1533-AE69-4500-8E65-B49467414835Q38600885-38962462-A6F6-4A02-8A86-3D1F981B487FQ38696932-929358E9-29B5-46D3-BE25-C5BBE8D60B0BQ38806399-F7E68F0B-3F02-42FD-8FF0-DB32A2866710Q38924713-C5F2D1E6-29AF-4A62-86F7-AA4285CC3910Q38975491-B0FB56FB-27C3-49C8-9C21-BA89FDCAB281Q39100888-8BF32D0D-6564-411D-95F1-0A2E08EAB4B4Q39118730-C2AC1211-EB93-43EB-885B-83449774CCFFQ39152245-32E1EBDD-2ED8-4D41-8601-88E27C4CFEB7Q39224666-C41F6B1A-44FF-4B5D-B460-84CDC7D6C98BQ39359785-1C45F43D-AE1E-4897-B98F-6250E30E4A97
P2860
Decitabine and suberoylanilide hydroxamic acid (SAHA) inhibit growth of ovarian cancer cell lines and xenografts while inducing expression of imprinted tumor suppressor genes, apoptosis, G2/M arrest, and autophagy.
description
2011 nî lūn-bûn
@nan
2011 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած
@hyw
2011 թվականի հոտեմբերին հրատարակված գիտական հոդված
@hy
2011年の論文
@ja
2011年論文
@yue
2011年論文
@zh-hant
2011年論文
@zh-hk
2011年論文
@zh-mo
2011年論文
@zh-tw
2011年论文
@wuu
name
Decitabine and suberoylanilide ...... s, G2/M arrest, and autophagy.
@ast
Decitabine and suberoylanilide ...... s, G2/M arrest, and autophagy.
@en
type
label
Decitabine and suberoylanilide ...... s, G2/M arrest, and autophagy.
@ast
Decitabine and suberoylanilide ...... s, G2/M arrest, and autophagy.
@en
prefLabel
Decitabine and suberoylanilide ...... s, G2/M arrest, and autophagy.
@ast
Decitabine and suberoylanilide ...... s, G2/M arrest, and autophagy.
@en
P2093
P2860
P921
P356
P1433
P1476
Decitabine and suberoylanilide ...... s, G2/M arrest, and autophagy.
@en
P2093
Ahmed Ashour Ahmed
Gary L Rosner
Michele N Washington
Min-Yu Chen
Violeta Hennessey
Warren S-L Liao
William G Bornmann
P2860
P304
P356
10.1002/CNCR.26073
P407
P577
2011-10-01T00:00:00Z